Neuro B5

Question 1

Ionotropic Receptor

Answer 1

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

Question 2

Metabotropic Receptor

Answer 2

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

Question 3

AMPA receptor

Answer 3

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

Question 4

NMDA receptor

Answer 4

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

Question 5

Excitatory Postsynaptic Potential (EPSP)

Answer 5

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

Question 6

Inhibitory Postsynaptic Potential (IPSP)

Answer 6

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

Question 7

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

Answer 7

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

Question 8

Exocytosis or quantal release of transmitter is governed by what?

Answer 8

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

Question 9

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

Answer 9

yes due to the increase with Ca2+

Question 10

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

Answer 10

at the muscle end plate

Question 11

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

Answer 11

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

Question 12

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

Answer 12

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

Question 13

Quantal Size

Answer 13

number of transmitter molecules in a vesicle

Question 14

Quantum Content

Answer 14

The number of quanta released by a single impulse

Question 15

Mean Quantum Content

Answer 15

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

Question 16

Is Botulinum Toxin considered a protease?

Answer 16

YES :)

Question 17

What is Botulinum Toxin produced by?

Answer 17

produced by Anaerobic Bacillus Clostridium botulinum

Question 18

What is the mechanism of action of botulinum toxin?

Answer 18

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)

Question 19

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

Answer 19

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

Question 20

what are some clinical uses of Botulinum Toxin?

Answer 20

treatment of destinies (muscle contractions) or wrinkle reduction

Question 21

Is Tetanus Toxin considered a protease?

Answer 21

Yes of course :)

Question 22

What is Tetanus Toxin produced by?

Answer 22

by the anaerobic bacillus Clostridium tetani (from soil)

Question 23

Does tetanus toxin enter the PNS or CNS?

Answer 23

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

Question 24

What is the mechanism of action of Tetanus Toxin?

Answer 24

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

Question 25

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

Answer 25

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

Question 26

What is the mechanism of action of the drug aminopyridine?

Answer 26

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

Question 27

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

Answer 27

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

Question 28

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

Answer 28

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

Question 29

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

Answer 29

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

Question 30

Where is the initiation zone for sensory neurons?

Answer 30

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

Question 31

Explain spatial summation

Answer 31

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)

Question 32

Explain temporal summation

Answer 32

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

Question 33

The firing rate of a neuron is dictated by what?

Answer 33

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

Question 34

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

Answer 34

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

Question 35

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

Answer 35

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

Question 36

Are peptide transporters found in blood brain barrier cells?

Answer 36

yes

Question 37

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

Answer 37

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