Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

BDS 1 > Neurophysiology > Flashcards

Neurophysiology Flashcards

1
Q

What is the function of the PM?

A

Defines boundaries of cell and differences between extracellular and intracellular responses

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is an organelle membrane?

A

Defines the boundaries of organelle and differences between intra and extra components and contents of organelle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Describe the structure of the PM

A

Very thin film of lipid and protein molecules
Phospholipid bilayer is common structural unit, provides basic structure
Highly dynamic, fluid structure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is the function of the dissolved proteins in the lipid bilayer?

A

Mediate most of the other functions of the cell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are the functions of the PM?

A

Maintain structural integrity and barrier function
Define shape
Control exchange
Site of chemical reactions (oxidative phosphorylation)
Site of ligand recognition
Cell-cell recognition
Facilitate cellular locomotion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the main components of the PM?

A

Lipids: phospholipid, cholesterol, glycolipid
Proteins: transmembrane, peripheral, integral
Glycolipids
Glycoproteins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is meant by amphipathic?

A

Has both polar (hydrophilic) and non-polar (hydrophobic) regions i.e. phospholipids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What determines if phospholipids will for a micelle of bilayer?

A

Number of tails
1 tail: form circular micelle
2 tails: lipid bilayer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Describe the movement of lipids within the bilayer

A 
Bilayer is highly dynamic 
Lipids can:
move, diffuse freely within bilayer
readily exchange place with neighbour in monolayer
rotate around long axis
hydrocarbon chain flexion
RARELY swap side of monolayer
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What determines the fluidity of the bilayer?

A

Composition and temperature

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What 2 lipids are usually highly expressed in bilayer?

A

Cholesterol and glycolipids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Describe the structure of cholesterol

A

Rigid molecule of 4 hydrophobic steroid rings interacts with fatty acyl chains of membrane phospholipids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is the function of cholesterol?

A

Highly expressed: up to 1 for every phospholipid to v important
Enhances permeability-barrier properties of the bilayer - tightly bound to phospholipid making membrane less soluble to v small water-soluble molecules

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Describe the effect of temp on cholesterol

A

At physiological temp. cholesterol limits fluidity of membrane
At lower temp. prevent membrane becoming less fluid by preventing hydrocarbon chains binding each other

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are lipid rafts and what are their functions?

A

Micro-domain of PM rich in cholesterol and sphingolipids

Help organise proteins for transport in small vesicles or enable to function together

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Explain the asymmetry of the bilayer

A

Outer layer of RBC have choline group

Inner layer have terminal primary amino group

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is the importance of the difference in symmetry?

A

Cytosolic proteins bind to specific lipid head groups thus different membranes won’t bind same proteins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are glycolipids?

A

Sugar-containing lipids, found only in outer layer

Thought to partition into lipid rafts, self associate into micro-aggregates by forming H bonds with each other

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is the importance of sugar group exposure?

A

On surface important for interactions of cell with surroundings

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Describe the 3 main types of membrane protein

A

Transmembrane: extend across bilayer, domains exposed both intra and extracellularly
Integral: exposed only on 1 side, usually tightly associated with membrane by lipid group
Peripheral: linked via non-covalent bonds with MP, easily released

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Give examples of transmembrane, peripheral proteins

A

Transmembrane multipass: band 3 in RBC
Single pass: glycophorin
Peripheral: spectrin 1/4 of MP mass

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What are glycoproteins?

A

Oligosaccharide chains bound to MPs (glycoproteins) and lipids (glycolipids)
Can also occur as polysaccharides bound to protein core forming proteoglycan (lots of sugar, little protein)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Describe the carb layer on the bilayer

A

Carbohydrate chains of glycolipids, glycoproteins and proteoglycans surround cell in thick coat allowing for protein binding

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Why is the PM selectively permeable?

A

Retain barrier to EC environment
Ensure essential molecules: lipid, glucose, AAs enter cells
Maintain ionic gradient
Intracellular organelles can also have selectively permeable membrane

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What is simple diffusion?

A

Diffusion of small molecules down conc. gradient without aid of MPs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What is the importance of membrane transport proteins?

A 
Allow passage of polar molecules into cell
Each transport only transports particular class of molecule, usually certain molecular species
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What are carrier and channel proteins?

A

Carrier: bind specific solute, undergo conformational change to transfer solute across membrane
Channel: weakly associated, form aqueous pores when open allow specific solutes to cross membrane

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What is passive diffusion?

A

Movement of molecules down conc. gradient without using energy usually just the conc. gradient dictates
If charged solute, both MP and conc. gradient (electrochemical gradient) will influence diffusion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What is active transport?

A

Movement of solutes up conc. gradient requiring energy
Carrier proteins can be active or passive, active tightly coupled to source of metabolic energy (ATP hydrolysis, ion gradient) and is directional

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Define uniport, symport, antiport

A

Uniport: passive, 1 solute in 1 direction
Symport: active, 2 solutes in same direction
Antiport: active, 2 solutes in opposite direction (uses energy of 1 going down gradient to push other up)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Describe transcellular glucose transport

A

Actively pumped into gut epithelium by Na+-powered glucose symport
Diffuse out via facilitated diffusion in basal-lateral membrane
Na+ gradient maintained by Na+ pump in basal-lateral membrane that keeps Na+ low

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Describe Na+/K+ATPase

A

Antiporter: pumps 3 Na+ out cell and 2 K+ in
Binding of intracellular Na+ changes conformation to E2 (low affinity for Na+), extracellular K+ binds to pump changing conformation back to E1 and K+ expelled in intracellularly
Maintains steep differences in Na+ and K+ concentrations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What is endocytosis?

A

Internal membrane system that allows uptake of macromolecules

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What are the 2 types of endocytosis?

A

Phagocytosis: ‘cell eating’, ingestion of large particles - micro organisms or dead cells via large vesicles phagosomes
Pinocytosis: ‘cell drinking’, ingestion of fluid and solutes via small pinocytic vesicles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Describe receptor mediated endocytosis

A

Macromolecules bind to complementary transmembrane receptor proteins
Accumulate in coated pits
Enter cell as receptor-macromolecule complexes in clathrin-coated vesicles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What is the importance of clathrin mediated endocytosis?

A

Allows specific uptake of minor components of ECF in large amounts without large amounts of ECF - is concentrating mechanism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What is exocytosis?

A

Delivery of newly synthesised proteins, carbs, lipids to cell exterior
Vesicles fuse with PM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

How does exocytosis function?

A

Products stored in secretory vesicles from trans Golgi network release products to exterior in response to extracellular signals

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What are cel junctions?

A

Protein complexes that occur at cell-cell/matrix contact points in tissues - particularly plentiful in epithelial

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What are the 3 functional groups of junctions?

A

Occuluding (tight): seal epithelial in way that prevents small molecules leaking from one side to other (gate) AND diffusion barrier within PM to maintain asymmetry (fence)
Anchoring (desomosomes): mechanically attach cells to neighbours OR ECM, strong cell adhesion, extensive mechanical strength to withstand mechanical strength
Communicating (gap): medicate passage of chemical/electrical signals

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What is the resting membrane potential?

A

Electrical gradient across the cell membrane

In nerve cells is usually -70mV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Define depolarisation and hyperpolarisation

A

Depolarisation: make MP less negative
Hyperpolarisation: make MP more negative

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Describe the function of the sodium pump

A

Any Na+ leaking into cell ejected by hydrolysis of ATP, 2K+ pumped into cell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Describe the function of the K+ channel

A

1 open at RMP allowing easy diffusion of K+ in/out cell

Even though pumped in by Na/K pump easily diffuse out

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Describe the intracellular and extracellular conc of Na, K, Cl

A

Na: 145 extra, 12 intra
K: 4 extra, 139 intra
Cl: 116 extra, 4 intra

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

How is K+ held in the cytoplasm?

A

Binds to protein anions (-ve) holding K+ ions in cell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

What is the effect of transporting ions across membrane?

A

Pumping ions has created electrical
Pumping +ve ions out has created chemical
Combined form electrochemical gradient

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

What is the Nernst equation?

A

Eion = RT/Fzln(Iout/Iin)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Describe how K+ contributes to the RMP

A

K+ leaks out conc gradient, -ve charge build up in cell as anions cannot cross membrane (electrical gradient formed)
-ve charge attract K+ back down electrical gradient
Net movement of K+ stops (equilibrium potential)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

What is equilibrium constant?

A

MO at which electrical gradient opposes chemical gradient

For K+ EK = -90mV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

How does Na+ contribute to RMP?

A

Na+ leaks in down conc. gradient, +ve charge builds up (electrical gradient) as Cl- can’t cross
Cl- attracts Na+ back down electrical gradient
Na+ movement stops
ENa = +60mV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Explain why RMP is -70mV?

A

Cell is ~40x more permeable to K+ than Na+ so closer to EK but small amount of Na+ still leaks into cell depolarises slightly

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Despite the small voltage how is the RMP strong?

A

Due to how thin membrane is electric field strength is very large (rate of voltage change over distance (V/d)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

What are ion channels?

A

Pore-forming membrane proteins

Establish and control voltage gradient across membrane by allowing flow of ions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Why are ion channels anchored to the cytoskeleton and ECM?

A

Keeps channel density constant in different subcellular compartments

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

What is special about ion channels?

A

Have aqueous pore that crosses membrane

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Describe the structure of ions channels

A

2-6 subunits associate to create functional channel

Pore-forming subunits contain a-helix made by ~20 hydrophobic AAs, interact with lipid bilayer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

What are the key components of an ion channel?

A

Selectivity filter: chooses ions to pass
Gate: shut/open (voltage/ligand) pore
Voltage sensor: detect MP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

Explain how ion selectivity works

A

Channel shape specialised to act as molecular sieve (selectivity filter)
At filter ion arrangement of AAs strip ion of waters forming weak chemical bond with charged/polar AA residues lining channel

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

Explain how the bacterial KcsA channel functions

A

-ve charges raise local K+ availability at entrance
Hydrophobic residues of pore allow water molecules to interact with K+
Pore precisely configured to contain K+ surrounded by 8 waters
4 CO O atoms in filter serve as surrogate water
Fine tuned for K+, can’t shrink to bind Na+

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

Describe the ion permeability and gating properties of VGIC

A

Permeability: Na+, K+, Ca2+
Properties
Sensitivity: strong/weak depolarisation, hyperpolarisation
Kinetics: slow/fast, inactivating or non-inactivating

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

Explains VGIC activation

A

+ve charged residues on voltage sensors rotated towards EC by depolarisation
Voltage sensors mechanically coupled to outer helix thus open cell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

Describe inactivation of VGIC

A

Have intrinsic blocking groups that enter permeability pore and prevent reopening

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

What is the importance of intrinsic inactivation?

A

Prevents repeated stimulation which uses lots of energy and high Ca2+ levels induces apoptosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

Describe LGC

A

Typically ion channels in postsynaptic cleft
Some respond to external ligands: ACh, GABA, glycine, glutamate
Or internal ligands: G-proteins, cGMP, cAMP, regulated by internal metabolites: PIP2, IP3, Ca2+, arachidonic acid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

Give an example of a LGIC

A

NAChR
Requires 2ACh to bind in order to open pore
Fluxes Na+, K+

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

What are signal gated channels?

A

Similar to ligand but the signal comes from inside the cell
Atrial M2 receptor - GiPCR is an example
ACh binds receptor, activates Gi protein, a-GTP inhibits adenylate cyclase less cAMP production, By opens K+ channels causing hyperpolarisation of cell slowing HR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

Describe modified of channel gating

A

Exogenous ligand can block - ir/reversible
Pore blockers - voltage dependent block of NMDARs by Mg2+

Exogenous modulators can alter action of endogenous ligands - in/dec opening period

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

What do cells need to communicate with and why is this important?

A

Immediate neighbours, cells in organ, distant organ systems

Enables body to respond in coordinated manner to internal or external environment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

What are the types of intercellular signalling?

A

Contact dependent/juxtacrine
Autocrine
Paracrine/Synaptic
Endocrine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

Describe juxtacrine signalling

A

Both ligand and receptor are membrane bound, require contract for info transmission
e.g. immune cell activation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

Describe autocrine signalling

A

Secreted signal acts back on same cell
Encourages cell group coordination - make same decision during development

Cancer cells stimulate own survival and proliferation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

Describe paracrine signalling

A

Secreted signal acts locally affecting cells in immediate environment
Can’t diffuse far, containment mechanisms: rapid uptake, destruction by EC enzymes, immobilisation by ECM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

Explain histamine and infection paracrine signalling

A

Mast cells have large secretory granules with histamine - secreted in response to infection/injury
Histamine binds H1 receptors on local arteriolar SM causing vasodilation, enhancing local blood flow, improves ability of immune cells to reach infection site

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

Why must histamine use paracrine signalling?

A

Localised effect is vasodilation and bronchoconstriction
Peptides released stimulate invasion of infection by WBCs
Excessive activation lead to anaphylactic shock (sudden drop in BP) and airways to constrict

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

Describe synaptic signalling

A

Axons terminate at synapses - specialised intercellular junctions with either more neurons or target cells in distant organs
Communicate using APs
Arrival causes presynaptic nerve terminal to secret NT
NT bind to receptors on postsynaptic membrane transmitting signal on

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

Name an example of neuronal signalling

A

ACh
Nicotinic: excitatory, activates ion channels
Muscarinic: excitatory and inhibitory slow synaptic transmission, G-protein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

Describe endocrine signalling

A

Form of whole body signalling

Secreted hormones into bloodstream, carries signal to distant target

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

How are hormones transported in blood?

A

Bind to carrier proteins (thyroid-globulin, cortisol-globulin)
Extends half life, increase plasma conc as otherwise rapidly eliminated by liver or kidney

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

Compare endocrine and CNS communication

A

Specific: E different cells must use different hormones; C nerve cells can use same NT still specific
Conc: E low conc diluted in blood, ECF; C high local conc
Affinity: E high affinity act at low conc; C low conc, dissociate rapidly
Speed: E slow; C faster, more precise

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

Describe intracellular signalling pathways

A

Extracellular signal binds receptor (usually on membrane)
Activates intracellular signalling pathway mediated by second messengers
1/+ interacts with target protein, altering behaviour invoking response in cell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

Name the 4 types of receptors

A

Ion channel
G-protein
Tyrosine kinases
Intracellular

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

Describe intracellular receptors

A

Bind lipophilic ligand that can diffuse across membrane
Many located in cytoplasm before translocation to nucleus
Some bound to nuclear DNA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

What are neurons?

A

Cells specialised for signal transport and processing
Collectively allow body to adapt behaviour
Basis for intelligence, independent thought, creativity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

Describe the structure of nerves

A 
Dendrites: inputs
Soma: cell body
Axon hillock: decision gate, whether propagate inputs to outputs (is threshold met?)
Axon: connector
Axon terminal: outputs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

Describe dendrites

A

Project from cell body, few organelles
Membrane abundant with proteins to control input via ion gates
Electrochemical conduction of signal to soma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

Describe the soma

A

Combines signals from dendrites
Large nucleus, abundant rER (Nissl bodies)
Axon hillock has lots of VGICs, threshold must be met for these to open

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

Describe axons

A

Transport between soma and axon terminal, very long (1m)
AP velocity increases as diameter increases
Contain microtubules
Transport: electrical charge, products made in soma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

Describe anterograde transport

A

Towards axon terminals
Fast: kinesin transports NT packaged in vesicle by Golgi
Slow: transport proteins to make microtubules

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

Describe retrograde transport

A

Terminals to soma
Dynein transports surplus PM where it is recycled and processed by lysosomes
Exocytosis of NT causes extra PM is removed and vesicles remade

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

What is a myelin sheath?

A

Electrical insulator between neuron and ECM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

Describe myelin sheath in PerNS

A

Schwann cells line axon, discontinuous myelin
Gaps called Nodes of Ranvier, high conc Na+ channels allow conduction over 1m, spacing optimised for efficiency
1 cell per segment

Provide mechanical support and insulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

Describe myelin sheath in CNS

A

Oligodendrocytes line axon
Nodes of Ranvier, discontinuous sheath
1 cell can wrap around 40-60 axons
Forms concentric rings of PM

Provides 3D scaffold

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

Describe the protection of nerve bundles in the PerNS

A

Epineurium extends from Dura and Arachnoid Mater contains nerve fascicles and blood vessels
Fascicles are bundles of axons protected by perineurium
Each axon is protected by endoneurium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

Describe afferent and efferent neurons

A

Afferent - sensory Arrive at CNS

Efferent - response Exit CNS to excite

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

Describe a simple reflex arc

A

Pain receptor receives stimulation
Neuron travels along afferent nerve (PNS) synapses in CNS
CNS outputs neuron that travels along efferent nerve, synapses at muscle/target

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

Describe nerve regeneration in PerNS

A

If endonerium intact, Schwann cells move along to find other Schwann cell, reconnect and axon regenerated
Not possible is endoneurium broken as Schwann cells unable to find next cell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

Describe nerve regeneration in CNS

A

Regeneration actively blocked in CNS
Astrocytes block regeneration
Get clubbed end of cut axons as can’t find other end
Prevents neuronal regeneration

Stabilise complex CNS - don’t want uncontrolled growth near brain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
99
Q

What are astrocytes?

A

Star shaped glial cell
Fibrous - white, protoplasmic - grey
Structural framework for migrating neurons during development
Transport fluid, ions from EC space to blood vessels
Energy metabolism of neurons by releasing glucose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
100
Q

What is an AP?

A

Electrical impulse that travels along nerve

Is responsible for transfer of info between 1 site and another

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
101
Q

How is the RMP maintained?

A

Na/K pump and K channels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
102
Q

Describe the process of how VGNaC allow AP propagation

A

Depolarisation opens Na channels in membrane, Na+ moves into cell
Na channels outnumber K channels so produces depolarisation of cell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
103
Q

Describe the structure of VGNaC

A

Very large, single protein a-subunit forms channel
4 sub-domains of a subunit form central pore
Most have small B subunit, modulates a sensitivity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
104
Q

How does K+ not pass through Na channel?

A

No proof

Thought to be due to lysine and asparagine residues at neck

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
105
Q

Describe the Na channel inactivation

A

To prevent excessive Na entry has intrinsic slow-acting, intracellular inactivation gate that closes pore
Occurs independently from channel opening mechanism
Hate resets slowly, preventing rapid reopening - refractory period

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
106
Q

What is the effect of Na channel inactivation?

A

MP falls back down to resting

Na inactivation is sufficient to restore RP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
107
Q

Why is there delayed opening of VGKC?

A

Opening allows MP to rapidly re-polarise
Reduces refractory period, allows more rapid repeat of AP
Causes hyperpolarisation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
108
Q

Define the 2 types of refractory periods

A

Absolute phase - Na channels inactivated
Cannot activate AP

Relative phase - after hyperpoalrisation
Need higher intensity depolarisation to trigger AP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
109
Q

When are Na/K pumps used for repolarisation?

A

After periods of extended stimulation - not normal for regular AP firing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
110
Q

How are AP initiated?

A

VGNaC at axon hillock

High conc of channels, slow inactivating, small diameter smaller currents required

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
111
Q

How are APs propagated?

A

Downstream Na channels triggered by changes in MP upstream

Inactivation prevents backwards propagation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
112
Q

What is saltatory conductance?

A

‘Jumping’ of AP from one myelin sheath to next due to nodes of ranvier

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
113
Q

What do myelin sheaths allow for?

A

Small axons have faster APs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
114
Q

How do nerves transmit messages?

A

Message transmitted between cells by NTs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
115
Q

Describe synaptic vesicles

A

Not free in cytoplasm
Small membrane bound vesicles containing NTs
Labelled with many intra-membrane and surface proteins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
116
Q

What are the advantages of using synaptic vesicles?

A

Allows concentration of NTs in small package: binding proteins, active accumulation against conc gradient, release all at once v rapid
Protects against proteases, esterases
Storage system allowing rapid response to AP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
117
Q

Explain the quantal hypothesis

A

NT release is not continuous - each vesicle is single unit

Greater strength of AP requires more vesicle release

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
118
Q

What are the 3 vesicle pools and what are their functions?

A

Reserve pool: mobilised by strong stimulation
Recycling pool: replenishes RRP upon mild stimulation
Readily-releasable pool: readily released

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
119
Q

What is the importance of Ca2+ in vesicle release?

A

Release is dependent on influx of extracellular Ca2+

AP opens Ca2+ channels, entry causes vesicle fusion, NT released, AP continues

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
120
Q

Why is Ca stored extracellularly?

A

Triggers too many processes (apoptosis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
121
Q

What is the most important subunit of VGCaC?

A

a1 - forms pore

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
122
Q

What are SNAREs?

A

Large family of membrane bound proteins involved in vesicle fusion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
123
Q

Describe the process of vesicle fusion

A
  1. Vesicles carry the v-SNARE - synaptobrevin
  2. Active zone PM target expresses t-SNAREs - syntaxin-1, SNAP-25
  3. RRP tethered by interaction between synaptobrevin, syntaxin-1, SNAP-25
  4. SNARE held by complexin- prevents vesicle fusion
  5. Ca2+ binds synaptotagmin causing displacement of complexin allowing vesicle to fuse, NT release
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
124
Q

Why must synaptic vesicles be recycled rapidly?

A

As the supply is limited

Recycled from PM by clathrin-mediated endocytosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
125
Q

Describe the lifecycle of a NT

A
  1. Precursors accumulate, NT produced
  2. NT packed into vesicle by selective transporters
  3. NT released into synaptic cleft, signal transmitted
  4. NT reuptake through neuronal or glial systems, degradation and recycling
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
126
Q

How does a NT signalling through postsynaptic receptor get converted into new AP?

A

Directly or indirectly activate ion channels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
127
Q

What are the 2 effect that a NT activating a ion channel can have?

A
  1. Excitatory post-synaptic potential

2. Inhibitory post-synaptic potential

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
128
Q

What is the difference between slow and fast EPSP/IPSP?

A

Fast: activate ion channels (direct)
Slow: GPCR activates ion channel (indirect) - M2 heart

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
129
Q

How are EPSP generated?

A

ACh binding nicotinic receptor causes Na+ influx, EPSP - membrane depolarisation
Fundamental for function of ANS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
130
Q

How are IPSPs generated?

A

Binding GABA to GABAA triggers Cl- influx - hyperpolarisation
How sedatives - benzodiazepines, barbiturates

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
131
Q

Describe the 3 different types of summation PSPs

A

Single EPSP not sufficient to trigger new AP

Temporal: fire another EPSP before last has died
Spatial: fire many EPSP in same area at once
Spatial (IPSP): cancel each other out, block responses

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
132
Q

What is the BBB?

A

Structural and functional barrier which impedes, regulates influx of most comoijds from blood to brain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
133
Q

How is the BBB formed and what is its function?

A

By brain microvascular endothelial cells, astrocyte end feet, pericytes

Maintains constant environment of CNS
Protection from foreign substances in blood, may damage brain
Protection from hormones, NT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
134
Q

Compare structural differences of cerebral and other endothelial cells

A

Absence of fenestrations - abundant TJs prevent anything moving past

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
135
Q

Compare the functional differences between cerebral and other endothelial cells

A

Impermeable to must substances
Sparse pinocytic vesicular transport
Inc expression of transport, carrier proteins - receptor mediated endocytosis
Only TJs
Limited paracellular and transcellular transport

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
136
Q

Describe TJs

A

Appear at sites of apparent fusion between outer leaflets of PM of endothelial
Continuous and anastomosing (joining together)
Components: claudin, occludin, accessory linking to cytoskeleton

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
137
Q

Describe junctional adhesion molecules

A

Integral membrane proteins with single transmembrane region
Belong to immunoglobulin superfamily
Regulate paracellular permeability and leukocyte (WBC) migration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
138
Q

What is homotypic and heterotypic binding in JAMs?

A

Homo: binding between adjacent endothelial cells acts as barrier for circulating leukocyte
Hetero: binding of JAM to leukocyte JAM guides leukocyte transmigration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
139
Q

Describe adherens junctions

A

Complex between membrane cadherin and intermediary proteins (catenins)
Cadherin-catenin complex joins to actin cytoskeleton

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
140
Q

What is the function of adherens junctions?

A

Form adhesive contacts between cells
Cadherins signal cell-cell, prevent excessive cell growth
Assemble via homophilic interactions between extracellular domains of Ca-dependent cadherins on surface of adjacent cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
141
Q

What are pericytes?

A

Cells embedded in basal lamina - interposed between endothelial and astrocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
142
Q

What is the function of pericytes?

A
  1. Mechanical/structural support
  2. Vasodynamic capacity - O2 sensors, shift blood supply to areas of high metabolic demand
  3. Barrier to passage of macromolecules
  4. Induce endothelial tightness by regulating endothelial proliferation, differentiation and formation of TJs
  5. Associated endothelial more resistant to apoptosis
  6. Phagocytic activity - may he involved in neuro-immune function
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
143
Q

What is the function of astrocyte end feet?

A

Lattice of fine lamellar closely supposed to outer endothelial surface - separate capillaries from neurons
Biochemical support for endothelial
Direct contact between endothelial and astrocyte necessary for BBB formation
Regulate BBB by secretion of soluble cytokines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
144
Q

Describe the different methods of transport across BBB

A

Diffusion: lipophilic, down conc gradient
Carrier systems: actively selected; essential AAs, glucose, neutral AAs, glycine glutamate (NTs)
Receptor mediated endocytosis: larger molecules (insulin) - overlaps with carrier systems

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
145
Q

What are efflux transporters?

A

Transporters that actively remove substances from brain
Impedes most drug delivery to brain
P-glycoprotein: removes waste products, binds whole range of molecules, most drugs fail due to function

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
146
Q

Describe the immune system present in the brain

A

NONE - if directly injected into brain tumours, bacteria, viruses evade immune recognition; no control mechanism to remove

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
147
Q

Why are there no immune cells in the brain?

A

They could damage neurons, synapses as not used to brain environment
Likely be activated by environment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
148
Q

What is the most superior region immune cells can reach in BBB?

A

Can reach perivascular space but can’t pass astrocyte

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
149
Q

Why are there regions with the BBB?

A

Regions that require hormones - circumventricular organs
Respond to factors in circulation or involved in neuroendocrine control of homeostasis
Neuroendocrine hormones pass easily, locally deliver hormone and hormones released directly into bloodstream

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
150
Q

What happens to the BBB during illness?

A

Enhanced permeability - blood borne bacteria can directly cause breakdown of inter-endothelial TJs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
151
Q

What can cause the significant enhancement of BBB permeability?

A

Ageing and chronic inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
152
Q

Compare acute inflammation with chronic inflammation

A

Acute invokes physiological sickness behaviour

Chronic pathological cognitive impairments

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
153
Q

How can drugs enter the brain?

A

Mimic substances for existing transporters: L-DOPA (dopamine precursor, Parkinson’s), gabapentin (AA transporter, epilepsy)

Injected intracerebrally: anti-cancer (doxorubicin)

Given into CSF: epidural anaesthetics (lidocaine)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
154
Q

What is the function of the Cerebrospinal fluid?

A
  1. Cushions, protects from trauma
  2. Mechanical buoyancy, support for brain
  3. Nutrients and ion supply
  4. Remove metabolic waste
  5. Protect against acute changes in arterial and venous BP
  6. Intra-cerebral transport of neuroendocrine hormones
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
155
Q

What is the composition of the CSF?

A

Similar to that of plasma but low protein, reduced glucose (used readily), inc CO2 (high respiration)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
156
Q

How is the CSF circulated?

A

Induced by pulsating blood vessels, respiration, changes of posture, aided by ependymal

Bathes the ependymal and pial surfaces of CNS, penetrates nervous tissue along blood vessels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
157
Q

What are some of the pathologies that can effect the CSF?

A

Increase pressure: physical blockage (tumours), haemorrhage, infection (meningitis)

Congenital hydrocephalus: accumulation of CSF in ventricles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
158
Q

Why are pressure changes of CSF serious medical problems?

A

Significantly impair neuronal viability - physical effects (squeeze tissue), obstruction of O2, nutrient supply

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
159
Q

What are the 3 parts of the brain stem?

A

Midbrain
Pons
Medulla oblongata

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
160
Q

Describe the anatomy of the midbrain

A

Cerebral peduncles: ascending sensory and descending motor pathways
Nuclei of oculomotor and trochlear nerves
Sup. colliculi - visual reflex centres; Inf. colliculi - auditory relay centres
Substantia nigra - regulate motor function
Red nucleus - control voluntary limb movement
Cerebral aqueduct - contains CSF, connects 3 and 4 ventricles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
161
Q

Describe the relationship between substantia nigra and Parkinson’s

A

Substantia nigra is part of basal ganglia - series of integrated brain nuclei that regulate fine control of motor activity
Has dopaminergic neurons that ascend to caudate putamen (striatum)
Degeneration of dopaminergic neurons leads to Parkinson’s

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
162
Q

Describe the anatomy of the pons

A

Pyramidal tracts: ascending and descending pathways
Nuclei of trigeminal, abducens, facial, vestibulo-cochlear nerves
Potine nuclei - neurones connecting cerebrum and cerebellum
Vestibular nuclei: components of balance pathways from ear
Pneumotaxic and apneustic areas of respiratory centre - control breathing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
163
Q

Describe the anatomy of the medulla

A

Ascending and descending pathways
Cranial nuclei
Inf. cerebellar peduncles: fibre tracts connecting medulla and cerebellum

Pyramids: bulges on ant. aspect of medulla
2 longitudinal ridges formed by corticospinal tracts passing between brain and spinal cord
site of decussation (X-over) of as/descending pathways

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
164
Q

What are the main centres of the medulla?

A 
Cardiovascular - heart rhythm 
Respiratory - breathing rhythm 
(Vomiting, swallowing, sneezing, coughing, hiccuping)
Inf. olivary nucleus 
Cuneate nucleus, gracile nucleus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
165
Q

What is the role of the inf. olivary nucleus?

A

Integrates input from cerebral cortex, midbrain red nucleus, spinal cord, sensory info from skeletal muscle

Helps regulate neural activity of cerebellum
Has role in leading new motor skills

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
166
Q

What is the role of the cuneate and gracile nuclei?

A

Carries touch pressure, vibration and proprioception info

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
167
Q

Name the nerves that originate in each region of spinal cord

A

Midbrain: 3, 4
Pons: 5, 6, 7
Medulla: 8, 9, 10, 11, 12

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
168
Q

What does the trigeminal nerve carry?

A

Facial sensation and oral motor functions (chewing and biting)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
169
Q

What are the 3 branches of the trigeminal?

A

Ophthalmic: sensory (positing of eye)
Maxillary: sensory
Mandibular: sensomotor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
170
Q

Where do the 3 branches of trigeminal converge?

A

On trigeminal/semilunar ganglion

Single sensory root enters brain stem at level of pons, smaller adjacent motor root emerges at same level

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
171
Q

What are the 4 nuclei of the trigeminal?

A

Sensory
Mesencephalic
Pontine
Spinal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
172
Q

Describe the sensory nucleus of CN V

A

Largest of cranial nuclei
Extends from midbrain to spinal cord
Has 3 parts, chief sensory nucleus in pons

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
173
Q

What is the role of the mesencephalic nucleus?

A

Proprioception of face and position of facial musculature

Info from mandible projected to motor trigeminal nucleus - mediates monosynaptic jaw jerk reflex

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
174
Q

What is unique about the synapses in the mesencephalic nuclei?

A

Are electrically coupled not chemically

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
175
Q

What is the role of the pontine nucleus?

A

Discriminative and light touch sensation and integrates with conscious jaw proprioception
Sensory info crosses midline and passes to contralateral thalamus
Oral cavity info passed to ipsilateral thalamus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
176
Q

What is the role of the spinal nucleus?

A

Deep/crude touch, pain, temp from ipsilateral face

Pain info from facial, glossopharyngeal and vagus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
177
Q

What is the light reflex and its importance?

A

Light entering 1 eye will elicit contraction of pupil in both
Damage to brain stem connecting neurons in oculomotor nerve leads to failure of reflex

Can be used to check life sign of patient: signs of optic nerve and oculomotor nerve damage, depressant drugs, brain stem death

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
178
Q

If a lesion is present in the brainstem what will the affect on the light reflex be? And if it is in the oculomotor nerve?

A

Brainstem: only 1 eye will respond
Oculomotor: neither eye responds

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
179
Q

What is the role of the facial (VII) nerve?

A

Signals voluntary movement of facial muscles, carried to facial motor nucleus in pons via corticobular tract

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
180
Q

What fibres of facial nerve project bilaterally and what do they control? Which project contralaterally?

A

Cortical fibres controlling forehead muscles project bilaterally meaning the control both halves
Fibres controlling other facial muscles project contralaterally

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
181
Q

What type of neuron lesion results in total paralysis of facial expression muscles ipsilaterally to lesion?

A

Lower Motor Neuron Lesion

Caused by damage to motor nucleus of facial nerve or its axons

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
182
Q

Damage to cortical neurons or their axons projecting to facial nerve motor neurons results in what?

A

Upper motor neuron lesion
Voluntary control of lower facial muscles lost on contralateral side but control of forehead muscles preserved due to bilateral innervation

183
Q

How is an upper motor neuron lesion usually caused?

A

Stroke

184
Q

What is the reticular activating system?

A

Diffuse network of nerve pathways in large parts of dorsal brainstem

185
Q

What is the function of the RAS?

A

Sleep arousal cycle: impulses sent to cerebral cortex to maintain consciousness and control sleep
Pain perception: modulates pain
Movement control: controls coarse motor movements
Visceral activity regulation: vasomotor, cardiac, respiratory centres regulate visceral motor functions
Filters out repetitive/weak stimuli

186
Q

What are the 2 ascending pathways?

A

Specific

Non-specific

187
Q

Which ascending pathway’s 2nd order neurons lie in the medulla and transmits sensory input for touch, joint stretch?

A

The specific
Sensory input can be precisely located
Axons X to other side of brain, ascend thalamus

188
Q

Describe the non-specific ascending pathway

A

Sensory input that is difficult to precisely locate: pain, temp, crude touch
2nd order neurons lie in dorsal horn of spinal cord
Axons X to other side of brain, ascend to thalamus

189
Q

What are the 2 descending pathways?

A

Direct/Pyramidal

Indirect/Extrapyramidal

190
Q

What descending pathway originates with neurons in cerebral cortex? Describe it

A

Direct pathway
Impulses sent through lateral corticospinal tracts and synapse in ant. horn of spinal cord
Ant. corticospinal tract descends on ipsilateral side of spinal cord, X at level it synapses
Lat. corticospinal tract X in medulla, descends to ventral horn of spinal cord

191
Q

Describe the extrapyramidal motor system

A

All motor pathways not part of pyramidal
Are complex, multisynaptic and regulate:
axial muscles that maintain balance and posture
muscles controlling coarse movements of prox. portions of limbs
H&N, eye movements that follow objects in visual field

192
Q

Describe 1st order neurons

A

Sensory neuron, delivers info from receptor to CNS

Cell body located in dorsal root ganglion
Axon passes to spinal cord through dorsal root of spinal nerve
Synapses with 2nd order in spinal cord or medulla

193
Q

Describe 2nd order neurons

A

Cell body in spinal cord or medulla oblongata

Axons decussate and terminate on 3rd order

194
Q

Describe 3rd order neurons

A

Cell body in thalamus

Axons terminate in ipsilateral cerebral cortex

195
Q

How and where are as/descending fibres organised?

A

In distinct bundles which occupy particular regions in white matter

196
Q

What tracts are located peripherally in white matter?

A

Long tracts

197
Q

Where are short tracts found?

A

Near grey matter

198
Q

What is a tract?

A

Bundle of nerve fibres (within CNS) having same origin, course, destination and function

199
Q

What does the name of a tract indicate?

A

Origin and destination of its fibres e.g. nigrostriatal from substantia nigra to striatum

200
Q

How are axons within a tract grouped?

A

According to body region innervated

201
Q

What is the composition and divisions of grey matter?

A

Composition: neuron cell bodies, dendrites, axons
Divisions: post. horn, ant. horn, lateral horn

202
Q

What is the composition and divisions of white matter?

A

Composition: myelinated axons
Divisions: ventral/ant., dorsal/post., lateral funiculi each divided into sensory or motor tracts

203
Q

What is the function of the dorsal column funiculi?

A

Carry impulses concerned with PROPRIOCEPTION, discriminative touch pressure and vibration from ipsilateral side of body

204
Q

What are the 2 tracts of the dorsal column funiculi?

A

Fasiculus gracillis

Fasicuclus cuneatus

205
Q

What axons do the dorsal columns contain?

A

Axons of primary afferent neurons that have entered cord through dorsal roots of spinal nerve

206
Q

Compare where the fasciculus gracillis and fasciculus cuneatus fibres are received

A

FG: sacral, lumbar, lower thoracic levels
FC: upper thoracic, cervical levels

Ascend w/o interruption and terminate on 2nd order neurons in nucleus gracillis and cuneatus, respectively

207
Q

Where do the 2nd order neurons decussate in the dorsal funiculi and how do they ascend?

A

Decussate in medulla as internal arcuate fibres

Ascend brainstem as medial lemniscus

208
Q

Where does the medial lemniscus terminate?

A

In ventral post. nucleus of thalamus on 3rd order neurons which project to somatosensory cortex

209
Q

What is the result of a left spinal cord injury in the dorsal funiculi?

A

Loss of sense: touch, proprioception
Patient will stagger, can’t perceive position or movement of legs, vibration in left leg

Test: cotton wool touch (light), joint position, vibration

210
Q

What are the 2 spinothalamic tracts and what info do they carry?

A

Lateral: pain, temp
Ventral: non-discriminative touch, pressure

211
Q

How are the fibres in the spinothalamic tracts arranged?

A

Highly somatotopically: lower limb superficial, upper limb deep

212
Q

Where do the thalamic neurons of both the lateral and ant. spinothalamic tracts project?

A

Primary sensory cortex - somatosensory cortex on opposite side of body

213
Q

Describe the lateral spinothalamic tract

A

Senses pain and temp
1st order neuron axons terminate in dorsal horn
2nd order axons decussate within segment of their origin
Terminate in 3rd order in ventral post. nucleus of thalamus

214
Q

Describe the ant. spinothalamic tract

A

Sense non-discriminative touch and pressure

1sr order terminate in dorsal horn
2nd order may ascend several segments before decussating

215
Q

What is the effect of a left spinal cord injury in the spinothalamic tracts?

A

Lose sense of touch, pain, warmth/cold in right leg

Test: pinprick, hot/cold stimuli

216
Q

What do the spinocerebellar tracts control?

A

Posture

Movement

217
Q

What are the 2 spinocerebellar tracts?

A

Posterior

Anterior

218
Q

Where do the spinocerebellar tracts carry info from?

A

Muscle spindles, Golgi tendon organs and tactile receptors to cerebellum
Both convey to same side of cerebellum

219
Q

Describe the post. spinocerebellar tract

A

Present only above L3
2nd order neurons lie in Clark’s column
Axons terminate ipsilaterally in cerebellum by entering through inf. cerebellar peduncle

220
Q

Describe the ant. spinocerebellar tract

A

2nd order cell bodies lie in base of dorsal horn of lumbosacral segments
Axons X, ascend to midbrain, X again to enter sup. cerebellar peduncle
Terminate in cerebellar cortex

221
Q

What are the symptoms of spinocerebellar damage?

A

Cerebellar ataxia
Clumsy movements
Incoordination of limbs
Wide based, feeling gait

222
Q

What is Romberg’s test?

A

Test for spinocerebellar ataxia

Stand upright and close eyes, if lose balance +ve result
Require vision, vestibular function and proprioception to maintain balance
Allows distinction between sensory and cerebellar ataxia

223
Q

Describe the spinal cord anatomy of afferent neurons

A

Enter spinal cord in dorsal root

Cell bodies in dorsal root ganglion

224
Q

Describe spinal cord anatomy of efferent neurons

A

Cell bodies in grey matter in ventral spinal cord

Axons exit in central root

225
Q

Describe the formation of plexuses

A

Dorsal and ventral roots fuse forming spinal nerves, exit via intervertebral foramina
Spinal nerves branch and fuse in plexuses forming peripheral nerves

226
Q

What are dermatomes?

A

Skin territory innervated by 1 dorsal root

227
Q

What is the clinical importance of dermatomes?

A

Overlap at edges ~50%

Total loss of sensation requires anaesthetising 3 successive spinal nerves

228
Q

How are dermatomes diagnostically useful?

A

Damage to spinal nerves changes skin sensation within dermatome allowing localisation of vertebral damage

229
Q

What are the 3 types of nerve fibre?

A

A: alpha, beta, gamma, delta
B
C

230
Q

Which type of nerve fibre is the only 1 to be unmyelinated?

A

C type

231
Q

Describe the relationship between diameter and conduction velocity

A

Directly proportional: greater diameter greater velocity

232
Q

Describe afferent and efferent A alpha and gamma motoneurons

A

Efferent
Alpha: muscle fibre
Gamma: muscle spindle - tells brain is muscle is contracted

Afferents project to 2 specialised sensory receptors in muscle and tendon
Muscle spindle: Ia afferent
Golfing tendon organ: Ib

233
Q

Describe A beta nerve fibres

A

General sensory afferents, mechanoreceptors
Myelinated, fast
Majority of fibres are A beta

234
Q

Describe A delta nerve fibres

A

Nociceptor or thermoceptor
Fast pain from skin, muscle, joints
Temp sensation

235
Q

Describe C fibres

A

Nociceptor or thermoceptor

Small, unmyelinated afferents
Conduct very slowly
Slow/aching/burning pain

236
Q

Describe the structure of a nerve

A

Individual nerve axons and Schwann cells covered by v thin connective membrane - endoneurium

Fibres grouped in fascicles, each surrounded by tough layer - perineurium

Fascicles and blood supply surrounded by tougher sheath - epineurium

237
Q

What are the 2 main locations of Schwann cells?

A
  1. Ensheathing single axon with myelin

2. Surrounding groups of unmyelinated C axons (Remak bundles)

238
Q

What is the function of Schwann cells?

A

Provide nutrient support to axons
Promote regeneration

Do NOT insulate or provide conduction velocity

239
Q

Describe myelin and its production

A

Fatty layer around axon that inc. conduction velocity

Produced by Schwann cells in spiral around axon

240
Q

Name the 6 somatic senses and 5 special senses

A

Somatic

  1. Mechanoceptors - touch, pressure, vibration, stretch
  2. Chemoceptors - chemicals
  3. Nociceptor - pain
  4. Thermoceptor - temp
  5. Proprioceptors - muscle stretch, balance
  6. Baroceptors - blood pressure

Special

  1. Vision
  2. Hearing
  3. Taste
  4. Smell
  5. Equilibrium - balance
241
Q

Define sensation

A

Sub/conscious awareness of changes in in/external environment

242
Q

What are the 3 classes of sensory receptor?

A
  1. Free nerve endings: pain, thermoceptor
  2. Encapsulated: pacinian corpuscles
  3. Separate: hair cells, photoreceptors, gustatory receptor cells
243
Q

Compare the AP production of free and encapsulate nerve endings and specialised receptor cells

A

Free
Generator potential produced, threshold met, AP triggered

Specialised
NT release from cell, AP triggered in sensory neuron

244
Q

What are the 2 main classes of skin mechanoceptors?

A
  1. Rapidly adapting

2. Slowly adapting

245
Q

What are the 5 main mechanoceptors? Are they rapidly or slowly adapting?

A
  1. Hair (follicle) receptors - rapidly
  2. Meissner’s corpuscles - rapidly
  3. Pacinian corpuscles - slowly
  4. Merkel’s discs - slowly
  5. Ruffini’s corpuscles - slowly
246
Q

Describe encapsulated receptors and give 3 examples

A

CT capsule around nerve fibre ending
Tunes fibre to respond to certain mechanical stimuli

  1. Meissner’s
  2. Pacinian
  3. Ruffini’s
247
Q

Describe pacinian corpuscles

A

Layers of elastin-containing cells around nerve ending
Mechanically filter tissue stretch or slow deformation

Leaves ending specifically sensitive to high freq. vibration

248
Q

Describe the receptive field of pacinian corpuscles

A

Periosteum: v large, detect vibration anywhere on limb

TMJ richly supplied, feel drilling across bone

249
Q

How are encapsulated sensory axon nerve endings activated?

A

Mechanosensitive ion channels
Physical distortion of terminal membrane activates ion channels triggering generator potential which can then initiate 1+ APs in axon

250
Q

Describe free nerve endings, give 2 examples of specialised types

A

Abundant in epithelial and underlying CT
Respond to pain, temp. slowly adapting

  1. Merkel discs: epidermis, slowly adapting for light touch
  2. Hair follicle: wrap around hair follicles, rapidly adapting
251
Q

Compare rapidly and slowly adapting fibres

A

Rapidly: fire short burst of APs then stop
Slowly: continually fire at slowly dec. rate

252
Q

Name 3 proprioceptors and their function

A
  1. Muscle spindle: changing length of muscle; embedded in perimysium between muscle fascicles
  2. Golgi tendon organs: tension within tendons; near muscle tendon junction
  3. Joint kinesthetic receptors: sensory within joint capsules
253
Q

What are receptive fields?

A

Area of skin where stimuli can influence a sensory receptor

Vary in size from tiny (hair follicle around single hair follicle) to very large (pascinian corpuscles)

254
Q

What is the importance of receptive field overlap?

A

Damage to single fibre does not leave any region of skin anesthetised

255
Q

Compare discrimination for many and few primary neurons converging

A

Many: converge into single 2ndary neuron create v large receptive field; stimuli perceived as 1 in same field
Few: much smaller receptive field; stimuli activate separate pathways, perceived as distinct

256
Q

Describe neighbour inhibition

A

Pathway closest to stimuli inhibits neighbours causing enhancement of stimuli

257
Q

Describe dental nerve endings

A

Tooth pulp sensory receptors arise from A delta and C fibres
Detect movement and chemical changes, signal temp and pain

Delta: enables tooth localisation
C: nociceptors mediate tooth pain (slow, throbbing tooth ache)

258
Q

Define motor unit

A

Motor neuron and fibres it innervates

259
Q

Describe the motor unit control of muscle

A

Muscles composed of muscle fibres
Alpha motor neuron innervates multiple fibres
Groups of alpha motor neurons innervate a muscle

260
Q

How is muscle contraction increased?

A

Rate coding and recruitment

261
Q

Compare fine and coarse movement motor unit size

A

Fine: multiple, small motor units
Coarse: fewer, each alpha motor neuron innervating up to 1000 muscle fibres

262
Q

Compare upper and lower motor neurons

A

Lower: cell body in ventral horn of spinal cord, project to SM
Upper: cell body in brain/brainstem, send axons down des. spinal tracts to target lower motor neurons

263
Q

What are the 3 main synaptic inputs of lower motor neurons?

A
  1. Descending tracts from UMNs
  2. Local interneurons (cells with all processes in CNS)
  3. Local sensory nerve fibres via reflexes
264
Q

Describe muscle spindle receptors

A

Specialised receptors found in all SM
Long, thin spindles running length of muscle from origin to insertion

Within there are intrafusal muscle fibres that sensory nerves wrap around non-contractile centres of

265
Q

Describe the activation of muscle spindle

A

Central receptor portion (no contractile machinery) activated by muscle stretch which activates Ia afferents inc. rate of AP firing

Contraction reduces AP firing

266
Q

What is the role of gamma motor neurons in muscle spindle?

A

Adjust sensitivity of Ia afferents (muscle spindle sensory receptor)

Innervate contractile parts of intrafusal fibres

267
Q

Describe the relationship between contraction of intrafusal fibres and sensitivity

A

Contraction inc. sensitivity of Ia afferents to stretch

268
Q

What is the alpha-gamma linkage?

A

When alpha motor neuron activated, gamma motor neuron activated

269
Q

What is the role of the alpha-gamma linkage?

A

Keeps spindle sensitive to stretch even at different absolute muscle lengths

270
Q

Describe the muscle spinal cord connection

A

Ia afferent project into ventral horn providing direct connection with motor neurons
All tendon reflexes are monosynaptic

271
Q

What is reciprocal inhibition?

A

Muscles on 1 side of joint reflex to accommodate contraction of other muscle
Flexor muscles inhibited by muscle spindle from paired extensor

272
Q

Describe the knee-jerk reflex

A

Tapping patella causes slight stretch activating quadriceps muscle spindle
Ia afferents excite quadriceps motor neurons via monosynaptic connection
Inhibit antagonistic muscles via inhib. reflex arc

273
Q

What is the importance of monosynaptic motor reflexes?

A

Maintain body posture in face of varying loads

E.g. holding glass that is then filled with fluid

274
Q

Describe Golgi tendon organs

A

2nd major proprioceptors in muscle, found in muscle tendon

275
Q

What is the role of Golgi tendon organs in muscle?

A

Prevent contracting muscles from applying excessive tension on tendons
Limits how contracted a muscle can get

276
Q

Describe the activation of GTO

A

Activated by muscle tension and resulting compression of axon fibres
Compression opens stretch-activated cation channels, trigger APs in Ib afferents

277
Q

Describe the connections of the GTO

A

Disynaotic connection to own motor neuron pool
Interneuron is glycinergic inhibitory neuron - glycine is inhibitory AA NT
Activation inhibits alpha motor neuron activity, preventing excessive contraction and damage

278
Q

What is muscle tone?

A

Continuous, passive minor contractions in muscle causing resistance even in passive state

279
Q

Compare damage to upper and lower motor neurons on muscle damage

A

Upper: exaggerated reflexes, pathological inc. in tone - muscle spasticity
Lower: reduces or absents tone - flaccid paralysis

280
Q

Name 3 motor system pathologies

A
  1. Spasticity: inc. tone and tendon reflexes, UML
  2. Clonus: series of jerky contractions of muscle following sudden stretching of muscle
  3. Hyperreflexia: abnormally, pathologically brisk tendon reflex seen in 1+ muscles
281
Q

What is the difference between pain and nociception?

A

Nociception: signal that something potentially dangerous has occurred
Pain: subjective, protective response triggered in the brain following nociceptive signals

282
Q

Describe nociceptive nerves

A

Distributed through skin, joints, muscles, viscera, blood vessels NOT brain
All free nerve endings

283
Q

What are the 2 types of fibres involved in nociceptive transmission?

A
  1. Thinly myelinated A delta fibres

2. Unmyelinated C fibres

284
Q

What are the 4 classes of nociceptor?

A
  1. Mechanonociceptor
  2. Thermonociceptor
  3. Chemonociceptor
  4. Polymodal nociceptors
285
Q

Describe mechanonociceptors

A

A delta and C fibres

Respond to mechanical injury accompanied by tissue damage

286
Q

Describe thermonociceptors

A

A delta and C fibres
Respond to heat/cold at range of temps
Range depends on what receptors present in neuron
Stimuli coded by firing rate - higher freq., greater damage

287
Q

Describe chemonociceptors

A

C fibres

Activated by endogenous mediators of tissue damage, inflammation and foreign agents (bee venom, capsaicin)

288
Q

Describe polymodal nociceptors

A

C fibres

Respond to mechanical, thermal and chemical stimuli

289
Q

Describe the activation of nociceptors

A

Tissue injury often immediate cause of pain

Resulting in local release of chemical agents that activate or enhance sensitivity of nerve endings to other stimuli

290
Q

Are nociceptors slowly or rapidly adapting?

A

Neither - non-adapting

Do not rapidly return to basal activity rates

291
Q

How is nociceptive transmission coded?

A

Nerve firing rate - greater exposure, greater freq.

292
Q

Why are nociceptors able to be activated by multiple chemical mediators?

A

As free nerve endings have variety of receptor proteins

293
Q

List some of the chemical mediators that can activate nociceptors

A

Capsaicin, K, H, ATP, histamine, bradykinin, substance P, eicosanoids

294
Q

Describe the nociceptive pathways

A

Run through spinothalamic tracts
1st order: synapse in dorsal horn of spinal cord
2nd order interneurones: decussate, ascend to brainstem parabrachial nucleus or thalamus
3rd order: project to cortex and limbic system

295
Q

Describe the lamina of the dorsal horn

A

Specific lamina where 1st order neurons synapse
A delta: lamina 1 and 5
C fibres: lamina 2

296
Q

What does substantia gelatinosa refer to?

A

Lamina 2-4 of dorsal horn of spinal cord

297
Q

What are the 2 classes of 2nd order neurons found in the dorsal horn?

A
  1. Nociceptive specific (NS) neuron

2. Wide dynamic range (WDR) neuron

298
Q

Describe nociceptive specific (NS) neurons

A

Receptive info. from A delta and C fibres
Receptive fields restricted to small areas
Somatotopically organised

299
Q

Describe wide dynamic range (WDR) neurons

A

Info. from nociceptive and non-nociceptive afferents
Innocuous stimuli will activate, noxious activate more strongly
WDR predominately found in lamina 5,6 some in 1,2,4
Important in linking A beta mechanoreceptor input with A delta nociceptive input

300
Q

What are the 3 main pathways from spine to higher centres?

A
  1. Spinothalamic
  2. Spinomescencephalic
  3. Spinoreticular
301
Q

Describe the spinothalamic tract

A

Terminates in med. and lat. thalamus
Outputs from thalamus terminate in somatosensory cortex
Arousal, motor responses, sensory discrimination, affective responses

302
Q

Describe the spinomesencephalic tract

A

Terminates at periaqueduct grey (PAG) and locus coeruleus
Outputs from PAG project to hypothalamus and limbic system
Unpleasantness/fear of pain

303
Q

Describe the spinoreticular

A

Targets the nucleus reticularis gigantocellularis in medulla
Outputs project to med. thalamus
Affective responses, autonomic responses

304
Q

Describe the substantia gelatinosa

A

V low level of myelination, high number of glial cells

305
Q

Many of what 2 types of receptors are found in the substantia gelatinosa?

A

Mu and Kappa opioid receptors found on pre and post synaptic nerves

306
Q

Explain how ascending control pain gating functions

A

Fast-adapting A beta fibres stimulate inhibitory interneurons and prevent excitatory transmission cell activation
A beta fibres convey non-nociceptive mechanical and thermal stimuli thus override weak pain stimuli

307
Q

What are the 3 major lower brainstem areas that the PAG projects?

A
  1. Nucleus raphe Magnus
  2. Locus coeruleus
  3. Nucleus reticularis paragigantocellularis
308
Q

Explain how the nucleus raphe magnus prevents nociceptive transmission

A

Projects 5-HT neurons to inhibit pain transmission in lamina 1,2,5

309
Q

Explain how the locus coeruleus inhibits pain transmission

A

Projects inhibitory noradrenergic neurons to lamina 1,5

310
Q

Explain how the nucleus reticularis paragigantocellularis inhibits nociceptive transmission

A

Projects inhibitory 5-HT neurons to spinal cord and excitatory 5-HT neurons to locus coeruleus

311
Q

What are the 2 reasons we have taste?

A
  1. Appetite: sugar; need carbs
    Salt; cell signalling, fluid balance
    Meat; proteins, AAs
  2. Protection: bitter/sour; avoid poisons, off food
312
Q

What are tastebuds?

A

Neuroepithelial cells grouped into mucosal projections

Not visible by naked eye

313
Q

Describe taste papillae

A

Groups of tastebuds seen as raised, red dots on tongue
Visible to naked eye
4 types

314
Q

What are the 4 types of taste papillae?

A
  1. Foliate
  2. Circumvallate
  3. Fungiform
  4. Filiform - not gustatory
315
Q

Describe tastebuds

A

Barrel-shaped epithelial cells w/ chemosensory cells (gustatory receptor cells)

3 cell components:

  1. Taste receptor
  2. Supporting cell
  3. Precursor/basal cell

Narrow apical end extend into taste pore on tongue

316
Q

Describe the function of each component of the taste bud

A
  1. Taste receptor: sensory transduction
  2. Supporting: possibly transitional cell
  3. Basal: differentiate into new receptor cells; derived from surrounding epithelium; renew every 10days
317
Q

What is the synaptic control on gustatory receptors?

A

Afferent nerve terminal derived from facial, glossopharyngeal, vagus (CN 7,9,10)

318
Q

Describe the central pathway of taste transduction

A

Afferents synapse in medulla

Ascend to thalamus and project to primary gustatory cortex

319
Q

What are the 5 tastes?

A
  1. Salt
  2. Sour
  3. Sweet
  4. Bitter
  5. Umami
320
Q

Define tastant

A

Soluble ions and molecules that activate gustatory neurons

321
Q

Describe the initiation of taste

A

Tastant diffuses into taste pore, binds receptor
Change in ion flow across taste cell PM
Different tastes change ion flow differently

322
Q

Describe salt taste transduction

A 
Na+ enters cell via Na channels
Depolarises cell
Ca2+ released from internal stores 
NT released
AP triggered in sensory nerve
323
Q

Describe the sour taste transduction

A

H+/acetic acid enter via Na channel/proton transmembrane protein
Cytoplasm acidified
Internal H+ block proton sensitive K+ channel
Influx H+/red. K+
Ca2+ released internally
NT released
AP triggered in sensory nerve

324
Q

What is different about the sweet, bitter and umami taste transduction?

A

Tastant doesn’t interact directly with channel

325
Q

Describe taste transduction of sweet, bitter and umami tastes

A 
Binding receptor activates G-protein
G-proteins activates PLC
PLC generates IP3 and DAG
Ca2+ released internally from smooth ER
Opens TrpM5 transmembrane action channel
AP triggered in sensory nerve
326
Q

What are the 4 functions of olfaction?

A
  1. Environmental sampling: alert danger, presence of food/person
  2. Recognition
  3. Detect bad, aversive smells
  4. Linked w/ memory
327
Q

What is the requirement of an odorant?

A

Volatile to reach and activate olfactory neuron in nose

328
Q

What are olfactory receptor neurons?

A

Neuronal cells embedded in olfactory epithelium with: basal cells and supporting cells

329
Q

Why do ORNs regenerate every month?

A

To regenerate sense of smell in case of damage

330
Q

Where are the odorant receptors located?

A

On cilia of ORNs

Cilia project from dendritic knob and bathed in mucous

331
Q

What are Glands of Bowman?

A

Olfactory serous gland under epithelium that secrete mucous that odoriferous substances dissolve in

332
Q

What is the odorant binding protein?

A

Protein found in secretory fluid w/ high affinity for many odorant molecules

333
Q

What is the function of the OBP?

A

Carry odorants to receptor
Remove odorants once sensed
Amplify odorant conc.

334
Q

What is the odorant receptor protein?

A

Transmembrane protein found in cilia PM

335
Q

Describe how the ORP functions

A 
Odorant binds to ORP
Activates G-protein 
Alpha subunit dissociates and activates adenylate cyclase
AC catalyses conversion of ATP to cAMP
cAMP open Na+ channels in cilia PM
Na+ influx depolarises cell
AP triggered at axon hillock
336
Q

Describe the connections of ORNs

A

Cilia project into mucous layer
10-100 axons form bundles that pass through ethmoidal cribriform plate and terminate in olfactory bulb at synaptic glomeruli

337
Q

What are glomeruli?

A

Spherical bundles of dendritic process from ~25 mitral cells

338
Q

What are mitral cells?

A

Principal neurons in olfactory bulb

Primary apical dendrite extends a glomerulus
Axons merge to for lat. olfactory tract

339
Q

What are periglomerular cells?

A

Cells that mediate lat. inhibition between glomeruli

340
Q

What are granule cells?

A

Inhibitory interneurons

341
Q

Describe the olfactory central pathway

A

Mitral cell axons run through lateral olfactory tract to forebrain:
Hypothalamus: physiological responses
Amygdala: emotional (feeding and mating)
Hippocampus: memory

Pyriform cortex: smell discrimination
Connections to frontal cortex required for conscious perception of smell

342
Q

What 2 things has the cortex evolved to do?

A
  1. Learn from environment

2. Generate activity patterns in response to specific patterns of thalamic and cortical activity

343
Q

Describe how cortex activity affects consciousness

A

Conscious when activity normal
Sleep: altered activity - not necessarily reduced
Coma: little/no activity

344
Q

What are the 3 association cortices?

A
  1. Post parietal: visual, agnosia
  2. Inferotemporal: memory formation, amnesia
  3. Frontal: executive functions and attention
345
Q

What role does the post. parietal lobe play in visual processing?

A

Separating object from background, relative location and orientation

346
Q

What is agnosia?

A

Inability to recognise an object

347
Q

What are the 2 types of agnosia?

A
  1. Apperceptive: R post. parietal lobe lesion

2. Associative: L post. parietal lobe lesion

348
Q

Describe apperceptive agnosia

A

Inability to recognise obscured object i.e. unusual orientations, on similar background
4 main types

349
Q

What are the 4 types of apperceptive agnosia?

A
  1. Piecemeal perception
  2. Optic apraxia
  3. Constructional apraxia
  4. Contralateral disregard
350
Q

Describe piecemeal perception apperceptive agnosia

A

Inability to recognise 1+ objects at a time

351
Q

Describe constructional apraxia

A

Inability to construct 3D object using other objects or when drawing, usually produce gross simplifications

352
Q

Describe optic apraxia

A

Inaccuracies reaching for objects
Inability to judge relative position and size
Clumsiness searching for object

353
Q

Describe contralateral disregard

A

Inability to recognise opposite side of body

354
Q

Describe associative agnosia

A

Inability to name/assign meaning to object from memory

Objects described in terms of physical appearance

355
Q

Why can associative agnosia be caused by a lesion in either post. parietal lobe?

A

In visual analysis pathway info 1st passes through R lobe where objection recognition occurs then passes to L side for association with memory

356
Q

What is amnesia?

A

Deficit in memory formation/recollection

357
Q

What are the 2 types of amnesia?

A
  1. Anterograde: inability to from new memories - memories not transferred to LTM
  2. Retrograde: inability to recall experiences prior to disorder
358
Q

How are memories transferred to LTM?

A

Takes few mins

Requires consciousness, consolidation

359
Q

How can memories be held in STM longer?

A

Verbal repetition, reinsert into STM via auditory stimuli and helps consolidation
Blocked by competing sensory input

360
Q

How does LTM differ from STM?

A

LTM is hard wired, not dependent on neuronal activity
After hypothermia patient will have severe retrograde amnesia from time they were cold but normal LTM; remember name, history, how to speak

361
Q

What is the hippocampus?

A

Subcortical structure that projects into temporal lobes in primates
Important role in consolidation

362
Q

What does damage to the hippocampus cause?

A

Severe anterograde amnesia and some retrograde

363
Q

What are the 2 frontal association cortices?

A
  1. Dorsolateral frontal

2. Orbitofrontal

364
Q

What is the role of the dorsolateral frontal association cortex?

A

Executive function: decision making, error correction, troubleshooting
Forward planning, ability to conceptualise future scenarios, think through consequences and choose most appropriate

365
Q

What can damage to dorsolateral frontal cortex cause?

A

Inability to retain attention

366
Q

What is the orbitofrontal cortex associated with?

A

Limbic system

Strongly inhibits primitive emotional and motivational behaviour to accepted social norms

367
Q

What are the cortices associated with the limbic cortex?

A
  1. Cingulate
  2. Parahippocampal
  3. Orbitofrontal
368
Q

What is the role of the cingulate cortex?

A

Emotional response to pain

369
Q

What is the role of the parahippocampal cortex?

A

Memory formation - emotional memories

370
Q

What is the role of the orbitofrontal cortex?

A

Integrates other limbic cortical areas, regulates output

371
Q

What is the amygdala and its function?

A

Partly cortical, partly subcortical structure embedded in med. temporal lobe at ateroventral end of hippocampus

Emotionally labels new experiences

372
Q

What can damage to the motor cortex result in?

A

Loss of movement with variable recovery

There is plasticity so muscle control will be taken over by new area

373
Q

What is the supplementary motor area?

A

Part of cerebral cortex that contributes to muscle control

Located med. of premotor cortex (ant. of primary motor cortex)

374
Q

What do lesions in the SMA result in?

A

Difficulty initiating movement and apraxia (normal reflexes but complex tasks difficult)

375
Q

What are the 5 brain areas involved in motor control?

A
  1. Post. parietal cortex
  2. Primary somatosensory cortex
  3. Premotor cortex
  4. Supplementary motor area
  5. Prefrontal cortex
376
Q

What is the function of post. parietal cortex in movement?

A

Respond to visual/somatosensory stimuli, current/future movements and mixture of both

377
Q

What is the function of the primary somatosensory cortex?

A

Integrates touch info. and movement

378
Q

What is the function of the premotor cortex?

A

Integrates info. about body position, organises direction of movement

379
Q

What is the function of the supplementary motor cortex?

A

Organising rapid sequence of movements

380
Q

What is the role of the prefrontal cortex?

A

Plan movement according to predicted outcomes of actions

381
Q

What is apraxia?

A

Inability to properly execute learned, skilled movements following brain damage

382
Q

What are the 5 types of apraxia?

A
  1. Ideomotor
  2. Ideational
  3. Orofacial
  4. Gait
  5. Constructional
383
Q

What is ideomotor apraxia?

A

Impaired performance of movements despite intact motor, sensory and language functions
Can describe action verbally but not physically

384
Q

Describe ideational apraxia

A

Inability to perform rapid sequence of movements in complex, multistep task (tea making)

385
Q

What is orofacial apraxia?

A

Difficulty in skilled movements of face, neck, mouth, tongue, larynx, pharynx

386
Q

What is gait apraxia?

A

Loss of normal function of lower limbs w/o sensory or motor neuron damage

387
Q

What is constructional apraxia?

A

R post. parietal lobe lesion

Difficulty drawing and constructing 3D objects

388
Q

What 2 groups do axons from motor cortex descend to spinal cord in?

A
  1. Lateral: independent limb

2. Ventromedial: gross limb

389
Q

What 3 tracts travel in the lateral group?

A
  1. Corticospinal: hand/finger movements
  2. Corticobulbar: face, neck, tongue, eye
  3. Rubrospinal: fore- and hind-limb muscles
390
Q

What 4 tracts travel in ventromedial group?

A
  1. Vestibulospinal: posture
  2. Reticulospinal: walking, sneezing, muscle tone
  3. Ventral corticospinal: muscles upper leg/trunk
  4. Tectospinal: eye and head/trunk movement
391
Q

Why are the cortical output pathways described as the ‘direct motor pathway’?

A

Neurons don’t synapse until reach spinal cord

392
Q

What are the 2 major pathways from motor cortex?

A
  1. Corticospinal: body regions, fine movement

2. Corticobulbar: facial regions

393
Q

What are the 2 corticospinal tracts?

A

Ant: cross over at level of synaptic contacts with spinal motor neurons
Lat: cross over to contralateral spinal cord in pyramids

394
Q

What does damage to corticospinal tract cause?

A

Red. of dexterity (fine finger/hand movement)

Loss of muscle strength

395
Q

Describe the corticobulbar tract

A

UMN project from cortex to medulla

Terminate on LMN within brainstem motor nuclei

396
Q

What is the role of the extrapyramidal system?

A

Modulate motor activity w/o directly innervating motor neurons

397
Q

How does the extrapyramidal system work?

A

Target motor neurons in spinal cord involved in locomotion, reflexes, complex movements and postural control

398
Q

How is the extrapyramidal system modulated?

A

By various areas in CNS: basal ganglia, sensory cortical areas, cerebellum, vestibular nuclei

399
Q

What are the 2 main extrapyramidal tracts?

A
  1. Reticulospinal: projects bilaterally

2. Vestibulospinal: projects ipsilaterally

400
Q

Describe origin and inputs of reticulospinal tract

A

From reticular formation in pons and medulla

Inputs: sensory and motor cortices, cerebellar, striatum and lat. reticular nuclei

401
Q

What is the role of the reticulospinal tract?

A

Mediate control over most movements not requiring dexterity/maintenance of balance
Important in modulating reflexes

402
Q

Describe the origin of the vestibulospinal tract

A

Med. and lat. vestibular nuclei in brainstem

403
Q

What is the function of the vestibulospinal tract?

A

Control balance, posture, locomotion

404
Q

How does the vestibulospinal tract function?

A

Fluid-filled semi-circular canals in ear detect movement and orientation of head, pass info. along CNVII to vestibular nuclei in pons and medulla
Muscle spindles detect body position

Vestibular nuclei compute motor programme to send commends to extensor muscles to keep centre of gravity above feet

405
Q

What is the basal ganglia?

A

Group of nuclei of different origin that act as cohesive unit

406
Q

What are the 4 nuclei in the basal ganglia?

A
  1. Striatum: caudate and putamen
  2. Globes pallidus: interior (med), exterior (lat)
  3. Subthalamic nucleus
  4. Substantia nigra: pars reticular, pars compacta
407
Q

How does the basal ganglia connect to the spinal cord?

A

SMA -> motor cortex and basal ganglia
Basal ganglia -> motor cortex via motor thalamus
Motor cortex -> spinal cord via corticospinal and corticobulbar tracts

408
Q

What does the cerebellum connect to?

A

Vestibulospinal and reticulospinal tracts in brainstem and (via motor thalamus) motor cortex

409
Q

What is the role of the cerebellum?

A

Coordinates movement initiated by basal ganglia and motor cortex

410
Q

What are the 3 connections of the cerebellum?

A
  1. Cerebrocerebellum: limbs and trunk
  2. Spinocerebellum: planning of movement
  3. Vestibulocerebellum: eye and head, balance
411
Q

What are the 3 intrinsic factors governing coronary artery diameter?

A
  1. Physical
  2. Metabolic
  3. Autonomic
412
Q

Describe the physical control of coronary perfusion

A

Only occurs during diastole when vessels contract pushing blood down coronary arteries

413
Q

Describe the metabolic control of coronary perfusion

A

Local, transient ischaemia causes release of vasoactive metabolites

414
Q

Describe the autonomic control of coronary perfusion

A

Larger arteries: a1 adrencoceptors, vasoconstriction

Smaller: B2 adrencoceptors, relaxation

415
Q

Describe the relationship between coronary stenosis and angina

A

Stenosis (narrowing of arteries) leads to O2 deprivation to cardiac muscle
Causes sensation of chest squeezing and pain (angina) but relationship between pain severity and myocardial O2 deprivation is weak

416
Q

What are the 2 types of angina?

A
  1. Stable: classic form

2. Unstable: escalates

417
Q

Describe stable angina

A

Pain minimal at rest, develops upon physical exertion or stress
Symptoms fade rapidly upon rest

418
Q

Describe unstable angina

A

Pain at rest and on minimal physical exertion
Severe and acute onset
Crescendo pattern: each episode worse than last

419
Q

Where does the difference between the 2 types of angina lie?

A

In their pathological process

Chronic atherosclerosis vs acute vascular blockade

420
Q

What are the 3 stages of plaque formation in atherosclerosis?

A
  1. Abnormal accumulation of lipid
  2. Fibrous tissue in vessel wall narrows or occludes vessel lumen
  3. Red. blood flow through vessel
421
Q

How can stable angina lead to myocardial infarction?

A

If left untreated will lead to unstable angina, loss of O2 supply to heart muscle causes necrotic cell death in area supplied downstream to plaque/clot

422
Q

What are the 6 risk factors of angina?

A
  1. Hypertension
  2. Hyperlipidaemia
  3. Smoking
  4. Obesity
  5. Diabetes
  6. Male
423
Q

What are the 3 contributing factors to angina?

A
  1. Stress
  2. Menopause
  3. Systemic infection: helicobacter pylori
424
Q

What is the ultimate goal in treatment of angina?

A

Red. heart workload thus O2 consumption

425
Q

What is heart workload?

A

stoke vol. * arterial pressure * HR

426
Q

What 3 factors is workload of the heart affected by?

A
  1. Preload: venous return
  2. Afterload: PR
  3. Sympathetic stimulation
427
Q

What are the 3 main classes of drugs used in pharmacological treatment of angina?

A
  1. Organic nitrate donors: glyceryl trinitrate, isosorbide dinitrate
  2. B2 adrenoreceptors antagonists: propranolol, atenolol
  3. Ca2+ channel blockers: nifedipine, nicardipine
428
Q

Describe the effects of organic nitrate donors

A

Widespread vasodilation: red. preload by action on venules, red. afterload by peripheral arterial relaxation

Some action on coronary artery dilation

Adverse: vasodilation, hypotension; met-haemoglobinaemia (red. o2 carrying capacity); tolerance

429
Q

Compare glyceryl trinitrate and isosorbide mono/dinitrate

A

Glyceryl: sublingual administration, 100% first-pass metabolism, t1/2 2mins

Isosorbide: slow release, t1/2 1hr

430
Q

What are the administration routes for organic nitrate donors?

A

Sublingual: fast acting acute attack

Oral/transdermal: slow, maintenance therapy

IV: maintenance of unstable angina or threatened MI

431
Q

What effects do B-adrenoceptor antagonists have?

A

Red. O2 consumption by red. workload

Adverse:
Hypotension, bradycardia, bronchoconstriction, hyperlipidaemia
Depression, fatigue, red. libido
Risk of MI in rapid cessation

432
Q

Compare propranolol and atenolol

A

Propranolol: non-selective B1&2 adrenoceptor antagonist, can target B2 receptors in bronchioles thus not used in asthmatics

Atenolol: cardio-selective B1 adrenoceptor antagonist

433
Q

What are the 2 types of Ca2+ channel blockers?

A
  1. Cardiac favouring: diltiazam, verapamil

2. Vessel favouring: nifedipine, nicardipine

434
Q

Explain how Ca2+ channel blockers treat angina

A

Prevent Ca entry into muscle cell, red. contractility, electrical impulse propagation and vascular tone

435
Q

How do cardiac favouring Ca2+ channel blockers work?

A

Diltiazam, verapamil

Dec. SAN automaticity, red. AVN conductivity causing dec. HR and myocardial contractility

436
Q

How do vessel favouring Ca2+ channel blockers work?

A

Relax blood vessels causing dec. BP and inc. coronary artery perfusion

437
Q

What are the adverse effects of Ca2+ channel blockers?

A 
Hypotension
Bradycardia
AV block 
Gastric distress
Constipation
438
Q

What 2 types of drugs are used to supplement angina treatment?

A
  1. Anti-platelets/anti-thrombotics: aspirin

2. Antilipidaemia agents: statins

439
Q

What are Broca’s and Wernicke’s areas?

A

Broca: specialised cortical ant. to premotor cortex, adjacent to motor area for mouth that controls language vocalisation (output)

Wernicke’s: L. post., sup. temporal gyrus, control language perception (input)

440
Q

What are the 2 types of aphasia?

A
  1. Expressive: difficulty saying words; Broca’s area

2. Receptive: speak fluently in meaningless way; Wernicke’s area

441
Q

Compare Expressive and Receptive aphasia

A 
Halting; fluent
Repetitive; no repetition
Disordered grammar; grammar ok
Disordered syntax; good syntax
Disordered word order; meaningless
Sense behind words; inappropriate words
442
Q

What is the arcuate fasciculus?

A

Bundle of cortico-cortical association fibres that connect Broca’s and Wernicke’s areas
Damage results in conduction aphasia

Parallel bundles run via area known as Geschwind’s area
Supplements and enhances language function

443
Q

What is conduction aphasia?

A

Impaired ability to repeat back heard/written words
Relatively preserved language comprehension
Speech characterised by word-finding difficulties

Patients recognise paraphasias and errors, attempt to correct

444
Q

What is paraphasia?

A

Substituting of 1 word for another, often inappropriately

445
Q

What are the 3 types of paraphasia?

A

Phonemic: papple for apple
Verbal: confusing husband/wife
Neologistic: completely new word

446
Q

What is the Wernicke-Geschwind model?

A

Sounds are decoded into words and meaning in Wernicke’s area

Ideas or concepts of words are formed in Wernicke’s areas, then sent via arcuate fasciculus to Broca’s area where they are converted to motor commands to vocal muscles

447
Q

What is Wada’s test?

A

Hemisphere dominance test in which anaesthesia injected into carotid artery on 1 side of face
Anaesthetises only 1 side supplied by middle carotid artery, functions lost are noted

448
Q

Describe the lateralisation of language specialisation

A

70-95% of people have L language specialisation

Rest either have R hemisphere language specialisation or bilateral specialisation

449
Q

What is the function of the non-specialised hemisphere?

A

R said to be emotional and creative area NOT TRUE no evidence

In recovered stroke in Broca/Wernicke area patients, show activation in equivalent R hemisphere areas
Damage to R equivalents has subtle effects on language processing, especially auditory info and context

450
Q

What is the corpus callosum?

A

Large fibre tract connecting R and L hemispheres

Info in the L visual field initially processed in R visual cortex
Info cross brain to Wernicke’s area for verbal recognition

451
Q

What is the result of a corpus callosotomy?

A

Patients could recognise image but not name it as info unable to cross brain to Wernicke’s area

452
Q

Describe the relationship between handedness and speech dominance

A

Dissociative

Majority L handers have Broca and Wernicke areas on L just like R handers

453
Q

What are the 2 theories for handedness?

A
  1. Psychological/Environmental: model parents, societal pressure
  2. Genetic: R handedness dominant trait since antiquity, L handedness apparently not fully heritable

BDS 1 (11 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions