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Neuroscience Flashcards

1
Q

What are the different lobes of the brain called

A

frontal lobe, temporal lobe, parietal lobe and the occipital lobe

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2
Q

What is the difference beteen grey and white matter

A

White matter is white due to high percentage of lipids. These are the primary sourse for axons which are lipidated as the result of myelination

grey matter is actually pink and it contains the cell bodies which are organised in layers.

There are bundles of axons connecting the different regions

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3
Q

What is the most important section of the brain

A

the bottom sector containing the medulla, spinal chord and cerebellum

this is because they have been evolutionary present since ancient times all animals have them and they are required for basic function to allow for life

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4
Q

how does information flow through nerve cells?

A

from the dendrites through the axon and to the presynaptic terminal

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5
Q

Why are there different types of neural cells

A

there are ~ 50 types
specialised shapes determine there interactions (how there recieve and transmit impulses)

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6
Q

What are Glia cells and there types

A

cells that provide structural and metabolic support for neurons

Astrocytes - most popular, involved in the blood brain barrier, take up K+ ions from synaptic cleft

Ogiodendrocytes - schwann cells in Peripheral nervous system axons sheathed with myelin

microglia - become activated during infection, injury or seizure.
the macrophage of the CNS

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7
Q

What did Ramon and Cajal do

A

used staining techniques to characterise cell types of CNS and develop neuronal theory

  • synapses exist and the nervous system isnt reticulated
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8
Q

Structural features of note in neurones

A

highly polarised - similar structural features to epithelial cells containing both an apical donain (axon in neuron) and a basolateral region ( dendrites in neuron)

this means that at the apical domain it is able to be highly involved in membrane trafficing and sensing whereas dendrites are less able to

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9
Q

componants of neuronal cytoskeleton

A

microtubials, neurofiliments and microfiliments (such as actin)

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10
Q

what is neural polarity dictated by

A

the neuronal cytoskeleton

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11
Q

how does axonal transport of mitochondria work

A

mitochondria and vesicles are loaded onto kinesin molecules and transported along the axon to the synaptic terminus where they are unloaded. Spend mitochondria are then transported back along to the cell body.

anterograde transport = to synaptic terminus
retrograde transport = to the cell body

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12
Q

what is required for fast transport in neuronal transport

A

important cargo such as neurotransmitter or mitochondria

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13
Q

what are the types of neuronal transport

A

anterograde, bidirectional, retrograde, slow component A and slow compartment B

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14
Q

How does Nissl stain work

A

stains DNA and RNA
- allows visualisation of cell nuclei and the rough ER (also called Nissl bodies)
- good for visualising neuronal architecture of the brain (how the brain is organised)
- NOT good for neuronal morphology

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15
Q

how does golgi stain work

A

silver based
- only stains small proportion of neurons but stain purkinje neurons
- the silver dichromates fill cell soma and reveal whole morphology of the cell

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16
Q

how does immunofluorescence staining work

A

antibodies are raised to bind to specific proteins (such as mitochondria)
allows for visualisation of that protein using the flurochrome which is covalently attached to antibody

-can be multicoloured using different antibodies that bind to different species together.

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17
Q

How do you calculate membrane resting potential and what is the healthy rate

A

Vm = voltage in - voltage out

the membrane potential is negative relative to the outside typically ~ -60 to -70mV is healthy at rest

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18
Q

what is nernst potential

A

also known as equalibrium potential

the membrane potential where there is no net flow of a particular ion from one side of the membrane to the other

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19
Q

how is resting membrane potential controlled

A

lipid bilayer is highly impermeable to ions
ions can only cross through ion channels
At rest ion movement is balanced so the membrane potential is constant - the balance is createdby the NA/K pump.
highly permeable to K due to tandem pore K+ channels that are always open
potential is the nernst potential for K+ (-75) being offset by slight permeability to Na+

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20
Q

how is membrane potential measured at rest and excitation

A

a current clamp
: current generator and a voltage amplifyer

injects known current into the cell and measures the change in membrane potential

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21
Q

what is voltage clamping

A

monitoring the voltage across a cell membrane while coinciding with injecting a known volume of current to clamp the transmembrane voltage to a desired level

intermal electron that is measuring is connected to voltage clamp amplifier which compares Vm with desired preset potential.
When it is different the amplifier injects current into the axon through secondary electrode

the feedback arrangement causes the Vm to become the same as the command
(used in squid axon action potential experiment by huxley)

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22
Q

what is the patch clamp technique

A

records the activity of single ion channels

it is cell-attached and places the electrode tip on the membrane to form a high resistance seal between the walls of the tip and the membrane

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23
Q

what is the whole cell patch clamp technique

A

suction is applied to a cell-attached patch causing rupture to the membrane and allows whole cell recording. Properties of specific channels can be studied in this technique by blocking other types via toxins or chemicals.

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24
Q

what are the 4 phases of membrane potential

A

depolarisation, overshoot, repolarising and hyperpolarizing

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25
how does voltage dependent activation work
when the membrane potential is depolarised it causes a conformational change as the charged voltage sensor helix S4 rotate outwards to open the channel gate. (this first opens the Na+ channels then the K+ channel. Hyperpolarization causes the closing of this by the the helix loses its positive charge
26
what direction do sodium and potassium ions move
sodium ions out, potassium ions in
27
how do you prove the role of Na+ and K+
you can use tetrodotoxin to inhibit the Na+ channel which when inhibited shows no "In" current. tetraethylammonium (TEA) inhibits the "out current component this shows the role of K+ moving in the cell and the Na+ out
28
what data do the electrophysiology techniques
current clamp: membrane potential, used to observe action potentials cell attached patch voltage clamp: single channel currents, kinetic information whole cell patch voltage clamp : whole cell currents creates a focus on a single type using inhibitors
29
how do different neurone connect to each other :the types
axo-dentritic - bind to the other dendrite axo-somatic - bind to the cell body of another neuron axo-axonic - bond to the axon of another neuron
30
what are the main features of the neuronal synapse
presynaptic terminal , post synaptic cell, active zones which contain synaptic vesicles and mitochondria
31
what are the main inhibitory and excitatory transmitters
GABA - main inhibitory Glutamate - excitatory
32
how does Ca2+ dependent neurotransmitter released
Action potential causes membrane depolarisation leading to the opening of Ca channels Ca causes synaptic vesicles to fuse to plasma membrane released neurotransmitter diffuses and binds to post synaptic receptors ~ can activate presynaptic auto-receptors the NT can spill over into adjacent synaptic vesicle membrane recycled by endocytosis neiropeptides released from dense cored granules
33
what is an end plate potential (EPP)
the change in membrane potential caused by an action potential in the presynaptic motor neurone which causes an imperminant depolarisation of post synaptic muscle fibre
34
name a technique that allows for real time analysis of synaptic vesivle cycle
fluorescent antibodies, fluorescent dyes and fluorescent proteins
35
where are synaptic vesicles located
in the presynaptic terminal in active zones
36
what makes neurotransmitter Ca2+ dependent?
the vesicle docks next to the presynaptic membrane the entering Ca2+ binds to synaptotagmin (this is the Ca2+ sensor) This allows for the formation of SNARE protein complexes which form and pull membranes together the Ca2+ bound synaptotagmin catalyses membrane fusion this allows for diffusion across the synaptic cleft
37
what are the steps of membrane trafficking in presynaptic nerve terminal
Neurotransmitter uptake translocation to the membrane and docking at the presynaptic membrane priming prefusion using ATP Ca2+ mediated fusion exocytosis Endocytosis of the vesicle back into the presynapse and translocation for endosome fusion
38
how does the binding of NT's cause a post-synaptic potential
they open channels in the post synapse either directly or indirectly this causes a small inward flow of Na+ current into the post synaptic membrane causing depolarisation (far below threshold doesnt cause action potential) this is also permeable to negative Cl ions therefore net increase in -tive charge is inhibitory Excitatory makes more likely for AP Inhibitory makes less likely A single EPSP cannot cause a AP however the action of numerous presynaptic neurone imputs can cause an AP
39
What are the different types of neurotransmitter receptor on a postsynaptic membrane
Ionotropic receptor - direct - produce fast responses - ligand-gated ion channels Metabotropic receptors - G-protein coupled receptors (modulate voltage gate channels) - made of large trimeric GTPases - can regulate enzyme activity -eg through interaction with cytosolic channel loops in both NT binding causes a conformational change of channels
40
examples of ionotropic and metabotropic receptors
ionotropic : nicotinic acetylcholine receptor - 5 subunits Glutamate receptors: -AMPA and Kainate -gated by glutamate binding - rapid depolarisation decays rapidly -NMDA -only open when two event s occur concurrently -binding of glutamate - strong depolarisation of PostSM relives block of Mg2+ - opens and closes quite slowly permeable to Ca2+ metabotropic : muscarinic acetylcholine receptor
41
how can you observe events in the synapse
FM dyes neurones are incubated in a FM buffer dye Neurones have action potentials stimulated this indroduces the dye to the synapse Synaptic vesicles containing the FM dye are exocytosised cells are washed to remove extracellular buffer neurones are stimulated again and dye is exocytosed the fluorescence signal decreases as vesicles are destained
42
extracellular sources of Ca2+
NMDA receptor post synaptic L-type voltage gated Ca"+ channels (l-type VGCC) sotre-operated channels
43
intracellular release channels on ER
IP3 receptors: activated by increase in IP3 levels ryanodine receptors: activated by Ca2+ entering through NMDA receptor causing Ca2+ induced Ca2+ release
44
how Ca2+ is removed from the cell
SERCA - Sarcoplasmic endoplasmic reticulum Ca2+ ATPase, pumps Ca2+ back into ER PMCA - Pumps Ca2+ out of the cell NCX - Na+/Ca2+ exchanger
45
how can Ca2+ be indicated/ tracked
Fura-2 ca2+ sensitive dyes
46
Why doesn't neuroscience measure pain
pain is subjective and therefore cannot be definitively measured so nociception is used instead pain recetion can be delayed and this isnt necesarrily any issues with the receptors
47
what is nociception?
the sensory nervous systems response to harmful stimuli the quantifiable experience of stimuli causing harm
48
what are the types of nociceptive stimuli
Chemical mechanical (cutting or crushing) thermal
49
where is the nociceptors located
the dorsal horn of the spinal cord specifically the cell bodies are in the dorsal root ganglion
50
what are the 3 main classes of nociceptive receptors
thermal mechanical polymodal
51
how are the 3 classes of nociceptors activated
thermal - >45 degrees <5 mechanical - intense pressure to the skin polymodal = high intensity mechanical, chemical or thermal stimuli
52
what are the main nociceptive fibers and describe them
A delta - small diameter - thinly myelinated - strong damaging stimulus - fast (5-30 m/s) C fibres - small diameter - unmyelinated - slower (<1 m/s) - slower action potential
53
what is first and second pain
first pain - sharp quick pain second pain - burning/ achy slow pain. pain that grows
54
how does noxious stimulus cause action potential
activation of TRP channels via conformational change, ligand binding or Ca2+ that is intracellular TRP channels can be triggered by multiple different types of stimulus
55
how can TRPV1 channels be activated
temperatures >43 acidification allyl isothiocyanate (mustard + wasabi) vanilloids capsaicin can bind to TRPV1 channel lowers the activation temperature to 37
56
what is hyperalgesia
pain over time peripheral tissue that's damaged can lead to increased pain sensitivity causes decreased threshold of nociceptor activation. This can also cause pain to occur in the absence of stimulation
57
how is nociception processed through the CNS
stimulus activates nociceptors stimulus is processed in spinal chord, thalamus and cortex spinal chord causes reflex cortex causes both behavioural response and subjective experience of pain.
58
what are the different types of sensory neurons in C.elegan
soft touch , multi-dendritic harsh touch (PVD), nose touch and foraging behaviour, sex specific touch
59
Expand upon PVD neurons
also known as menorah cells found in the hypodermis under pressure the branded structure moves inducing opening of ionic channels
60
how has genetic screening for touch sensitivity identified the MEC complex
identified a complex of ion channels attached to cytoskeletal microtubules and extracellular matrix proteins (one of which is collagen) this suggests that the channels are anchored in a fluid membrane by stiff intracellular and extracellular structures this allows touch gated channels with pressure the cysteine rich domains can be mimiced by snake toxins which open the channel
61
The presence of snake toxins or a substitution from alanine to valine at position 713 can cause neuron death. why?
valine is more bulky than alanine so it keeps the channel open allowing for free flow of K+ (instead of Na+) activating action potential. This can cause the sensory neuron to die from excitotoxicity. - overstimulation of neuron leading to apoptosis (these are therefore called degenerin channels)
62
how can hair act as a tranducer
hairs are anchored and attach to neurons via neuronal dendritic cap therefore the movement of the hair from touch moves the cap activating a current in the neuron. this similarly occurs in whiskers though these use merkel cells
63
how do merkel cell generate a stimulus
release neurotransmitter from the dense core vesicles to the slowly adapting type 1 afferents made by inactivating Piezo2 channels
64
how does sound get through in the ear
sound moves towards the tympanic membrane this sound vibrates the menbrane to move the auditory ossicles the ossicles moves which vibrates the oval window fluid is incompressible causing the movement around the vestibular canal and tympanic canal round window allows an outlet for the compression
65
how is the vibration detected
the cochleal vibration causes a shearing force between the tectorial membrane and the basilar membrane via hairs the kinocilium and sterocilium in the hair cells detect the stress caused by the vibration tip link molecular links the sterocilium and kinocilium links to a channel complex movement of cilia towards the kinocilium open the channel complex allow potassium entry depolarises the cell opening voltage gated calcium channels release chemical transmitter to the afferent nerve fibres
66
what is olfaction
detection of chemicals from a distance - smell ->detects a large number of odorants
67
what is gustation
taste requires direct contact with relevant chemical -> organised into categories (sweet, salty, sour)
68
what are the different taste qualities mediated by
bitter : poison GPCRs sweet: sugar, carbohydrates GPCR sour: organic acids (ion channels) salty: sodium (ion channels) umami: L-amino acids, nucleotides (GPCRs) fats: mechanism unknown
69
what is the organisation of the taste bud
each one comprised of up to 100 polarised neuroepithelial cells which form columnar islands in the oral cavity
70
how many different types of taste bud cells are there
3
71
what are the differences between the types of taste bud cells
type 1 : express ion channels allowing the transportation of Na ions into cells (salty) type 2: conduct different responses based on which GPCR they express. Ligand binding triggers G-protein signalling type 3: neuron like: protons from acidic tastes enter via proton channels and organic aicds enter the plasma membrane accumulation blocks the K+ channel to depolarise membrane releasing seratonin
72
how do taste cells cope when a food is complex with multipul different flavour profiles
cross talk between different types of taste cell allow them to dissifer the prominant taste and generate a signal
73
how does olfaction work in mammels
air resirculation possible from shape of turbinate bones in nose. odors bind to receptors in the olfactory epithelium activating the olfactory neurones which send signals through the cribriform plate to the olfactory bulb
74
why do organisms phototransduce
creates vision circadian rhythm metabolism vitamin production
75
how do primitve eyes process light/see
strength of light triggers simple reflexes or phototaxic responces can detect strength of light and direction meadiated through membrane rich cilium or rhabdomere where it can be harvested
76
what are the two major types of photoreceptor
rhabdomeric photoreceptors ciliary photoreceptors the difference is in the orientation of cillia polarity
77

biochem y2 (4 decks)

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