Module B-05 Flashcards
What is Synaptic delay?
The time (0.5ms) btw arrival of an impulse at the end of an axon and the postsynaptic response
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.
Number of neurotransmitter molecules in a vesicle
Quanta
What effects the probability of exocytosis of transmitter from a vesicle
intracelllar Ca2+ concentration
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
What happens when [Mg2+] at NMJ is increased
blocks voltage-gated Ca2+ channels and reduced EPPs
Number of quanta released by a single impulse is the _________
quantum content
Equation for Mean quantum content
Mean Quantum Content = (Mean size of EPP) / (Mean Size of MinEPP)
What is effect of Botulinum Toxin
- Irreversibly Blocks Ach Release
How does Botulinum Toxin block Ach release
- Binds to cholinergic nerve endings
- enters cell
- breaks down synptobrevin => prevents docking IRREVERSIBLY
Symptoms of Botulism
- double vision,
- dysphagia,
- dry mouth,
- dysarthria followed by weakness of limbs and trunk.
- Paralysis of ventilatory muscles => death
Clinical use of Botulinum toxin
- treat dystonias (dysfunctional and sometimes disfiguring contractions of muscle)
- cosmetically to reduce facial wrinkles
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
Symptoms of Tetanus
powerfully sustained muscular contratcions
What is effect of Tetanus Toxin
Blocks Glycine release
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
How can Effect of Neomycin and streptomycin be reversed
By increasing extracellular Ca2+ conc.
What is effect of 4-Aminopyridine
Prolongs the duration of an impulse
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)
where do EPSPs (excitatory postsynaptic potentials) occur
in Dendrites and somata
EPSPs spread with ___________
decrement
where is the highest conc of voltage gated Na+ channels?
Axon Hillock (near sensory nerve ending for sensory neurons)
Where is region of lowest threshold for excitation?
Axon Hillock (near sensory nerve ending for sensory neurons)
Temporal summation of PSPs
impulses arrive in series add up to produce an EPSP because they arrive before the previous impulse has lapsed
Spatial summation of PSPs
impulses arrive at different synapses simultaneously and their depolarizing current summates
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
How are peptides removed from synaptic zones
- Peptide transporters found in blood-brain barrier cells.
- Diffusion
- extracellular proteases
Slowest removed transmitters
ACh, peptides and gases
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
How is Serotonin (5-HT)degraded?
MAO
