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Neuro Pre midterm > Neuro B5 > Flashcards

Neuro B5 Flashcards

1
Q

Ionotropic Receptor

A

Receptor that, when activated by an appropriate agonist, functions as an ion channel when appropriately stimulated.

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2
Q

Metabotropic Receptor

A

Receptor that, when activated by an appropriate agonist,interacts with a G protein to produce a change of enzyme activity within the postsynaptic cell

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3
Q

AMPA receptor

A

ionotropic glutamate receptor that is activated selectively by the agonist alpha-amino-3-hydroxy-5methyliosxazole-4-propionic acid (often called a non-NMDA receptor)

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4
Q

NMDA receptor

A

ionotropic glutamate receptor that is activated selectively by the agonist N-methyl-D-aspartate

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5
Q

Excitatory Postsynaptic Potential (EPSP)

A

excitatory depolarizing graded potential driving membrane potential towards the threshold for action potential

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6
Q

Inhibitory Postsynaptic Potential (IPSP)

A

inhibitory hyperpolarizing graded potential driving the membrane potential away from threshold for action potential

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7
Q

why is there a small synaptic delay between arrival of the impulse and a postsynaptic response?

A

time required for release, diffusion and binding of transmitter, opening of ion channels, movement of ions and changes in enzyme activity.

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8
Q

Exocytosis or quantal release of transmitter is governed by what?

A

P- probability that the contents of a given vesicle will undergo release
N- number of vesicles available for release
Therefore the number of vesicles participating in exocytosis is given by pn

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9
Q

Can the value of p be non zero even in the absence of impulses in the nerve terminal?

A

yes due to the increase with Ca2+

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10
Q

small spontaneous (without nerve stimulation) transient depolarizations can happen where? (Also called minEPPs)

A

at the muscle end plate

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11
Q

What is a standard way of lowering P (probability of release) at the NMJ (neuromuscular junction)?

A

replace Ca2+ with Mg2+ —-> this will reduce influx of Ca2+

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12
Q

When the P (probability of release) is low, what do the EPPs (end plate potentials) look like?

A

have amplitudes that are multiples of a set minimum (referred to as quantal fluctuations)

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13
Q

Quantal Size

A

number of transmitter molecules in a vesicle

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14
Q

Quantum Content

A

The number of quanta released by a single impulse

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15
Q

Mean Quantum Content

A

mean size of EPP (end plate potential) / mean size of MinEPP

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16
Q

Is Botulinum Toxin considered a protease?

A

YES :)

17
Q

What is Botulinum Toxin produced by?

A

produced by Anaerobic Bacillus Clostridium botulinum

18
Q

What is the mechanism of action of botulinum toxin?

A

Prevents vesicular release of ACh irreversibly. does this by binding to the cholinergic nerve endings, entering the cell and suppressing the docking mechanism by breaking down synaptobrevin (remember that is a v-SNARE protein)

19
Q

What are some signs and symptoms of a patient several hours after ingestion of botulinum toxin?

A

double vision, dysphagia, dry mouth, and dysarthria followed by weakness of limbs and trunk

20
Q

what are some clinical uses of Botulinum Toxin?

A

treatment of destinies (muscle contractions) or wrinkle reduction

21
Q

Is Tetanus Toxin considered a protease?

A

Yes of course :)

22
Q

What is Tetanus Toxin produced by?

A

by the anaerobic bacillus Clostridium tetani (from soil)

23
Q

Does tetanus toxin enter the PNS or CNS?

A

PNS via a cut or wound then passes to CNS by retrograde axonal transport

24
Q

What is the mechanism of action of Tetanus Toxin?

A

Enters glycinergic interneurons and suppresses the docking of vesicles by breaking down synaptobrevin. The suppression of glycine release disinhibits lower motor neurons.

25
Q

What is the mechanism of action of aminoglycoside antibotics? (neomycin and streptomycin)

A

Inhibit exocytosis of ACh at motor nerve terminals by blocking presynaptic calcium channels. Therefore raising extracellular calcium

26
Q

What is the mechanism of action of the drug aminopyridine?

A

K+ channel blocking drug prolongs the duration of the impulse and thereby enhances Ca2+ entry tin the motor nerve ending. Hence enhancing quantum content

27
Q

Explain what happens in EPSPs? (excitatory post synaptic potentials)

A

positive charge flows into the neuron at the dendrite and sonata and passes to adjacent cellular surfaces

28
Q

As the current spreads further from the synaptic sites do depolarizations decline or increase?

A

decline, duh! (EPSPs spread with decrement) ;)

29
Q

Where is the density of voltage-gated sodium channels the highest?

A

At the axon hillock (therefore this is the initiation zone for action potentials)

30
Q

Where is the initiation zone for sensory neurons?

A

close to the sensory ending rather than at the junction of the cell body and axon

31
Q

Explain spatial summation

A

more then one input into the same cell, however, we are adding inputs from different parts of space( could be sufficient to provoke an action potential)

32
Q

Explain temporal summation

A

perhaps 10 impulses at 20ms intervals that serially arrive at the excitatory synapse on a motor neuron

33
Q

The firing rate of a neuron is dictated by what?

A

by the combined effect of the spatial and temporal summation of EPSPs (excitatory post synaptic potentials) and IPSPs (inhibitory post synaptic potentials)

34
Q

Do both the transmitter release and the cellular effects of transmitters occur briskly?

A

No, transmitter release occurs briskly but cellular effects of transmitters may linger for 20ms or far longer

35
Q

The transmitter, glutamate, is rapidly removed from the synapatic cleft by transporters, explain the process

A

Glutamate when taken up by transporters into astrocyte, is metabolized to glutamine, which has its own neuronal transporter

36
Q

Are peptide transporters found in blood brain barrier cells?

A

yes

37
Q

How are norepinephrine, epinephrine, dopamine, and serotonin (5-HT) absorbed and then degraded in the outer membrane of mitochondria in the nerve endings?

A

absorbed via transporters and then degraded by monoamine oxidase (MAO). NOTE—> can also be degraded by COMT

Neuro Pre midterm (12 decks)

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