Module B-05 Flashcards Preview

Neuroscience > Module B-05 > Flashcards

Flashcards in Module B-05 Deck (30):
1

What is Synaptic delay?

The time (0.5ms) btw arrival of an impulse at the end of an axon and the postsynaptic response

2

What causes Synaptic delay?

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

3

Number of neurotransmitter molecules in a vesicle

Quanta

4

What effects the probability of exocytosis of transmitter from a vesicle

intracelllar Ca2+ concentration

5

What are mini End plate potentials(mini EPPs)?

-spontaneous small transient depolarizations about 1 mV in
size in a muscle at rest
- caused by the motor nerve terminal releasing ACh
spontaneously

6

What happens when [Mg2+] at NMJ is increased

blocks voltage-gated Ca2+ channels and reduced EPPs

7

Number of quanta released by a single impulse is the _________

quantum content

8

Equation for Mean quantum content

Mean Quantum Content = (Mean size of EPP) / (Mean Size of MinEPP)

9

What is effect of Botulinum Toxin

- Irreversibly Blocks Ach Release

10

How does Botulinum Toxin block Ach release

- Binds to cholinergic nerve endings
- enters cell
- breaks down synptobrevin => prevents docking IRREVERSIBLY

11

Symptoms of Botulism

- double vision,
-dysphagia,
-dry mouth,
- dysarthria followed by weakness of limbs and trunk.
- Paralysis of ventilatory muscles => death

12

Clinical use of Botulinum toxin

- treat dystonias (dysfunctional and sometimes disfiguring contractions of muscle)
- cosmetically to reduce facial wrinkles

13

How does the Tetanus toxin act

- enters PNS and moves retrogradely to the CNS
- enters Glycinergic interneurons (inhibitory
- suppresses ( irreversibly) vesicle docking by breaking down synaptobrevin
- prevents inhibition of lower motor neurons

14

Symptoms of Tetanus

powerfully sustained muscular contratcions

15

What is effect of Tetanus Toxin

Blocks Glycine release

16

Effect of Neomycin and streptomycin

- Block Presynaptic Ca2+ channels => blocks release of Ach at motor nerve terminals
- At high concentrations, both antibiotics also can block postsynaptic nAChRs

17

How can Effect of Neomycin and streptomycin be reversed

By increasing extracellular Ca2+ conc.

18

What is effect of 4-Aminopyridine

Prolongs the duration of an impulse

19

How does 4-Aminopyridine prolong impulse

it is a K+ channel blocker
enhances ca2+ entry into the motor nerve ending
this increases Ach release ( quantum content)

20

where do EPSPs (excitatory postsynaptic potentials) occur

in Dendrites and somata

21

EPSPs spread with ___________

decrement

22

where is the highest conc of voltage gated Na+ channels?

Axon Hillock (near sensory nerve ending for sensory neurons)

23

Where is region of lowest threshold for excitation?

Axon Hillock (near sensory nerve ending for sensory neurons)

24

Temporal summation of PSPs

impulses arrive in series add up to produce an EPSP because they arrive before the previous impulse has lapsed

25

Spatial summation of PSPs

impulses arrive at different synapses simultaneously and their depolarizing current summates

26

The firing rate of a neuron is dictated by the combined effect of the ______ and _______summation of _____ and _____ (inhibitory post-synaptic potentials)

spatial ; temporal ; EPSPs ; IPSPs

27

How are peptides removed from synaptic zones

- Peptide transporters found in blood-brain barrier cells.
- Diffusion
- extracellular proteases

28

Slowest removed transmitters

ACh, peptides and gases

29

How are Norepinephrine, epinephrine and dopamine degraded

1) Monoamine Oxidase (MAO) in the outer membrane
of mitochondria in the nerve endings (also in astrocytes and liver). Some extracellular MAO also exists
2) catechol-omethyltransferase(COMT)which methylates teh catechol ring; located in presynaptic mitochondria, postsynaptic nerve endings, astrocytes and liver

30

How is Serotonin (5-HT)degraded?

MAO