Conduction and Synapses

Question 1

What is the morphology of neuron?

Answer 1

Soma - cell body, dendrite - receive and process signal, axon - AP conduction, hillock - signals are summated to see if AP will occur, synapse

Question 2

Have many receptors/channels that are activated by a NT ligand…

Answer 2

dendrites

Question 3

Densely packed with channels activated by changes in membrane voltage…

Answer 3

axons

Question 4

Action potential shape is due to…

Answer 4

properties of Na+ and K+ voltage channels

Question 5

Sodium channel open states

Answer 5

no delay, stays open for msec

Question 6

Opens with 1 msec delay, stays open as long as membrane is depolarized, this efflux leads to repolarization

Answer 6

voltage K+

Question 7

How does refractory period form after AP?

Answer 7

previous action potential (depolarized) area is returned to resting potential via K+ efflux. This creates an orthodromic propagation

Question 8

What affects conduction of propagation?

Answer 8

axon diameter (larger the faster), myelination thickness, and temperature (speed increase w temp)

Question 9

What is purpose of Nodes of Ranvier?

Answer 9

Allow for saltatory conduction which is where in those gaps the AP is regenerated, without this the whole membrane would need to be depolarized (continuous conduction) which is slow

Question 10

What are components of electrical synapse?

Answer 10

gap junctions which are made of connexons and allow ions, metabolites to pass through. This is important for things like cardiac muscle. This changes post synaptic potential immediately but is small

Question 11

What are components of post and pre synaptic terminals?

Answer 11

Pre-synaptic is axon terminal release of NTs triggered by Ca2+ channels. Post-synaptic can be dendrites, or NT receptors

Question 12

This opens when action potential reaches the presynaptic terminal and there’s depolarization of presynaptic terminal membrane…

Answer 12

Ca2+ channels causing calcium influx and can stay open during depolarization. This leads to synaptic vesicle fusion

Question 13

How does Ca2+ trigger synaptic vesicle fusion?

Answer 13

Ca2+ binds to synaptotagmin on vesicle which initiates engagement of SNARE complex to fuse to active zone, then exocytosis. (SNARE proteins: synaptobrevin, Snap-25, Syntaxin)

Question 14

Ionotropic vs metabotropic postsynaptic receptors

Answer 14

iontropic is ligand gated ion channel, quick, but short and metabotropic is GPCR, slower, but longer lasting

Question 15

step wise, passive change in membrane potential that varies and is proportional to input stimulus; can be inhibitory or excitatory

Answer 15

graded potential

Question 16

What are examples of graded potentials?

Answer 16

PSPs, End Plate potentials -generated in motor endplate (muscle) in response to motor signal and is greater than EPSP, and receptor potential

Question 17

Why do graded potentials degrade quicker than AP?

Answer 17

because signals degrade and the summation of signals is important; need convergence of input

Question 18

How does ACh affect NMJ?

Answer 18

ACh release binds to ionotropic nicotinic receptors which then open for Na+ influx; agonist is nicotine

Question 19

Why are EPPs larger?

Answer 19

multiple axons releasing NTs, motor endplate has larger surface area, and more channels open this leads to APs in adjacent cells, not the EP

Question 20

How does alpha latrotoxin affect NMJ?

Answer 20

increases Ca causing uncontrolled exocytosis of ACh, prolonged depolarization then depletion, death from respiratory paralysis

Question 21

Organophosphates

Answer 21

bind to AChE so no breakdown of ACh leads to seizures, drooling, respiratory failure, constriction

Question 22

Myasthenia gravis

Answer 22

antibodies against NMJ AChrs, fewer motor units activated, and ACh is degraded before is can bind to the few receptors; treat with anti AChE (pyrdostigmine)