Csf - Excitable Membranes - Synaptic Transmission/nmj

Front 1

What NT's precipitate an EPSP?

Back 1

Glutamine and Acteylcholine

Front 2

What NT's are involved in IPSP?

What kind of channels do these use?

Back 2

GABA and Glycine -

LIGAND GATED ION CHANNELS.

Front 3

What effect does increase in permeability to Cl- have on synaptic transmission?

Back 3

This is INHIBITORY. GABA and Glycine are used in this inhibitory pathway.

Front 4

Which kinds of presynaptic contacts are inhibitory?

Back 4

AXOSOMATIC and AXOAXONIC are usually inhibitory.

Axodendritic with contact at the shaft is inhibitory as well.

Front 5

Which kinds of presynaptic contacts are excitatory?

Back 5

AXODENDRITIC - axon to dendrite end (not shaft) are excitatory

Front 6

How many EPSP's does it take to get to an action potential?

Back 6

These are GRADED...so more than one.

Front 7

What is spatial summation?

When is this most effective?

Back 7

EPSP's arising simultaneously at multiple synapses on the dendrites or soma.

Spatial summation is most effective when LENGTH CONSTANT IS LONG.

Front 8

What is temporal summation?

When is it most effective?

Back 8

When a single NT is released at a single synapse frequently enough to get electrical summation of individual EPSP's.

Temporal summation is most effective when TIME CONSTANT IS LARGE.

Front 9

When there is a large time constant, what kind of summation is most effective?

Back 9

Temporal summation - the one with ONE
synapse getting fired on many times in a row.

Front 10

When there is a long length constant - which kind of summation is most effective?

Back 10

Spatial summation.

Front 11

In the CNS, is there a low or high probability that an AP will evoke the release of a vesicle?

Back 11

Probability is low in the CNS.

Front 12

What opens Ca+ channels?
What happens when they are open?

Back 12

Action potential opens Ca+

Entry of Ca+ into the cell will release NT into synapse.

Front 13

What has bigger impact on amount of neurotransmitter release - the gating properties of Ca+ or the duration of the AP?

Back 13

The duration of the AP has the biggest effect on amount of NT released.

Front 14

What are three examples of peptide NT's?

Are there more kinds of small-molecule neurotransmitters or peptide NT's?

Back 14

ex) substance P, enkephalin and LHRH

there are many more kinds of peptide NT's than small molecules like Ach/Glu

Front 15

What is classic presynaptic inhibition?

Back 15

Usually axoaxonic inhibition.

Front 16

What is this:

T=RmCm

Back 16

Time constant = loss of current through leak channels X capacitance

Front 17

Are time constant and length constant affected by voltage-gated Na+ channels?

Back 17

NO these are passive properties.

Front 18

Why does it makes sense that spatial summation is most effective when length constant is long?

Back 18

When length constant is long - the decrement over the length of the axon is LOW - so over that span - a greater number of spatially separated EPSP's can sum.

Front 19

Where do you find peptide neurotransmitters vs. small-molecule NT's?

Back 19

small-molecule NT's are found localized to active zones.

peptide NT's (called dense-core vesicles) are distributed around the periphery of the synaptic terminal.

Front 20

What is responsible for termination of NT action in the CNS?

Back 20

Termination occurs via reuptake of NT into synaptic terminal by transporters SPECIFIC for the NT and diffusion.

They are co-transported with Na+ who's concentration gradient provides the energy.

Front 21

what is a motor endplate?

What is the junctional cleft?

Back 21

The area on the muscle fiber that is directly under the axon terminal.

The space between these two regions.

Front 22

Where are active zones found in the NMJ?

Where is a junctional fold?

Back 22

on presynaptic structures

a fold in the motor endplate

Front 23

How does an EPP arise?

Back 23

Ach is released into the junctional cleft and diffuses to the motor end plate.

Front 24

What kind of ion channel is an Ach receptor?

Back 24

Ach receptor is a LIGAND GATED ion channel.

Front 25

What surrounds the muscle fiber and axon terminal to maintain the fold structures?

What enz does this space contain?

Back 25

Lamina Basliaris = surrounds these tissues and contains acetylcholinesterase

Front 26

Where does inhibition occur in the CNS or PNS?

Back 26

ALWAYS CNS - there are NO INHIBITORY neurons in the PNS. PNS contains all excitatory motor neurons.

Front 27

Are EPP's or EPSP's graded?

Back 27

EPSP's are graded. EPP's always result in an AP in muscle.

Front 28

How do EPP's terminate?

How is this different than EPSPs?

Back 28

EPP's terminate bc acetylcholinesterase cleaves.

Both EPSPs and EPPs use diffusion...but only EPPs use acetylcholinesterase.

Front 29

What guarantees EPP at NMJ?

Back 29

The amount of Ach released is more than necessary

Front 30

What is an MEPP?

Back 30

When vesicles randomly fuse with the internal surface of the axon membrane (not requiring Ca+) - each vesicle that fuses with the membrane releases a single quantam of ACh - gives rise to MINIATURE ENDPLATE POTENTIAL.

Front 31

The acetylcholine receptor is made of what?

What is desensitization of ACh receptors?

Back 31

Integral membrane proteins.

Desensitization = the net depolarizing current through the channel gradually decreases despite continued binding of ACh by the receptors.

Front 32

Why are the ACh-sensitive ion channels in the endplate region not affected by voltage changes?

Back 32

ACh-sensitive ion channels are LIGAND GATED. The motor endplate does not generate an AP - but it does depolarize the muscle membrane to threshold so an AP will fire next to it.

Front 33

What is gallamine?

Back 33

Gallamine is a competitive neuromuscular blocking agent - it inhibits Ach binding resulting in muscle paralysis.

Front 34

Are AP's generated with competitive neuromuscular inhibitors?

Back 34

No AP. Just paralysis.

Front 35

Does succinylcholine cause an AP before blocking ACh receptors?

How do these work?

Back 35

Yes (unless administered slowly which takes advantage of desensitization).

Much slower to dissociate from receptor so voltage gated Na+ inactivate in muscles = tissue now REFRACTORY.

Front 36

What is nerve gas?

Back 36

blocks acetylcholinesterase = increase ACh in junction = paralysis by depolarization block and desensitization.

LETHAL.

Front 37

What is myasthenia gravis?

Back 37

degenerative muscle weakness caused by antibodies that attack ACh receptors.