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BISC 307 > Final Review Deck - Lecture I - Synaptic Transmission > Flashcards

Final Review Deck - Lecture I - Synaptic Transmission Flashcards

1
Q

What is an ionotropic receptor and what is a metabotropic receptor?

A

-In an ionotropic receptor the receptor is an ion channel and a NT can bind to a ion. channel and cause them to open or close
-in a metabotropic receptor the receptor is slower and yields long term effects and it is where an NT binds and causes an activation in second messenger pathway and causes an intracellular response

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2
Q

If an ion channel open in an ionotropic receptor what two things can happen?

A

EPSP = more sodium in
IPSP = more K+ out or Cl- in

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3
Q

If an ion channel closes in an ionotropic receptor what two things can happen?

A

IPSP - less sodium in
EPSP - less potassium out or less chloride in

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4
Q

If ECl is more negative than the resting membrane potential what direction is chloride moving?

A

chloride is moving into the cell and get an outward current

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5
Q

If ECl is more posiitve than the resting membrane potential in what direction is chloride moving?

A

chloride is moving out of the cell get an inward current

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6
Q

What kind of ionotropic channels are the photorecptors of the eyes?

A

when an NT binds the sodium channels closes causing hyperpolarization or IPSP

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7
Q

What is the secondart transmitter at the NMJ released with ACh?

A

alpha MSH - a co peptide

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8
Q

What are the different types of AChRs?

A

nicotinic and muscarinic (brain)

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9
Q

What are the two types of adrenergic receptors and which one causes vasoconstiction? How many subtypes are there?

A

alpha and beta
alpha causes vasoconstriction
5 subtypes

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10
Q

How many glutamate receptors are there?

A

3 total
2 ionotropic
one metabotropic

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11
Q

How many inputs are there per cell in the CNS and what is the relative strength of each input?

A

-each input is weak
-there is 100-1000 inputs per cell

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12
Q

Over what time course are inputs into the CNS active and what determines the overall effect?

A

-many inputs are spontaneously active and the integration determines all of the effects
-it is a mix of excitation and inhibition
-there are different transmitters and different receptors for each transmitter
-there are ionic and metabotropic effects as well

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13
Q

Where is the density of sodium channels high?

A

at the nodes of rnavier and the highest at the axons hillock whicjh is the trigger zone so it has the lowest threshold and makes it the easiest to get more inward current than outward current

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14
Q

Why are there more inhibitory synapses on nerve cells?

A

cause they are always teetering on the brink of excitation

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15
Q

How can you excite and inhibit a neuron in regards to excitatory synapses?

A

excite - by activating excitatory synapses
inhibit - by activating less excitatory synapses

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16
Q

Where can different receptors be found on the postsynaptic membrane?

A

different receptors can be found on the same patch of postsynaptic membrane or they can be found on different parts of the cells and i all cells the receptors are localized under the patch of presynaptic membrane that releases its respective NT - the nerve cells are really good at trafficking protein where they need to go such as where on the postsynaptic membrane a receptor protein needs to go

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17
Q

If you have a postsynaptic cell that receives both excitatory and inhibitory inputs what happens when it receives the excitatory input?

A

it will depolarize and there will be a release of glutamate which will bind to AMPA receptor and causes an inward sodium current and when current flows in ad then it depolarizes the cell enough to get an AP to trigger from the hillock of the axon and propagate down the length of the axon

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18
Q

If you have a postsynaptic cell that receives both excitatory and inhibitory inputs what happens when it receives the inhibitory input?

A

the GABA or glycine NT binds to its receptor and the current increases of potassium leaving or chloride coming in which causes an outward current and the cell gets hyperpolarized and get an IPSP

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19
Q

If you have a postsynaptic cell that receives both excitatory and inhibitory inputs what happens when it receives both of the inputs?

A

if you stimulate both together you get a flat line where there is no effect, a slight EPSP or an IPSP
-no PSP occurs because the cell remains at the resting membrane potential and there is no driving force

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20
Q

What is the reversal potential?

A

a point between ENa and Ek where there is not net current cause some of the channels are permeable to both sodium and potassium - this is the potential where the current reverses direction - if the permeability of an ion increases simultaneously the membrane potential will reach the reversal potential for that combination of ions

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21
Q

What happens if you have reached the reversal potential for a neuron but you add more NT?

A

nothing the cell will stay more at that reversal potential and the more channels which open which will keep the cell more anchored at that reversal potential if the channel is equally permebale to both ions

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22
Q

What does it mean if you still get inhibitory current even if those channels are closed?

A

some current is leaking out

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23
Q

What is spatial summation of synapses?

A

the currents of two synapses in different places summate due to firing at same time

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24
Q

What is temporal summation of synapses?

A

-when a neuron receives multiple input from the same place if they are fired in close temporal succession

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25
Q

What about a synapse also contributes to the effectiveness of a synapse and why is this the case?

A

the position of the synapse
-this is the case because most potentials are graded and they tend to decay along greater distances

26
Q

What is the efficacy of the synapses in the image in terms of ranking and why?

A

1>2>3>4
-this is because 1 is closest to the axon hillock or the trigger zone and this is the place where there is the greatest concentration of sodium channels making the threshold potential lower since it is easier to get the inward currents to exceed the outward currents
-4 is the furthest from the synapse so trigger zone so it decays a greater extent and is weaker

27
Q

How does the bulbous spine of dendrites affect current?

A

-makes the currents go through the high resistance neck before it can flow out and depolarize the trigger zone

28
Q

Why do neurons have dendritic spines?

A

cause they allow for more postsynaptic membrane to create synaptic inputs

29
Q

How is the dendritic spine a place for regulation and modulation?

A

-if the spine is short and fat then current can flow more easily but if it is long and skinny current cannot flow as easily

30
Q

What channels do dendrites have?

A

voltage gated sodium and calcium and potassium channels

31
Q

What channels does the cell body of a neuron have?

A

has the same channels that are found along the length of an axon but in smaller density so they can generate an AP but it is much harder

32
Q

What type of channels do dendrites tend to lose and what do they tend to keep and what effect does that cause?

A

they tend to lose their sodium channels and keep their calcium channels and they generate calcium dependent APs and this can amplify or cancel the effects of the presynaptic AP they receive

33
Q

Where are the voltage gated channels that can generate their own AP located?

A

the heart like pacemaker cells,

34
Q

How many neurons are there in the digestive tract compared to that of the brain and spinal cord?

A

there are more neurons in the digestive tract compared to that of the brain and spinal cord combined

35
Q

What is presynaptic inhibition and an example of it?

A

-sensory neurons which project to the drg motor nuclei have a presynaptic terminal that synapses onto the postsynaptic dendrite of motor nuclei ad and the presynaptic nerve terminal also has a excitatory neruon synapsing with it and what it does is is cause a small depoalrization of the nerve terminal but not enought to release NT but enpugh where the current spreading in from the major AP is shunted out from open sodium channels which opened due to the small AP which first came in and this overall causes a smaller presynaptic AP and less NT mobilization

36
Q

What is use dependent or activity dependent plasticity?

A

-the way a synapse works is dependent on activity so using a synapse will produce a persistent change in the synaptic function - this is the candidate mechanism for learning and memory

37
Q

Is synaptic plasticity always structural?

A

no but it can be

38
Q

What is facilitation?

A

stimulate the synapse repeatedly and get a response that gets stronger with time can get a bigger epsp that goes back down to baseline - this is due to the residual epsp getting bigger an bigger because of the summation

39
Q

What is the time course of facilitation?

A

measured in ms and is quick to emerge but not a long lasting form of plasticity

40
Q

What is potentiation?

A

-tends to last longer than facilitation - if you stimulate a synapse for a long period of time - the effect persists longer than facilitation
-time course is seconds

41
Q

What is the residual calcium hypothesis for potentiation?

A

-calcium ions that enter the presynaptic terminal are there for a longer period of time in which the calcium is sequestered but when you do stimulate close together in a short period of time there is more calcium present because there is not enough time for it to be sequestered and transmitter release is sensitive to it so small increases in calcium cause more transmitter release
(in squid giant axon the transmitter release increase by n^4 with n more calcium)

42
Q

What is depression?

A

the succesive epsps decline in amplitude the later steps for transmitter release such as docking and priming cause depression because there is depletion of the vesicle pool if you wait for 10-100ms the depression will fade because the vesicle pool is restored

43
Q

What dictates whether a synapse will undergo depression or potentiation?

A

how much of the vesicle pool is released or depleted in on stimulation

44
Q

What are short term forms of plasticity based on?

A

presynaptic changes

45
Q

What are long term forms of plasticity based on?

A

postsynaptic changes

46
Q

What is the basis of learning?

A

LTP, LTD (mins to days)

47
Q

When is LTP observed?

A

stimulate glutamatergic synapses in the CNS that use glutamate at a high frequency and get facilitation and stimulate again days later and it remains facillitated even days later and it can even have permanent effects

48
Q

What are the receptors for glutamate?

A

-metabotropic receptor which is a hormone receptor and causes secondary signaling in the cell
-kainate receptor and is ionotropic
-NMDA receptor and is permeable to calcium and sodium and this inward current does not cause a potential change but it does allow calcium to come in

49
Q

What happens when glutamate binds to the kainate receptor and NMDA receptor?

A

they cause an inward current and calcium activated kinases are activated and this causes greater localization of kainate receptors in the postsynaptic membrane and the structural changes that make spines shorter and fatter allow for more feasibility in conductance
-calcium also changes protein expression and translation and circuits start to behave in a more predictable manner in LTP

50
Q

In regards to sound localization with what accuracy can we determine where a sound is coming from?

A

50% accuracy level within about 2 degrees accuracy level of sounds

51
Q

What is sound and how does it create the production of tones?

A

-pressure waves in the air and it creates tones through a certain frequency of peaks and troughs of pressure waves

52
Q

What do place encoding neurons in the brain do?

A

they receive excitatory input from both ears and they are subthreshold inputs so can only get an AP if both ears inputs fire simultaneously to produce an AP and then go to higher learning centers in the brain

53
Q

Which input in the diagram as binaural input?

A

input c

54
Q

Based on the diagram if a sound source is coming from the right then activity in which neuron will be strong enough to make an AP and send it to the higher learning centers?

A

neuron A due to the left ear being able to generate an AP with delay and the right ear will receive a string enough input to travel to neuron A in time

55
Q

Based on the diagram if a sound source is coming from the left then activity in which neuron will be strong enough to make an AP and send it to the higher learning centers?

A

input e

56
Q

What is the maximum delay of arrival between the two ears?

A

when the sound is perfectly 90 degrees on one side compared to another given the spacing of the human ears and the speed of sound being 400m/s there is a 1 microsecond (1us) delay between the two ears in this case

57
Q

When the sound is perfectly in front of a person what is the maximum delay of arrival?

A

0 microseconds

58
Q

When the sound is 45 degrees in front of a person what is the delay?

A

0.5 microseconds

59
Q

What is in the brainstem’s medial superior olive?

A

-10,000 place encoding neurons and input comes in from the left ear and branches these five neurons and goes to the other ear and signals time delay

60
Q

How does the frequency of the sound they are most sensitive to map out?

A

in a logarithimic way

61
Q
A
  1. In the Ia afferent depends on the concentration of Cl in and out the cell
  2. it will be more positive cause more ECl will want to leave the cell then
  3. GABA will cause chloride to leave via the channel and will cause an inward current cause negative charge is leaving the cell
  4. depolarize the Ia afferent terminal cause chloride is leaving

Summary: NKCC increases intercellular Chloride and this causes ECl to be more positive and want to leave the cell causing an inward current and depolarization cause negative current is leaving the cell

62
Q
A

BISC 307 (17 decks)

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