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Neuro > Unit I, Week 1 > Flashcards

Unit I, Week 1 Flashcards

1
Q

Gray matter or white matter?

Nucleus - ?
Lemniscus - ?
Ganglion - ?
Peduncle - ?

A

Nucleus - gray matter
Lemniscus - white matter
Ganglion - gray matter
Peduncle - white matter

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2
Q

Gray matter or white matter?

Cortex - ?
Funiculus - ?
Body - ?
Fasciculus - ?
Tract - ?
A 
Cortex - gray matter
Funiculus - white matter
Body - gray matter
Fasciculus - white matter
Tract - white matter
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3
Q

Astrocyte

A

large glial cell with long processes that insinuate between neural elements

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4
Q

Astrocyte functions (5)

A

1) Maintain ionic equilibrium by taking up K+ and neurotransmitters (e.g. glutamate)
2) Role in transport of nutrients from blood vessels to nearby neurons
3) Role in local regulation of blood flow
4) Central role in response to injury - prevent axonal regrowth
5) Maintain blood-brain-barrier

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5
Q

Astrocyte and uptake of glutamate

A

Astrocytes take up glutamate and convert it to glutamine → glutamine back to local neurons → neurons convert glutamine back to glutamate

Glutamate uptake also regulates local blood flow

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6
Q

Microglia

A

major phagocytic cells in CNS, undergo rapid proliferation to clear debris from brain in response to tissue damage

Arise embryologically outside neural tube, from hematopoietic tissues

Major role in brain plasticity via synapse editing - glial cell dysfunction can cause neurological/psychological disorders

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7
Q

Oligodendrocyte

A

form myelin in CNS, may myelinate several nearby axons

Prevents regeneration of axons in CNS

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8
Q

Schwann cell

A

glial cell in PNS, form myelin in PNS, myelinates only one axon

Determine if axon can regrow, creates path new axon can grow on

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9
Q

Dendrite

A

Passive conductors of electrical energy (signal decreases with distance)

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10
Q

Axon

A

Contains voltage-sensitive ion channels capable of propagating AP

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11
Q

Nissl substance

A

distinctive rough endoplasmic reticulum in neuronal cell bodies

Neurons have lots of protein production in cell body that can then be transported down axon to peripheral terminals

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12
Q

Autoregulation of cerebral blood flow:

increased BP –> ?

A

increased BP → mechanical stretch of arteriole wall → activation of second messenger cascade → inhibition of calcium-activated-K+ channel → prevent K+ out = depolarization → Ca2+ influx → activation of arteriole muscle wall

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13
Q

Functional Hyperemia

A

Local increase in neuronal activity → increase in local blood flow (basis for fMRI and PET scans)

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14
Q

Two mechanisms causing functional hyperemia

A

1) NO released by neurons diffuses to reach local vessels to cause dilation
2) Astrocytes

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15
Q

Why substances in circulatory system do not freely enter brain parenchyma

A

Capillaries in brain are NOT fenestrated, connected by tight junctions → requires diffusion or transport through endothelial cell

BBB maintained by astrocytes - tell endothelial cells to maintain tight junctions

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16
Q

How astrocytes regulate local blood flow in proportion to neuronal activity:

increased neuronal activity –> ??

A

Astrocyte “foot processes” extend towards local blood vessels, contact vessel walls → carry nutrients and oxygen to from vessels to neurons and regulates vessel function

Increased neuronal activity →

1) increased astrocytes uptake of glutamate (most prevalent NT)
2) → causes release of arachidonic acid in astrocytes
3) → arachidonic acid converted by P450 enzyme to form epoxyeicosatrienoic acid (EET)
4) → astrocyte EET released and acts to hyperpolarize arteriole membrane
5) → decrease vascular tone → larger lumen → increased blood flow

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17
Q

Nerve regeneration in the PNS

A

Minor damage → distal portion of nerve ending degenerates, but regeneration begins from end still attached to cell body

Long term effects: alterations in sensory perception in affected area (hypersensitivity, hyperalgesia, allodynia)

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18
Q

What type of cells are responsible for nerve regeneration in the PNS

A

Schwann cells

Regeneration of axons along course of original nerve, facilitated by Schwann cells

Schwann cells clear myelin debris, then line endoneurium to form substrate for outgrowth of axons from cut stump of nerve

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19
Q

Nerve regeneration in the CNS

what cells are responsible for this process?

A

Damage →

Oligodendrocytes do not clear myelin debris - proliferate and upregulate expression of molecules (chondrotin, sulfate proteoglycans) that inhibit axonal outgrowth
-Axons do not regrow!

Microglia activate local astrocytes to form glial scar → chemical and physical barrier to neuronal regeneration

Capacity for CNS regrowth remains, but is limited

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20
Q

Anterior circulation is supplied by what artery and brings blood to what part of the brain?

A

from internal carotid artery → entire cerebral hemisphere except medial occipital lobe and inferior part of temporal lobe

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21
Q

Internal carotid artery branches into ________ and ________

A

anterior and middle cerebral arteries

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22
Q

Anterior cerebral artery supplies blood to where?

A

Anterior cerebral → longitudinal fissure to supply anterior ⅔ of medial face of cerebral hemisphere and orbital cortex

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23
Q

Middle cerebral artery supplies blood to where?

A

Middle cerebral artery → lateral fissure to supply lateral face of cerebrum (frontal, parietal, and temporal lobes)

Gives off penetrating branches to supply deep white and gray matter of cerebral cortex

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24
Q

Posterior circulation of the brain gets blood from what artery and supplies blood to what region of the brain?

A

from vertebral arteries → brainstem, cerebellum, some cortex (medial occipital, inferior temporal lobe)

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25
Q

At the level of the _____, vertebral arteries fuse to form the ________ → splits at base of midbrain to form paired ________ → which 2 regions of the brain?

A

At level of pons, vertebral arteries fuse to form basilar artery → splits at base of midbrain to form paired posterior cerebral arteries → medial face of occipital lobe and inferior surface of temporal lobe

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26
Q

Along course of vertebral/basilar system, circumferential branches wrap around brainstem

What are the 3 named circumferential branches?

A

All circumferential branches supply blood to dorsal brainstem and overlaying cerebellum

1) Posterior Inferior Cerebellar Artery (PICA)
2) Anterior Inferior Cerebellar Artery (AICA)
3) Superior Cerebellar Artery (SCA)

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27
Q

Posterior Inferior Cerebellar Artery (PICA):

branch off of ______ artery, wraps ______ and supplies ________

A

branch off vertebral artery, wraps medulla and supplies most caudal cerebellum

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28
Q

Anterior Inferior Cerebellar Artery (AICA)

branch off ______ and wraps _______ and supplies ______

A

branch off basilar artery, wraps caudal pons, supplies anterior/inferior cerebellum

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29
Q

Superior Cerebellar Artery (SCA)

branch off ______ and wraps _______ and supplies ______

A

branch off basilar artery, wraps around rostral pons, supplies superior face of cerebellum

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30
Q

Vertebral arteries split into _______ and _______ to supply blood to the _________

A

Vertebral arteries → Anterior and posterior spinal arteries → rostral spinal cord

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31
Q

Posterior and Anterior circulation systems are INTERCONNECTED via what two mechanisms?

A

1) End-to-End Anastomosis between terminal vessels of two systems where they abut across cerebral cortex
2) Circle of Willis

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32
Q

Entire blood flow to CNS can be supplied via any of 3 major vessels: _______, _______ or ________

A

L Carotid, R Carotid, or Basilar artery

A slow occlusion will not cause problems, because blood supply can compensate via a different pathway

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33
Q

Review venous drainage images

A

DO IT

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34
Q

Review circle of Willis diagram

A

MEMORIZE THAT SHIT

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35
Q

Lateral Ventricles

A

Paired ventricle

include former 1st and 2nd ventricles

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36
Q

Interventricular foramen connects ______ with _______

A

connects lateral ventricles with 3rd ventricle (one for each lateral ventricle)

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37
Q

Cerebral aqueduct connects ______ with _______

A

connects 3rd and 4th ventricles

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38
Q

what connects the 4th ventricle with the subarachnoid space?

A

Three apertures (two lateral, one caudal) connect 4th ventricle with subarachnoid space

CSF gets reabsorbed through subarachnoid space

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39
Q

Ependyma

A

single cell layer lining ventricles

Leaky → CSF in ventricles exchanges freely with ECF in interstitial space in brain

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40
Q

Choroid Plexus

A

specialized ependymal cells that produce CSF

Brain capillaries lose their tight junctions in choroid plexus and ependymal cells acquire tight junctions → solutes diffuse out of capillaries, and actively transported across ependymal cells to get into CSF

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41
Q

CSF

A

buoys up brain, dampens shock of blows to head

500 ml of CSF produced daily by choroid plexus

Ionic composition very close to plasma, but highly regulated and stabilized because it is ECF for neurons

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42
Q

Resorption of CSF

A

by arachnoid granulations that line principal dural sinuses in subarachnoid space

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43
Q

Blockage in CSF flow or failure in resorption → ??

A

increase intracranial fluid pressure → hydrocephalus (CSF non-compressible, but brain tissue is compressible → ventricles expand at expense of brain tissue)

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44
Q

Non-Communicating Hydrocephalus

A

flow of CSF interrupted (e.g. by block of interventricular foramen of cerebral aqueduct)

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45
Q

Communicating Hydrocephalus

A

CSF gets into subarachnoid space, but isn’t resorbed properly into the bloodstream

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46
Q

Meninges: inside to outside = ______, ______ then ______

A

(inside) pia, arachnoid, then dura (outside)

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47
Q

Pia

A

single cell layer covering outside of CNS, not separable from brain surface

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48
Q

Arachnoid

A

loose spongy layer between pia and dura

Subarachnoid space filled with CSF

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49
Q

Dura

A

leathery layer closely applied to cranium, but loose on spinal column

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50
Q

EPSP/IPSP (inhibitory/excitatory post synaptic potential) vs. action potential

A

EPSP/IPSP:

  • longer duration
  • fluctuations in potential causing electrical current, but may or may not cause an AP

Action Potential:

  • brief duration
  • propagated along axon
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51
Q

Pyramidal cells

A

where summation of electrical potential changes in cerebral cortex occurs

Vertically oriented neurons

Cell body in deep layer, dendrites extend through all layers of cortex → guide flow of currents generated by postsynaptic potentials through entire thickness of cortex

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52
Q

Electroencephalography (EEG)

A

measures electrical potential fluctuations at scalp surface

Fluctuations produced by temporal and spatial summation of electrical currents caused by slow postsynaptic potentials (EPSPs, IPSPs)

  • APs are very short and contribute very little
  • Captures “field potentials”, which represent synchronized activity across many neuronal elements and include subthreshold synaptic potentials
  • Measure populations of partially synchronized neurons, and not individual neuronal activity
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53
Q

Event Related Potentials (ERP)

A

EEG recording obtained during specific task

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54
Q

Magnetoencephalography (MEG)

A

measures small magnetic fields induced by electrical current flux

Measure populations of partially synchronized neurons, and not individual neuronal activity

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55
Q

Techniques for evaluating brain activity using ELECTROMAGNETIC properties (3)

A

1) EEG
2) ERP
3) MEG

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56
Q

Techniques for evaluating brain activity using HEMODYNAMIC properties (2)

A

1) PET

2) fMRI

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57
Q

Positron Emission Tomography (PET)

A

Inject positron-emitting radionuclide labeled tracer → radionuclide in radiotracer decays, releasing positrons that contact and annihilate electrons → each annihilation produces 2 photons traveling in opposite directions that then encounter detectors arranged circumferentially around subject

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58
Q

Types of radionuclide labeled tracers that can be used for PET scan and what they show

H2(15)O → ?
18-Fluorodeoxyglucose (18-FDG) → ?
18-Fluorodopa (18-FD) → ?

A

H2(15)O → rough measure of cerebral blood flow
18-Fluorodeoxyglucose (18-FDG) → map of glucose metabolism
18-Fluorodopa (18-FD) → loci in brain where L-dopa converted to dopamine

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59
Q

Functional MRI (fMRI)

A

Signal changes due to regional changes in deoxyhemoglobin concentration associated with synaptic activity

BOLD = Blood Oxygen Level Dependent Signal

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60
Q

fMRI - oxy vs. deoxy hemoglobin?

A 
Oxyhemoglobin = diamagnetic, does NOT distort magnetic field
Deoxyhemoglobin = paramagnetic, distorts magnetic field
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61
Q

Diffusion Tensor Imaging (DTI)

A

Allows direct examination, in vivo, of some aspects of tissue micro-structure

Quantitative measure of integrity of white-matter fiber tracts

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62
Q

Connectomics

A

comprehensive description of structural relationships within nervous system, represented graphically

Graphs altered in a number of diseases, can be useful biomarkers for disease

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63
Q

Driving force

A

difference between reversal potential and actual potential

Nernst Equation used to calculate the reversal potential

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64
Q

Electrical Synaptic Transmission

A

couple and synchronize cells that need to fire together via gap junctions between cells

Cytoplasmic continuity between cells

Rare in nervous system of mammals

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65
Q

Advantages of Electrical Synaptic Transmission (5)

A

1) Very fast transmission, delay is virtually absent
2) Simple
3) Bidirectional
4) Easy to trigger synchronous activity
5) No delay

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66
Q

Examples of electrical synaptic transmission (6)

A

1) Escape reflexes in animal kingdom
2) Cardiac muscle contraction
3) CNS: dear learning, emotional memory in hippocampus
4) Contribution to establishment of theta rhythms
5) Other synchronously firing networks
6) Development of retina and inner ear

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67
Q

Limitations of electrical synaptic transmission (4)

A

1) In order to provide enough current to depolarize postsynaptic cell to threshold, presynaptic terminal has to be comparable in size to postsynaptic cell
2) Electrical transmission is ALWAYS excitatory - no complex integration of excitatory and inhibitory signals
3) Signal cannot be amplified
4) Cannot modulate signal

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68
Q

Steps of synaptic transmission

from AP arriving in presynaptic terminal → until NT diffuses into cleft

A

→ terminal depolarizes → depolarization causes voltage gated Ca2+ channels to open

→ Ca2+ flows into cell

→ Ca2+ encounters docked and primed synaptic vesicles → Ca2+ binds synaptotagmin and triggers fusion of lipids of vesicle with surface membrane = fusion pore opening

→ NT diffuses out of vesicle into synaptic cleft via exocytosis

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69
Q

Steps of synaptic transmission after NT released into synaptic cleft

A

→ diffusion across synaptic cleft

→ NT binds postsynaptic membrane at receptor

→ receptors open and allow positive ions to enter cell (in case of NMJ)

→ Depolarization (EPSP)

→ if threshold reached causes AP

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70
Q

Postsynaptic receptor determines…

A

Postsynaptic receptor determines if signal is: excitatory or inhibitory, fast or slow, membrane potential change brief or persistent

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71
Q

SNARE complex

A

SNARE complex holds vesicle to presynaptic terminal to ensure that vesicle fuses with the membrane, and fuses only when you want it to

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72
Q

Synaptobrevin

A

protein on vesicle that interacts with corresponding molecules in presynaptic membrane

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73
Q

Synaptotagmin

A

protein on vesicle that senses calcium

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74
Q

SNAP25 and Syntaxin

A

SNAP25 and Syntaxin (binds synaptobrevin): in presynaptic membrane

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75
Q

How is Ca2+ pumped out of the cell after AP (2)

A

1) ATP driven Ca2+ pump (primary active transport)

2) Na-Ca exchanger (secondary active transport)

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76
Q

How can NT be removed from the synaptic cleft? (3)

A

1) Diffusion out of cleft into ECF
2) Recycled
3) Destroyed

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77
Q

NT recycling

A
  • Pumped back into presynaptic terminal and back into synaptic vesicles (and neighboring glial cells)
  • Least important at NMJ, most important in CNS

EX) Drugs like amphetamine, cocaine, and Prozac block reuptake of monoamine transmitters like dopamine and serotonin

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78
Q

NT destruction in synaptic cleft

A

NT destroyed by tethered extracellular degradative enzyme (Acetylcholine esterase destroys ACh at NMJ)

*Does not occur in CNS

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79
Q

After releasing their contents into the synaptic cleft, how are vesicle membranes re-internalized?

A

Vesicle membrane re-internalized (endocytosis) and refilled with NT

Clathrin shapes vesicle, while dynein pinches off new vesicle

Synaptic vesicle recycling can take several seconds in well rested synapse or up to a minute in a hard working one

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80
Q

How can NTs be produced?

A

Synthesized locally by enzymes in nerve terminal cytoplasm, then pumped back into vesicle via sodium-coupled transporter proteins in vesicle membrane

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81
Q

NMJ vs. CNS synapses:

Speed
Effect
Strength
Transmitter
Transmitter termination
"Intelligence"
A

NMJ

  • Speed = fast
  • Effect = excitatory
  • Strength = strong
  • Transmitter = ACh
  • Transmitter termination = diffusion, degradation, minimal to no reuptake
  • “Intelligence” = stupid

CNS

-Speed = fast or slow
-Effect = excitatory or inhibitory
-Strength = weak (many inputs required to have AP, no safety factor)
-Transmitter = many different kinds
-Transmitter termination = reuptake, diffusion, minimal to no degredation
“Intelligence” = smart

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82
Q

Motor unit

A

Single motor neuron branches to innervate many individual muscle fibers

axon + muscle fibers = Motor Unit

(smallest unit of force in skeletal muscle)

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83
Q

ACh receptor

A

ligand gated ion channel only located at synapse on muscle fiber

Permeable to ALL cations (non-selective cation channel, NSC) (Na+ and K+)

Synaptic reversal potential = -10 mV (between Ek/ENa)

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84
Q

Structure of ACh receptor

A

pentameric, 5 subunits arranged around central pore

2 ACh molecules must bind simultaneously, one to each of 2 alpha subunits

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85
Q

If threshold for AP (-50mV) in a muscle fiber is reached then…

A

→ voltage gated sodium channels open and AP propagates

Single muscle fiber twitch if threshold is reached regardless of how much threshold is exceeded

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86
Q

Acetylcholinesterase

A

located inside synaptic cleft, breaks down ACh

Breaks down half of ACh before it gets to postsynaptic side

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87
Q

Job description for motor nerve terminal

A

every time an AP arrives from CNS, you must secrete enough ACh to depolarize the muscle fiber you innervate to threshold for an AP (requires SAFETY FACTOR)

Depolarize muscle by 30 mV (-80 to -50 mV)

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88
Q

Amplification of Neuromuscular Signal - why do we need it, and how do we do it?

A

Nerve terminal is much smaller than muscle fiber it innervates → wouldn’t provide enough current needed to depolarize muscle by necessary 30 mV

**CHEMISTRY provides the amplifier

-Electrical signal converted to chemical signal with ACh release from up to 100 synaptic vesicles (each vesicle = 1 mV depolarization)

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89
Q

_______ and _______ are two opposing processes that occur together during repetitive stimulation

A

Synaptic facilitation and depression

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90
Q

Synaptic facilitation

A

During high frequency stimulation Ca2+ concentration inside nerve terminal increases because it can’t get pumped out fast enough → more Ca2+ to bind vesicles → number of quanta secreted INCREASES during repetitive stimulation

**Effect recovers within milliseconds

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91
Q

Myasthenic syndrome

A

antibodies to presynaptic Ca2+ channels - patients are weak and become stronger with exercise

facilitation allows stronger signals with repetitive stimulation

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92
Q

Synaptic Depression of Transmitter Release

A
  • reduction of number of available vesicles during periods of high frequency activity
  • Nerve terminal cannot replenish synaptic vesicles from reserve pool fast enough to keep up with demand

**Effect recovers in seconds up to about 1 minute

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93
Q

Myasthenia gravis

A

antibodies to postsynaptic acetylcholine receptors - patients are weak and become weaker with exercise

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94
Q

Direct (fast) Synapses

aka ionotropic

A

neurotransmitter directly binds gate, instantly changing membrane permeability

Underlies our immediate conscious behavior and ability to respond quickly to sensory stimulation

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95
Q

Indirect (slow) Synapses

aka metabatropic

A

neurotransmitter receptor protein is NOT an ion channel, but a transmembrane protein that undergoes structural rearrangement when transmitter binds → G protein (second messenger) molecules diffuse and bind to nearby ion channels

  • Slower to turn on, and turn off - 2nd messengers stay in cytoplasm longer than NT in synaptic cleft
  • 2nd messengers can also cause changes in gene expression in nucleus
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96
Q

________ and _______ are examples of NTs that act via metabotropic receptors

A

Catecholamines (epi, norepi, and doapine)

Serotonin

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97
Q

_________ is a NT that can cause both fast (direct) and slow (indirect) activation in the same cell

A

Acetylcholine

Fast excitation via NSC channel = Nicotinic ACh receptor

Slow excitation via G protein channel = Muscarinic ACh receptor

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98
Q

Inhibitory synapses

A

membrane potential is below threshold - can be hyperpolarizing, depolarizing, or shunting (nothing happens)

EX) K+ selective channel

Some inhibitory nerve terminals synapse on other (excitatory) presynaptic terminals INHIBITING presynaptic transmitter release

EX) Cl- channels opened by GABA on presynaptic neuron, causing fewer Ca2+ channels to open in response to AP and thus less excitatory transmitter release

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99
Q

________ and ______ are the major inhibitory transmitters and open what kind of channels?

A

GABA and Glycine = major inhibitory transmitters

Opens Cl- channel

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100
Q

Inhibition is more powerful than one might predict from the size of an IPSP because…

A

Typically located closer to axon hillock

Reversal potential of inhibitory synapses near resting potential such that inhibitory postsynaptic potentials are small, BUT inhibition is powerful

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101
Q

Excitatory synapses

major NT is ______ and opens ______ channel

A

membrane potential more positive (closer to threshold)

EX) Na+ selective channel

Glutamate = major excitatory transmitter
-Opens NSC (nonselective) channel

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102
Q

Factors influencing neural integration (5)

A

1) Reversal potential (excitatory or inhibitory)
2) Size of each synapse
3) Distance of each synapse from soma/axon hillock
4) Number of excitatory vs. inhibitory synapses active
5) Leakiness of neuron

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103
Q

Spatial summation

A

individual synaptic inputs converge to summate, driving postsynaptic membrane potential towards threshold for AP, two or more different inputs contribute

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104
Q

Temporal summation

A

same individual input/synapse stimulated in succession (both facilitation and summation cause larger depolarization) → cell depolarizes more and more until threshold is reached

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105
Q

Smart synapses

  • excitatory or inhibitory?
  • what is NT?
  • what types of receptors?
A

Involved in synaptic plasticity

  • excitatory
  • Glutamate is transmitter
  • Contains two types of glutamate receptors:

NMDA receptor

AMPA receptor

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106
Q

AMPA receptor

A

NSC channel, gated open by glutamate transmitter

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107
Q

NMDA receptor

3 important properties

A

coincidence detector (requires two events to happen simultaneously before conducting ions)

1) Binds glutamate
2) Have pore plugged by magnesium ion
3) High permeability to Ca2+

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108
Q

What two events are required to open NMDA receptor

A

Requires presynaptic activation via glutamate binding to ligand gate, AND postsynaptic AP electrically “popping out” Mg2+ from pore → clears way for Ca2+ to enter cell

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109
Q

After NMDA receptor is opened and once Ca2+ is in postsynaptic cell, it STRENGTHENS the synapse by…(2)

A

1) 1) Insertion of additional AMPA receptors into postsynaptic membrane
2) Presynaptic strengthening by NMDA receptor activation

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110
Q

How are additional AMPA receptors put into postsynaptic membrane?

A

Ca2+ influx triggers exocytosis of vesicles containing AMPA receptors → increased size of glutamate induced synaptic potentials

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111
Q

How does presynaptic strengthening by NMDA receptor activation happen?

A

Requires RETROGRADE signal from postsynaptic cell to presynaptic terminal = postsynaptic NO synthesis → diffuses back across synapse to potentiate transmitter release

→ more transmitter quanta released in response to presynaptic AP

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112
Q

Silent synapses

A

no AMPA receptors, only NMDA receptors → only active with both pre and postsynaptic activation

Can become un-silent with insertion of AMPA receptors

Important in developing brain

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113
Q

Tetanus Toxin Mechanism of Action

A

Tetanospasmin binds peripheral nerve terminal

→ transported via axons and across synaptic junction to CNS → becomes fixed to gangliosides at presynaptic inhibitory motor nerve endings and taken up by endocytosis

→ blocks release of inhibitory neurotransmitter with zinc dependent endopeptidases that selectively cleave synaptobrevin protein on synaptic vesicles → spasms

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114
Q

Botulinum Toxin Mechanism of Action

A

Toxin is specific for PERIPHERAL nerve endings, prevents release of acetylcholine across synaptic cleft by selectively cleaving synaptobrevin protein via zinc dependent endopeptidase

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115
Q

Safety factor at NMJ

A

many more vesicles are released than are necessary to cause 30 mV depolarization to reach threshold

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116
Q

Is there a safety factor in CNS?

A

NO

  • CNS synapse is weak, each presynaptic terminal (bouton) contains a single active zone, and a few dozen releasable vesicles
  • A single AP in a CNS bouton often fails to produce exocytosis of any vesicles at all
  • Each postsynaptic cell weight combined input from many separate individuals before deciding whether to fire an AP
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117
Q

Long Term Potentiation (LTP)

A

increase in synaptic current produced by a synapse after a pairing event

Associative plasticity that results when a presynaptic signal is combined with a unique signal from the postsynaptic cell

Relies on NMDA receptor (coincidence detector)

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118
Q

Long Term Depression (LTD)

A

decrease in synaptic current produced by synapse after pairing event

Low frequency stimulation causes synaptic responses to become smaller and stay smaller

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119
Q

What is the difference between synaptic facilitation and LTP?

A

Both increase amplitude of synaptic response

Facilitation is increased synaptic response amplitude due to higher Ca2+ concentration in presynaptic terminal, short term

LTP is increased synaptic response amplitude due to more postsynaptic receptors, longer term

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120
Q

How can you discriminate between facilitation and summation?

A

Facilitation is second synaptic event being larger due to Ca2+ in terminal

Summation is slow increase in membrane potential due to frequent stimulation - may or may not result in AP

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121
Q

Curare

A

competitively and reversibly inhibits nicotinic acetylcholine receptor at NMJ (competitive antagonist of N-M receptor)

-used to be used as a paralytic

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122
Q

Do curare or rocuronium stop the release of minis (basically NT incontinence)?

A

NO - curare and rocuronium work on post-synaptic membrane and minis come from presynaptic terminal

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123
Q

How does GABA-A and GABA-B signaling work differently?

A 
GABA-A = iontropic, direct
GABA-B = metabotropic, indirect
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124
Q

Synthesis of Acetylcholine

A

Acetyl-CoA + Choline → ACh + CoA via Choline Acetyl Transferase (CAT)
Choline uptake is rate limiting step

125
Q

Acetylcholine receptor types

A

Muscarinic Receptors

Nicotinic Receptors:
N-N (open receptor gated cation channel)
N-M

126
Q

Muscarinic receptor subtypes and their general mechanism of action

A

M1-M3 (Gq → stimulate PLC activity)

M2-M4 (Gi/o → inhibit AC activity)

127
Q

_______ is the rate limiting step in the synthesis of catecholamines (NE and dopamine)

A

Tyosine hydroxylase catalysis of tyrosine –> L-Dopa

128
Q

Dopamine receptors general mechanism

D1 –>
D2 –>

A

D1 (Gs → stimulate AC activity)

D2 (Gi/o → inhibit AC activity)

129
Q

Norepinephrine receptors general mechanism

a1 adrenergic
a2 adrenergic
B1 adrenergic
B2 adrenergic

A

a1 adrenergic (Gq → stimulate phospholipase C)

a2 adrenergic (Gi/o → inhibit AC activity, K+ channel opening)

B1 adrenergic (Gs → stimulate AC activity)

B2 adrenergic (Gs → stimulate AC activity)

130
Q

Rate limiting step in the synthesis of serotonin

A

Tryptophan hydroxylase catalysis of conversion of tryptophan –> 5-OH-tryptophan

131
Q

Receptors for serotonin general mechanism

5HT-1A, 1B, 1D –> ?
5HT-2A, 2B, 2C –> ?
5HT3 –> ?
5HT4 –> ?

A

5HT-1A, 1B, 1D (Gi/o → inhibit AC activity, open K+ channel)

5HT-2A, 2B, 2C (Gq → stimulate PLC activity, close Ca2+ channel)

5HT3 (Ligand-gated cation channel, excitatory)

5HT4 (Gs → stimulate AC activity)

132
Q

Monoamines (serotonin, NE, dopamine) are taken up and stored in vesicles by ________ and is degraded by _______

A

VMAT - vesicular monoamine transporter

Monoamine oxidase (MAO)

once serotonin is taken back up into cytosol, inactivated by MAO or transported into vesicles by VMAT

133
Q

inhibition of VMAT results in…

A

block vesicular uptake of monoamines = increased degradation by MAO → decreased monoamine release/action

134
Q

inhibition of MAO results in…

A

decrease degradation by MAO = more vesicular storage → increased monoamine release/action

135
Q

GABA synthesis

A

Precursor = Glutamate

Glutamate → GABA via GAD (glutamic acid decarboxylase)

136
Q

GABA-A vs. GABA-B receptors

A

GABA-A: opens ligand-gated Cl-channel → decrease neuronal excitability (IPSP)
-Postsynaptic only

GABA-B: Gi/o → inhibit AC, decrease Ca2+ conductance, open K+ channel
-Pre and postsynaptic

137
Q

Benzodiazepines mechanism of action

A

AMPLIFY GABA EFFECT

bind GABA-A receptor, increase GABA inhibitory action

Treat seizures caused by depressed GABA activity and anxiety caused by excessive amygdala activity/depressed GABA activity)

138
Q

Tiagabine mechanism of action

A

inhibit reuptake of GABA

139
Q

Vigabatrin mechanism of action

A

inhibit degradation by GABA-transaminase (GABA-T)

140
Q

Glutamate synthesis

A

Glutamine → glutamate via Glutaminase in nerve endings, stored in synaptic vesicles

Dependent on interaction between nerve terminals and glial cells

141
Q

Ionotropic glutamate receptors (3)

A

NMDA (Ca2+ influx)
AMPA (Na+ and Ca2+ influx)
Kainate (Na+ influx)

142
Q

Metabatropic glutamate receptors

R1-R5 –> ?

R2-R3 –> ?

R4-R6-R7-R8 –> ?

A

R1-R5 (Gq → increase PLC activity)

R2-R3 (Gi/o → decreased AC activity, inhibit VSCC, activate K+ channels)

R4-R6-R7-R8 (Gi/o → decreased AC activity, inhibit VSCC)

143
Q

Hierarchical Systems

A

Clearly delineated pathways directly involved in motor control and sensory perception

Large myelinated neurons with rapid conduction velocity

Sensory info processed sequentially and integrated successively at relay nuclei on the way to cortex - lesion disrupts pathway

Relay and local circuit neurons present at each nuclei

144
Q

Relay neurons

A

in pathways that transmit signals over long distances, feed forward

Excitatory → NT = glutamate

145
Q

Local circuit interneurons

A

synapse on relay neuron cell body or on axon in spinal cord

Inhibitory → NT = GABA

146
Q

Diffuse Systems

A

Modulate the function of hierarchical systems

**Neurotransmitters: ACh, monoamines

Produced in neurons whose cell bodies lie in small discrete nuclei (usually in brainstem)

Axons very divergent, single neuron can innervate functionally distinct parts of CNS

CANNOT convey topographically specific information

Affect vast CNS areas simultaneously, subserving global functions - e.g. attention, sleep-wake cycle, appetite, emotions

147
Q

Primary vesicles

A

Prosencephalon (forebrain)
Mesencephalon (midbrain)
Rhombencephalon (hindbrain)

  • Segmentation of hollow neural tube along rostrocaudal axis
  • Gives rise to 5 secondary cerebral vesicles
148
Q

5 secondary cerebral vesicles

A 
Telencephalon
Diencephalon
Mesencephalon
Metencephalon
Myelencephalon
149
Q

Prosencephalon –> ________ and ________

A

telencephalon and diencephalon

150
Q

Paired telencephalon –> what adult brain structures?

A

cerebral hemispheres each with lateral ventricle

151
Q

Diencephalon –> what adult brain structures?

A

thalamus, hypothalamus, subthalamus, epithalamus, and third ventricle

152
Q

Mesencephalon –> what adult brain structures?

A

mesencephalon and cerebral aqueduct

153
Q

Cephalic flexure

A

Bending of neural tube occurs between diencephalon (prosencephalon) and mesencephalon, prosencephalon bends 80 degrees forward

154
Q

Rhombencephalon –> _______ and _______ as well as the ______ ventricle

A

metencephalon (cranial) and myelencephalon (caudal)

fourth ventricle

155
Q

Metencephalon → what adult brain structures

A

pons, cerebellum

156
Q

Myelencephalon → what adult brain structures

A

medulla

157
Q

The spinal cord and central canal come from what embryologic structure

A

neural tube

158
Q

Review of embryogenesis:

Inner cell mass –> _________ –> ___________

A

two layered germ disc (epiblast + hypoblast)

three layered germ disc (ectoderm, mesoderm, endoderm)

159
Q

Primitive streak

A

formed when caudal half of epiblast (part of two layered germ disc) thickens and elongates via addition of cells

Cranial end → Primitive Node (aka Primitive Knot, Hensen’s node)

160
Q

Primitive groove

A

formed in middle of primitive streak

161
Q

Notochord is formed what what layer of the germ disc?

A

mesoderm

162
Q

Notochord secretes ______ and influences the _____ layer to divide rapidly and form _________

A

sonic hedgehog

ECTODERM

thickened NEURAL PLATE

163
Q

How is neural tube formed?

A

ECTODERM (of germ disc)→ NEURAL PLATE

Neural groove forms in center of neural plate → neural folds → folds fuse → NEURAL TUBE

164
Q

What does the neural tube from?

A

the nervous system!

Cerebral hemispheres, segments of brainstem, spinal cord, and their respective fluid-filled cavities (ventricles)

Undergoes rostrocaudal patterning

165
Q

Dorsoventral Patterning in Spinal cord

A

Neural progenitors develop into different cell populations based on distinct position along dorsal-ventral axis

Divide populations into alar plate and basal plate on each side of tube, separated by sulcus limitans

166
Q

Basal Plate

A

Ventral aspect of neural tube

→ motor neurons (efferent)

167
Q

Alar plate

A

Dorsal aspect of neural tube → afferent neurons receiving sensory input from cells of dorsal root ganglion carrying sensory information

168
Q

Sulcus limitans

A

separates alar plate and basal plate on neural tube

169
Q

Notochord secretes sonic hedgehog with higher concentration _______, contributing to what forebrain developmental dorsoventral pattern

A

Notochord secretes SHH, with higher concentration VENTRALLY than it is dorsally → dorsally get telencephalic vesicles forming

Without SHH, vesicles don’t form properly

170
Q

3 discrete proliferative zones of forebrain that undergo dorsoventral patterning

A

1) Cortex (dorsal)
2) Lateral and medial ganglionic eminences
3) Basal forebrain

171
Q

The ganglionic eminences form what adult brain structures?

A

Ganglionic eminence → subcortical gray matter (caudate, putamen, globus pallidus)

172
Q

Rostrocaudal Patterning of Neural Tube

A

-Initial definition of RC patterning occurs with implantation (leading edge is caudal end of embryo)

RC patterning results in enlargements of rostral end of tube → primary cerebral vesicles (see above)

173
Q

Rhombomeres

A

8 morphologically distinct elements of rhombencephalon

Cells in each rhombomere differ in morphology, axonal trajectory, NT synthesis, NT selectivity, firing properties, and synapse specificity

Specific combination of Hox genes expressed in particular rhombomere varies with position along AP (rostral-caudal) axis

174
Q

Hox genes

A

transcription factors, activate expression of downstream genes → activate specific/distinct programs of differentiation
Trigger different programs of differentiation along rostrocaudal axis

175
Q

Morphogens

A

secreted by anterior and posterior structures of neural tube, establishing a concentration gradient along AP axis

176
Q

Morphogens are secreted from where and results in what type of development?

A

1) Primitive node –> Wnts, FGFs, Retinoic Acid → Caudal structure development
2) Anterior Visceral Endoderm (underlying prechordal plate) = Cerebrus, dickkopf → Forebrain development

177
Q

Neuroepithelial cell layer

A

pseudostratified ectoderm of neural tube

Neuroepithelial cell layer will form all cellular elements of CNS (except microglia)

Period of rapid cell replication of daughter cells in this layer → cell migration

178
Q

Radial migration

A

migration away from inner multiplication zone to outer edges of growing wall of neural tube

179
Q

Telencephalon “inside out” development

A

Telencephalon develops in “inside-out” fashion to form cortex

Cortex = 6 cell layers, each with distinct pattern of organization and connections

Deepest layer formed first, each successive migration ascends farther, forming more superficial layers

Cells follow radial glial guides → important preceding cells “get off” the ladder before others can follow

180
Q

Motor or sensory?

Precentral gyrus
Postcentral gyrus

A

Precentral gyrus = primary motor cortex

Postcentral gyrus = somatosensory cortex

181
Q

Internal Capsule

A

pathway of axons that separate caudate nucleus and thalamus from putamen and globus pallidus

182
Q

Pathway of axons from cerebral cortex:

_______ —> _______ –> ______ —> ________ –> _____

A

Corona radiata (above caudate and putamen)

→ internal capsule (separating caudate and putamen)

→ Crus cerebri

→ through pons

→ pyramid of brainstem (ventral surface of medulla) - where axons cross midline

183
Q

Lateral corticospinal tract (aka pyramidal tract)

A

axons that travel from precentral gyrus (primary motor cortex) and descend into spinal cord

184
Q

Describe the pathway of the lateral corticospinal tract (4)

A

1) Cells in precentral gyrus (primary motor cortex) stimulated (output cells in bottom layer of 6 layered cortex)
2) → cells project through white matter, continue down into brainstem where they cross midline at the decussation of the pyramid
3) → lateral corticospinal tract descends spinal cord and synapse on alpha-motor neuron (output cells on VENTRAL gray matter)
4) → joins spinal nerve and innervates contralateral muscle

185
Q

alpha motor neuron

A

output cells on VENTRAL gray matter, large fiber diameter and fast conduction velocity

186
Q

what determines where the lateral corticospinal tract terminates in spinal cord?

A

lateral corticospinal tract descends spinal cord and terminates in spinal cord depending on where in the cerebral cortex they originated

187
Q

Anterior corticospinal tract

-how is this different from lateral corticospinal tract?

A
  • Do not cross, remain ipsilateral
  • Innervate alpha-motor neurons in more MEDIAL gray matter of spinal cord that are responsible for core muscle groups that maintain posture
  • Innervate IPSILATERAL alpha motor neurons and cross at ANTERIOR WHITE COMMISSURE to other side
188
Q

Anterior white commissure

A

where anterior corticospinal tract crosses midline in the spinal cord

189
Q

What happens to your anterior and lateral corticospinal tract if you have a stroke on the R hemisphere?

A

1) lose lateral corticospinal input to L side
2) lose anterior corticospinal tract in R side
3) BUT anterior corticospinal tract on L side still intact and can maintain core muscle groups on R side by doing double duty via anterior white commissure

190
Q

How do you determine what level in the spinal cord you are?

A

Cervical: large ventral gray matter to innervate arm

Thoracic: has narrow ventral gray matter (minimal muscles) and has sympathetic nervous system preganglionic sympathetic neurons from C8-L2 → has little notch of white matter

Lumbar: large ventral gray matter to innervate lower extremities

191
Q

Upper motor neuron syndrome

A

(brain to spinal cord neuron damaged)

hyporeflexia or areflexia → emergence of hyperreflexia a few days later

Will produce weakness of all muscle groups innervated by UMNs

Immediate muscle weakness and hypotonia, hyporeflexia or areflexia

Followed by spasticity and HYPERreflexia in days to weeks (including extensor plantar response: Babinski)

SPASTIC PARESIS

192
Q

Lower motor neuron syndrome

A

(spinal cord to muscle signal damaged)

permanent flaccidity (loss of motor tone) and long term loss of reflexes those motor neurons participate in

Will produce weakness in muscles innervated by those neurons

Long-term loss of reflexes that those LMNs participate in, and long term loss of muscle tone (FLACCIDITY) in those muscle groups

FLACCID PARESIS

Can also produce fasciculations

193
Q

What happens if you damaged your cord at C5-C6? (in terms of upper and lower motor neuron syndrome)

A

everything above and below will be in tact

Weakness to all muscle groups innervated from C5 and below

Everything below will have UMN injury characteristics (hyporeflexia → hyperreflexia/spasticity)

For c5 and c6 segments will have LMN characteristics

194
Q

Brown-Sequard Syndrome

A

Only destroy ½ of spinal cord → destroy pain and temperature info from contralateral side and dorsal column information from ipsilateral side

Crossed sensory deficit

195
Q

Posterior/dorsal column medial lemniscal system transmits what kind of sensation?

A

Sensation of touch, vibration sense, and joint position sense

196
Q

Posterior/dorsal column medial lemniscal pathway:

1) Big toe receptors in skin for different modalities → different axons depending on modality go to L5 _______
2) → L5 _______ (between ___ and __ vertebral body)
3) → spinal canal between two vertebrae → L5 _______ (near ____ vertebrae)
4) → enter ______ of spinal cord
5) → continue up in column of white matter called _________
6) → bottom of brainstem → synapse with second neuron in ________
7) → _______ neuron discharges and crosses midline, ascends _________ pathway
8) → synapses in ______
9) → 3rd neuron in pathway from sends signal to ______________

A

1) Big toe receptors in skin for different modalities → different axons depending on modality go to L5 dermatome (dermatome for toe)
2) → L5 dorsal root ganglion (between L5 and S1 vertebral body)
3) → spinal canal between two vertebrae → L5 segment of spinal cord (near T12 vertebrae)
4) → enter dorsal horn of spinal cord
5) → continue up in column of white matter (Fasiculus gracilis)
6) → bottom of brainstem → synapse with second neuron in nucleus gracilis
7) → N. gracilis neuron discharges and crosses midline, ascends medial lemniscus pathway
8) → synapses in thalamus (VPL, ventral posterior lateral)
9) → 3rd neuron from VPL sends signal to somatosensory cortex

197
Q

What happens to the posterior/dorsal column medial lemniscal system above the T6 dermatome?

A

white matter dorsal column in spinal cord is FASICULUS CUNEATUS
-(just LATERAL to fasiculus gracilis in dorsal column)

→ NUCLEUS CUNEATUS in brainstem just lateral to nucleus gracilis

→ medial lemniscus

→ VPL sensory thalamus

→ somatosensory cortex

198
Q

Pathway for sensation of pain and temperature

1) Heat/pain in foot → _____________ → enter L5 segment
2) → In dorsal horn, travel up or down in thin bundle of white matter = ____________
3) → synapse in _____________ contains second neuron cell body
4) → sends axons across midline via ___________
5) → signal then ascends via white matter in anterior/lateral spinal cord via ________ or aka _________
6) → up to _______ → cortex

A

same system for upper and lower extremities

1) Heat/pain in foot → small c-fibers (unmyelinated) with cell body in L5 dermatome → enter L5 segment
2) → In dorsal horn, travel up or down in thin bundle of white matter = Lissauer’s fasiculus
3) → synapse in Substantia gelatinosa gray matter contains second neuron cell body
4) → sends axons across midline via anterior white commissure
5) → signal then ascends via white matter in anterior/lateral spinal cord via spinothalamic tract or Anterior Lateral System (ALS)
6) → up to thalamus → cortex

199
Q

Nuclear Movement

A

as cells divide, they undergo nuclear movement

As nuclei move, portion of progenitor cell with nucleus encounters different environments - determines if cell will become post-mitotic

200
Q

S phase, M phase, G1, and G2 phase location of nucleus in nuclear movement

A

S Phase: DNA being synthesized, nuclei situated most superficially (nearest to pia)

M phase: mitosis, when cell division occurs, nuclei situated most deep (nearest to ventricle)

G1 and G2 gap phases: nuclei occupy intermediate position

201
Q

What determines when a cell stops dividing and begins differentiating? (4)

A

1) Nuclear Movement - different environments based on nucleus location
2) Process detachment (from ventricular and external surface)
3) Plane of cleavage
4) Asymmetric inheritance of cytoplasmic proteins, mRNA, and other factors

202
Q

Process detachment in neuronal cell proliferation and differentiation

A

Each dividing cell has processes attaching them to medially to ventricular surface, and laterally to external surface

During division, one process has detached from external surface, and remains attached to ventricular surface

After M phase, daughter cells can re-attach to external surface and continue dividing OR can detach other process from ventricular surface and cease dividing

203
Q

Plane of cleavage in neuronal cell proliferation and differentiation

A

perpendicular vs. parallel to ventricular surface

-Perpendicular cleavage to ventricular surface → both daughter cells remain attached to ventricular surface and continue dividing in cell cycle

  • Parallel cleavage to ventricular surface → only one daughter cell still attached to ventricular surface → exit cell cycle and begin differentiation
  • -> ASYMMETRIC DIVISION
204
Q

Asymmetric inheritance of cytoplasmic proteins, mRNAs and other factors

A

Asymmetric division → asymmetric inheritance of cell components → different cell fates

Helps determine if a cell exits cell cycle in M phase and begins differentiating

205
Q

Neuron’s birthdate

A

the time a cell undergoes its last round of DNA synthesis (S phase)

After a cell’s “birthdate” it divides and exits the cell cycle from M phase

Cell then begins neuronal differentiation

Neurons that are born at the same time tend to end up together in the same layer, and follow similar programs of differentiation

206
Q

Brain Regions of Secondary Neurogenesis (3)

A

1) External Granule Layer (Cerebellum)
2) Subventricular zone (olfactory neurons)
3) Dentate Gyrus (hippocampal neurons)

207
Q

External Granule Layer

A

area of secondary neurogenesis until age 2

Granule layer initially located near rim of 4th ventricle, but cells migrate very high on top (near pia) before they are postmitotic to form a new neurogenic “secondary” region = External Granule Layer

External granule cell progenitors proliferate and once they exit the cell cycle, migrate to cerebellum (further down toward ventricle)

208
Q

Subventricular Zone

A

area of secondary neurogenesis

cells initially located in ventricular zone of lateral ventricles → migrate very small distance before exiting mitotic cycle to subventricular zone

Cells in subventricular zone give rise to olfactory bulb neurons

Cells exit cell cycle and migrate rostrally to location of olfactory bulb

209
Q

Dentate Gyrus

A

Cells migrate from ventricular zone to dentate gyrus secondary zone of neurogenesis –> hippocampal neurons

210
Q

All 3 cell types of secondary zones of neurogenesis share 3 characteristics:

A

1) Arise in ventricular zone
2) migrate before exiting mitotic cycle to a new non-ventricular location
3) Proliferate postnatally in non-ventricular zone locations

211
Q

Neurogenesis in the adult brain

A

= Secondary Zones of Neurogenesis

Majority of neurogenesis occurs prior to birth

212
Q

Neurogenesis

A

the process of generating neural cells

We have 10^12 neurons in the adult brain, we only start with 10^5 → need to proliferate exponentially before differentiating

Begins after neuroectoderm rounds up and forms neural tube

Proliferating cells are located in ventricular zones (layer nearest to neural tube lumen/ventricle or central canal)

213
Q

Radial Glia

A

cells that extend from deep ventricular zone to surface

Guide neurons during radial migration after preplate has formed

Reason why cortical cells that serve similar functions are arranged in columns → single progenitor found in clusters

Facilitate “inside-out” development of cortex (earlier born cells in inside layers, and later born ones in outside layers)

214
Q

Tangential migration

EX?

A

causes single progenitor found dispersed throughout cortex tissue

EX) inhibitory GABA-containing cells in cerebral cortex

215
Q

Chain Migration

A

neurons migrate from subventricular zone near lateral ventricle to olfactory bulb - does not involve radial glial cells, migrate in ROSTRAL MIGRATORY STREAM

Strands of cells moving on top of each other over large distances

216
Q

Preplate

A

First postmitotic cells migrate from ventricular zone to form preplate at 8-9 weeks of embryogenesis

Post-mitotic cells accumulate in preplate → preplate divides into zones

217
Q

Zones after preplate division (5)

A

1) Marginal Zone
2) Cortical Plate
3) Intermediate Zone
4) Subplate
5) Deep Ventricular Zone

218
Q

Marginal zone

A

superficial zone adjacent to pial surface

219
Q

Cortical plate

A

internal layer, forms 6 layers of cortex

Successive waves of neurogenesis produce new neurons in CP organized in specific layers

220
Q

Intermediate zone

A

contains neuronal and radial glia processes, becomes white matter

221
Q

Subplate

A

between ventricular zone and cortical plate

Earliest born cells, act as “pioneering” cells in circuit formation

Cells die once pioneering role is played out

Transient neuronal population

222
Q

Deep ventricular zone

A

contains proliferating cells

223
Q

For both the cerebral cortex and retina, describe where the first‐born cells are found with respect to the ventricular zone

A

Cerebral Cortex = Inside-Out - earliest born cells in deepest layer

Retina = Outside-In - earliest born cells on outside layer
-Ganglion cells born first, and photoreceptors last

224
Q

Neural crest

A

forms between neuroectoderm and epidermis

Neural crest cells give rise to PNS and many other cell types (pigment cells, cartilage and are found in very diverse locations (gut, skin, dorsal root sensory ganglia)

225
Q

Neural crest cell migration

A

Does not use radial glia cellular guides - migration fate influenced by neural crest cell’s position along rostral-caudal axis

Neural crest cells recognize proteins in the environment over which they migrate

ventral stream vs. dorsal stream

226
Q

Dorsal Stream (neural crest cell migration)

A

flows dorsolaterally underneath ectoderm, but lateral to myotomes that give rise to pigment cells

227
Q

Ventral Stream (neural crest cell migration)

A

flows ventro medially, dives under dorsal dermamyotomes (DM) → gives rise to sensory, autonomic, and enteric ganglia

228
Q

What are some examples of proteins that neural crest cells recognize in the environment over which they migrate?

A

LAMININ and FIBRONECTIN found in ECF → INTEGRINS found on neural crest cells → act as permissive factors

Inhibitory “non-permissive” surfaces keep neural crest cells on track

CADHERINS expressed in final destination, act as adhesion molecules

229
Q

Neural crest migration vs. Radial migration

A

Neural crest migration uses expression and recognition of proteins in the environment while radial migration uses radial glial cells as a guide scaffold by which neurons travel

230
Q

Somatic Nervous System

A

voluntary skeletal muscle

- Single neuron connects CNS with peripheral tissues

231
Q

Autonomic nervous system

A

Sympathetic (SANS) and Parasympathetic (PANS)

232
Q

Function of autonomic nervous system

A

involuntary, unconscious, automatic portion of nervous system

Regulate involuntary visceral smooth muscles, cardiac muscle, and glandular secretions (CO, blood flow to organs, digestion, etc.)

233
Q

Double neuron connection: Autonomic nervous system

A

Pre/Post-ganglionic nerves connect at a ganglion

234
Q

CNS origin: Parasympathetic

A

cranial nerve nuclei (tectal region of brainstem) and sacral segments (S2-S4)

235
Q

Location of ganglia: parasympathetic

A

innervated organs

236
Q

Length of pre/postganglionic neurons: parasympathetic

A

preganglionic LONG, postganglionic SHORT

237
Q

Ratio of pre to postganglionic neurons: parasympathetic

A

1:1, discrete function

238
Q

Neurotransmitter/receptors: parasympathetic

A

Preganglionic neurons release ACh → nicotinic cholinergic (N-N) receptors in ganglia

Postganglionic neurons release ACh → muscarinic cholinergic (M1-5) receptors in end organs

239
Q

CNS origin: Sympathetic

A

Thoracic (T1-T12) and Lumbar (L1-L2) segments

240
Q

Location of ganglia: Sympathetic

A

two paravertebral chains along spinal cord or in prevertebral ganglia in abdomen

241
Q

Length of pre/postganglionic neurons: sympathetic

A

preganglionic SHORT, postganglionic LONG

242
Q

Ratio of pre to postganglionic neurons: sympathetic

A

1:20-50, diffuse/widespread function

243
Q

Neurotransmitter/receptors: Sympathetic

A
  • Preganglionic neurons release ACh → nicotinic cholinergic (N-N) receptors in ganglia and adrenal medulla
  • Postganglionic neurons release:

NE → a1-adrenergic receptors (blood vessels, eye, GI tract), B1-adrenergic (heart, low affinity), B2-adrenergic (smooth muscle)

ACh → muscarinic cholinergic (M) receptors in sweat glands

Dopamine → Dopamine D1 receptors in kidney vascular smooth muscle

  • Adrenal medulla releases epinephrine and NE into general circulation → adrenergic synapses with a1, B1, and B2 receptors
244
Q

Nicotinic receptor: ionotropic or metabotropic?

A

Ionotropic

245
Q

3 types of nicotinic receptors

A
  1. Ganglionic (Nn)
  2. Skeletal muscle (Nm)
  3. Neuronal CNS (Nn)
246
Q

Muscarinic- ionotropic or metabotropic?

A

metabotropic

247
Q

Where are muscarinic receptors located?

A

Postganglionic effector organs

248
Q

Where are M1 receptors located?

A

CNS, enteric nervous system

249
Q

Where are M2 receptors located?

A

Atria, SA, AV node

NOT VENTRICLES

250
Q

Where are M3 receptors located? (5)

A

Glands, smooth muscle, bronchial muscle, GI/Gu tract, eye

251
Q

G protein class coupled to M1

A

Gq

252
Q

G protein class coupled to M2

A

Gi

253
Q

G protein class coupled to M3

A

Gq

254
Q

Muscarinic effect on the cardiovascular system

A

Decrease HR and AV conduction rate, and atrial contractility

Vasodilation (ONLY via production of NO → cGMP, NOT via innervation with PNS) = decrease BP (Note: this is an M3 effect)

255
Q

Muscarinic effect on the respiratory system

A

bronchial muscle contraction, stimulate glands

256
Q

Muscarinic effect on the GI tract

A

increased secretory and motor activity

257
Q

Muscarinic effect on the GU tract

A

relax sphincters, contract detrusor muscle (promote voiding)

258
Q

Muscarinic effect on the eyes

A

miosis (pupil constriction), accommodation (focus near vision), outflow of aqueous humor → decreased IOP

259
Q

What are the receptors on:

  1. dilator muscle of the eye
  2. constrictor muscle and accommodation for near vision
  3. thing on the eye that make aqueous humor
A
  1. a1
  2. M3
  3. B2
260
Q

Nicotinic neuronal (N-N) receptors are located where?

A
  1. In autonomic ganglia

2. In CNS

261
Q

N-N receptors effect in autonomic ganglia (2)

A
  1. Cardiovascular: sympathetic effects (vasoconstriction, tachycardia, elevated BP)
  2. GI/GU tract: parasympathetic effects (nausea, vomiting, diarrhea, urination)
262
Q

N-N receptors effect in CNS

A
  1. Mild alerting effect, tremor, emesis, respiratory stimulation
  2. Activate “reward” pathway in limbic system (addicting potential)
  3. Convulsions can occur at toxic doses
263
Q

Peripheral adrenergic receptors in the vasculature (3)

A
  1. a1 → vasoconstriction, increase in total peripheral resistance and BP (reflex bradycardia)
    - Cutaneous, mucous membranes, splanchnic vasculature
    - Renal vasculature constriction
  2. B2 → vasodilation, decrease TPR and BP (reflex tachycardia)
  3. D1 → renal vasculature relaxation
264
Q

Peripheral adrenergic receptors in the heart (2)

A
  1. B1 → increase SA node chronotropy, increase AV node conduction velocity, increase atrial/ventricular contraction (positive inotropy)
  2. a2 → decrease in SNS outflow via CNS, decreases BP
265
Q

Fight or flight

A

Sympathetic

i. Continuously active with level of activity constantly changing
ii. Widespread physiologic responses

266
Q

Effects of fight or flight (5)

A

1) Increase HR, raise BP
2) Shift blood flow fro skin and splanchnic regions to skeletal muscle
3) Rise in blood glucose
4) Dilate bronchioles and pupils
5) Decrease GI/GU system activity

267
Q

Rest and digest

A

Parasympathetic

i. Conservation and restoration of energy
ii. Single organ system, discrete, localized discharges

268
Q

Effects of rest and digest

A

1) Slow HR, lower BP
2) Stimulate GI motility, secretions and nutrient absorption
3) Empty bladder and rectum
4) Protect retina from light (pupil constriction), focus for near vision

269
Q

Tone

A

intrinsic level of activity determined by dominant branch

also Billy’s body, he’s a toned motherfucka

270
Q

Predominant tone in the body… any exceptions?

A

Predominant control almost always parasympathetic (exception = sympathetic control of blood vessels - do not have any parasympathetic innervation)

271
Q

What are the questions you ask in at screen for PTSD?

A

1) Have had nightmares about it or thought about it when you did not want to?
2) Tried hard not to think about it or went out of your way to avoid situation that reminded you of it?
3) Were constantly on guard, watchful, or easily startled?
4) Felt numb or detached from others, activities, or your surroundings?

272
Q

In the Diagnostic Criteria for PTSD, what is trauma defined as?

A

Exposure to actual or threatened death, serious injury, or sexual violence - direct exposure, witnessing, or learning of it.

Patient must view it as a trauma.

273
Q

What are the main diagnostic categories of PSTD? (5)

A
  • Trauma
  • Intrusion
  • Avoidance
  • Negative alterations of cognition and mood.
  • Arousal and reactivity
274
Q

With regards to PSTD, what Sx are associated with Intrusion?

A

can’t get trauma out of their head, problems sleeping, nightmares, dissociative reactions, flashbacks

275
Q

With regards to PSTD, what Sx are associated with Avoidance?

A

avoid distressing memories, thoughts, or feelings associated with traumatic event - can lead to isolation

276
Q

With regards to PSTD, what Sx are associated with Negative alterations of cognition and mood?

A
  • Inability to remember important aspect of the event
  • Dissociative amnesia. Not other factors like head injury or drugs/alcohol)
  • Persistence and exaggerated negative beliefs/emotional state (fear, horror, anger, built, shame)
277
Q

With regards to PSTD, what Sx are associated with alternations in Arousal and reactivity?

A
  • Irritable and angry outburst
  • Reckless/self-destructive
  • Hypervigilance
  • Exaggerated startle response
  • Problems w/ concentration
  • Sleep disturbances; falling/staying/restless sleep
278
Q

With regards to PTSD, disturbance lasts for a minimum of ___ days, maximum of ___ month, and occurs within ___ weeks of traumatic event

A

3 days
1 month
4 weeks

279
Q

What are the main diagnostic categories of PSTD? (5)

A

-Trauma-Intrusion-Avoidance-Negative alterations of cognition and mood.-Arousal and reactivity

280
Q

With regards to PSTD, what Sx are associated with Negative alterations of cognition and mood?

A
  • Inability to remember important aspect of the event- Dissociative amnesia. Not other factors like head injury or drugs/alcohol)- Persistence and exaggerated negative beliefs/emotional state (fear, horror, anger, built, shame)
281
Q

With regards to PSTD, what Sx are associated with alternations in Arousal and reactivity?

A
  • Irritable and angry outburst- Reckless/self-destructive- Hypervigilance- Exaggerated startle response- Problems w/ concentration- Sleep disturbances; falling/staying/restless sleep
282
Q

What are the mechanism by which ANS drugs act? (3)

A

Direct Agonist- Antagonist - Indirect Agonist/Antagonist

283
Q

ANS drugs that act to mimic NT action at receptor level are ?

A

Direct Agonist

284
Q

ANS drugs that act to block NT action at receptor level are ?

A

Antagonist

285
Q

What is the MOA of Indirect Agonist/Antagonist ANS drugs?

A

Change normal action of NT.

286
Q

Indirect Agonist/Antagonist ANS drugs change normal action of NT, in what ways do they/can they do this?

A
  • Synthesis of NT.
  • Storage and release of NT.
  • Inactivation of NT following release. (*Less clinically useful because they affect all synapses for that particular NT regardless of which specific postsynaptic receptor subtype is present.)
287
Q

Most clinically useful are drugs that act at the ____ (post or pre?)–synaptically at specific receptor subtypes as agonists or antagonists

A

POST!

288
Q

Between a direct agonist and a direct antagonist ANS drug, which one is more clinical useful?

A

antagonist! More clinically useful, act post-synaptically at specific receptor subtype

289
Q

Botulinum toxin*: ____1____ ACh release

Black Widow Spider toxin*: ____2____ ACh release.

A
  1. blocks

2. increases

290
Q

What are the two subtypes of Cholinergic Receptors?

A

Nicotinic ReceptorsMuscarinic Receptors

291
Q

ligand gated, alter ionic permeability are the actions of what type of Cholinergic Receptors?

A

Nicotinic Receptors:

292
Q

G-protein coupled receptors, alters enzyme activity are the actions of what type of Cholinergic Receptors?

A

Muscarinic Receptors:

293
Q

Nicotinic Receptors: ?

A

ligand gated, alter ionic permeability

294
Q

Muscarinic Receptors: ?

A

G-protein coupled receptors, alters enzyme activity

295
Q

Gq → ____1___ PLCGi → ___2____ AC

A
  1. increase

2. decrease

296
Q

What [M] subtype is associated with Gq and what type of cell/organs are they on?

A

M1 = neuronal, GI glands

M3 = exocrine glands, smooth muscle

297
Q

What [M] subtype is associated with Gi and what type of cell/organs are they on?

A

M2, M4 = heart, CNS

298
Q

What are the direct acting Muscarinic Cholinergic Receptor Agonists?

A

Choline Esters:

 - Acetylcholine*: not used, rapid hydrolysis by AChE
 - Bethanechol*: synthetic analog of ACh, resistant to AChE.

Parasympathetic Alkaloids:- Pilocarpine*

299
Q

What are the Nicotinic Neuronal (ganglionic) Receptor Agonists

A
  • Nicotine* → increase BP, HR, vasoconstriction, increase GI motility, arousal, euphoria, increased attention Prolonged or toxic dose can cause antagonism due to persistent depolarization → renders membrane unresponsive
  • Acetylcholine*
300
Q

What is the MOA of Muscarinic Cholinergic Receptor Antagonists?

A

antagonize ACh, reversible (competitive) inhibitors (aka anticholinergic and antimuscarinic)

301
Q

What are the Muscarinic Cholinergic Receptor Antagonists?

A

Alkaloids:

 - Atropine*
 - Scopolamine*Semi-Synthetic Agents: higher selectivity of antagonism particularly parasympathetic function (bladder especially).
 - Oxybutynin*, Ipratropium*
302
Q

What is the overall MOA of Acetylcholinesterase Inhibitors?

A

Indirect agonist?

303
Q

List the Acetylcholinesterase Inhibitors. (4)

A
  • Physostigmine
  • Neostigmine, Pyridostigmine
  • Edrophonium
  • Organophosphates (nerve gas, insecticides) act indirectly to inhibit acetylcholine esterase → too much acetylcholine
304
Q

nerve gas, insecticides are what type of Acetylcholinesterase Inhibitors?

A

Organophosphates

305
Q

List the adrenergic agonist drugs:

A
  • Epinephrine
  • Pseudoephedrine
  • Norepinephrine
  • Phenylephrine
  • Clonidine
  • Isoproterenol
  • Albuterol
  • Dobutamine
  • Dopamine
306
Q

List the adrenergic antagonist drugs:

A
  • Doxazosin
  • Propranolol, Timolol = Non-selective B1 and B2
  • Metoprolol, Atenolol = B1 cardioselective (only at lower doses)
  • Labetalol, Carvedilol
307
Q

What adrenergic antagonist drug is non-selective for beta1 and beta 2?

A

Propranolol, Timolol

308
Q

What adrenergic antagonist drug is beta1 cardio-selective? (only at lower doses)

A

Metoprolol, Atenolol

Neuro (8 decks)

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