Flashcards in Lecture 5 Deck (143):
This type of synapse is separated by a Gap-junction channel:
This type of synapse is separated by a synaptic cleft:
Majority of synapses in the CNS and PNS are mediated by:
This type of synapse involves a presynaptic cell whereas this type involves a presynaptic cleft:
This type of synapse is formed by hemichannels:
electrical (also called connexons)
T or F? A synapse transmits intracellular signals.
Intercellular signals can be either:
electrical or chemical
These mediate electrical or electronic transmission:
Gap junctions are generally (excitatory/inhibitory)
T or F? Chemical signals mediate only excitation.
F. either excitation or inhibition
What type of channel does an AP open in the nerve terminal of a presynaptic cell?
What causes vesicle fusion?
What causes transmitter release?
Wat type of channel does an AP open in the postsynaptic cell?
This type of channel is both receptor and channel:
How do currents from a presynaptic AP affect the postsynaptic PM?
they don't, they are shunted in the synaptic cleft
T or F? transmitter-receptor binding can produce a depolarization or hyperpolarization of the PM.
This is a special synapse bw neuron and skeletal muscle:
Where is the cell body of the neuron located?
This is a 'giant' excitatory synapse:
What ensures high transmission reliability at the NMJ?
large size of synapse
In the absence of disease, 1 nerve AP generates:
1 muscle AP
Another name for NMJ
1 motor neuron + all fibers it innervates
T or F? Each muscle fiber can be innervated by multiple motor neurons.
F. Only one
Does an alpha neuron typically innervate one or more than one muscle fiber?
more than one
Is the motor neuron cell body in the dorsal or ventral horn?
A motor neuron is connect to a ____ via a NMJ:
Are NMJ junctions bigger the in the CNS or PNS?
PNS (check, note just say "huge compared to CNS")
Do small neuron or large neurons have a higher reliability of transmission?
What type of cell is the outer surface of the presynaptic terminal bouton made of?
Schwann cells, a sheath
This allows for the axon terminal to contact a large MF surface area:
Axon terminal boutons lie in:
gutter-like invaginations with in-foldings of the MF surface
What forms primary and secondary synaptic clefts?
unfolded junctional surface
How much transmitter does each vesicle contain?
How many AcH molecules are in one quantum?
Vesicles are divided into these 2 pools:
small readily releasable and large stationary (slow releasable)
Are the sole releasable pool vesicles located nearer or farther from the PM?
Another name for large stationary vesicles:
What anchors AChE?
These cleft are blank spaces while these contain AChE:
What is the transmitter release site called?
The majority of AChRs are this type of receptor, each made up of this many subunits:
Nicotinic receptors - 5 subunits (pentameric)
What type of channel is nAChR?
an ACh-gated non-selective cationic channel
List the subunit of the nAChR:
2 alpha, 1 beta, 1 gamma, 1 delta
Where is there a high density of AChRs?
in the crests of postsynaptic folds
T or F? Negative charged ions will flow through the cACHRs:
F. Positively charged will
this is a non-conductance state:
How long of a delay is there with chemical transmission?
about 0.5 msec
What triggers exocytosis of vesicles docked at the active zones?
increase in Ca conc.
How many active zones are found in one NMJ?
What is an active zone?
a release site
How many quantum are released at the active zone per nerve AP?
1 quantum (200-300 quanta)
Another name for muscle AP:
How can you mobilize more vesicles from the stationary pool?
increase nerve AP freq. (increase Ca conc)
Are nicotinic receptors both receptor and channel?
EPP are due to:
activation of AcH receptor
T or F? The threshold for an EPP is always bigger (more negative) than the threshold for firing an AP of the muscle.
T or F? Frequency codes for amplitude.
What does frequency code for?
Is the activation threshold larger at the presynaptic end or postsynaptic end?
post (-80 vs. -70)
What type of channels are activated by a NAP?
voltage-gated Ca channels
Does the K driving force get bigger or smaller with the influx of Na?
Does the Na driving force get bigger or smaller with the influx of Na?
T or F? Na/K channels are selective.
Neurons going to EPP are only (excitatory/ inhibitory)
In normal conditions, an EPP is always a _______ potential that produces an AP in the skeletal muscle.
Does an EPP have a large or small safety margin, and how big is it?
large, about 30mV
At which point of the graph is the current of the EPP zero?
at the peak, the driving force of Na and K cancel each other out
At what point on the graph do the AChRs deactivate?
at the reversal potential, peak of the graph
T or F? EPP is presynaptic.
The amplitude of the EPP (decreases/increases) as it moves away from the EP region.
The safety margin for generating a MAP is the voltage separation bw the:
threshold and the reversal potential
How can you determine the EPP?
block more and more receptors until it will no the tablet o pass threshold
EPP is an example of a ___ electronic (local) potential.
A large enough ___ must be created to pass threshold:
How can you decrease a graded potential?
reduce activated receptors or block release of transmitter
2 types of AcHR's:
nicotinic and GPCR
What does the graded potential depend upon?
the amount of ACh released and the number of nAChR activated
T or F? The graded potential is an all-or-nothing potential.
T or F? The EPP will continue to increase in size at a high rate of stimulation.
F. Increase at first then decrease due to depletion of vesicles
Why do the number of vesicles deplete at high frequency stimulation over time?
can't recycle the vesicles fast enough
A high rate of stimulation produces:
What causes an increase in the amount of quanta released?
increase in Ca conc
About what fraction of ACh is hydrolyzed upon release?
3 fates of ACh after release into the junctional cleft:
1. diffusion out of cleft
2. AChE (reuptake)
3. AChR (at the post junctional fold)
AcH breaks down to:
acetate and choline
This is the only example in which transmitter action is terminated by enzymatic action:
List reversible ACh inhibitors:
physostigmine (eserine) and neostigmine
List irreversible ACh inhibitors:
organophosphorus (used in sarin gas & insecticides)
How would an increase in ACh function affect Alzheimers pts?
it would help cognition
What does termination of transmitter action depend upon?
diffusion out of cleft
Can ACh participate in multiple bindings if the transmitter remains in the cleft?
How is the vesicle membrane retrieved after fusion with the PM?
Vesicle endocytosis is ______ dependent.
Vesicle membrane is linked to clathrin endocytic machinery via:
What happens to vesicles that are not recycled?
They are depleted
2 pathways recycled vesicle membrane can take:
direct or indirect (back to membrane or to ER)
Nicotinic receptor is AKA:
This type of cholinergic receptor directly activates an ion channel:
This type of cholinergic receptor indirectly affects conductance of many channels via intracellular signaling:
This type of cholinergic receptor is located in the NMJ:
All autonomic ganglia and some CNS synapses use this type of cholinergic receptor:
Are nicotinic receptors ionotropic or metabotropic?
Are muscarinic receptors ionotropic or metabotropic?
This type of receptor can only activate GpCoupled intracellular signaling:
how do muscarinic metabotropic receptors affect conductance of many channels?
via intracellular signalling
This type of receptor is located at neuroeffector junctions:
muscarinic metabotropic (glands, s.m. tissues and some CNS synapses
Agents that activate receptors:
T or F? succinylcholine is hydrolyzed by AChE:
Prolonged exposure to an agonist leads to:
These can bind but can't activate receptors:
Agonists and antagonists compete by:
mass action for binding the same receptor
Toxins blocking neuromuscular transmission:
botulinum toxin and alpha-bungarotoxin
botulinum toxin blocks:
exocytosis of vesicles
activation by ACh
How does botulinum toxin block exocytosis of vesicles?
proteolytically cleaving components of vesicle fusion machinery in presynaptic terminals
How does alpha-bungarotoxin block activation by ACh?
a small basic peptide binds AChR irreversible
This toxin block neuromuscular transmission bc there is no release of transmitter;
botulinum toxin is produced by:
alpha-bungarotoxin is produced by:
banded krait snake, Bungarus multicinctus
Focal intoxication with botulinum toxin produces:
a chronic denervated state
This toxin works postsynaptically:
This toxin works presynaptically:
This toxin is a receptor agonist:
This is an autoimmune postsynaptic disease that impairs NM transmission:
Effect of myasthenia gravis:
2 diseases of the neuromuscular junction:
myasthemia gravis and Lambert-Eaton myasthenic syndrome
Autoantibodies against AChRs cause:
1. loss of AChRs and increased rate of turnover in junctional PM
2. local inflammatory reaction and widening of synaptic clefts
The effect of myasthenia gravis lead to the loss of the:
Why does myasthenia gravis lead to muscle weakness?
bc the loss of safety margin makes it harder to reach the threshold
T or F? Autoantibodies increase the reliability of signal transmission.
What do autoantibodies block?
Do nicotinic receptor desensitizes quickly or slowly?
This is autoimmune presynaptic disease that impairs NM transmission:
Lambert-Eaton myasthenic syndrome
This NM disease is presynaptic while this is one postsynaptic:
Lambert-Eaton myasthenic syndrome, myasthenia gravis
in this NM disease autoantibodies are against specific class of Ca2+ channel:
Lambert-Eaton myasthenic syndrome
In Lambert-Eaton myasthenic syndrome autoantibodies are against:
specific class of Ca2+ channel
The only 2 agents that are excitatory at the NMJ:
ACh and nicotine
Effect of tetra toxin:
block nerve AP
Affect of bungarotoxin: