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KINE2011: Human Physiology > Module 3: Lecture 6 > Flashcards

Module 3: Lecture 6 Flashcards

1
Q

what is an ionotropic receptor?

A

anytime we have a neurotransmitter triggering an ion channel to open and allow ions to flow

essentially
- respond to a ligand or a neurotransmitter binding to them to all ions to flow through them. they are a channel
- the receptor itself can be an ion channel DIRECTLY

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2
Q

what is a metabotropic receptor?

A

still respond to a ligand or a neurotransmitter binding to them but they are not an ion channel
- receptor can INDIRECTLY act on an ion channel
- it is a second messenger

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3
Q

what are the two types of subsynaptic receptors on the subsynaptic membrane?

A
  1. ionotropic receptors
  2. metabotropic receptors
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4
Q

what are ligand-gated channels/chemically gated ion channels?

A
  • active or respond in response to a neurotransmitter or chemical or ligand binding
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5
Q

what determines if an excitatory or inhibitory synapses is created?

A

depending on what neurotransmitter is released and what receptor it binds to

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6
Q

what is an EPSP?

A

an excitatory postsynaptic potential
- a graded potential that will decrementally spread from the synapse by local current

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7
Q

what is an excitatory synapses?

A

the post-synaptic response to the neurotransmitter is a depolarization
- neurotransmitter is binding to an ion channel (ionotropic receptor) inducing depolarization

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8
Q

what is the net movement of excitatory synapses?

A

net movement of positive charges inside the cell

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9
Q

can the activation of ONE excitatory synapse lead to an action potential?

A

no, it is not sufficient to lead to an action potential (it can be as small as 0.5mV)
- HOWEVER, it brings the membrane closer to the threshold such that additional EPSPs could eventually trigger an action potential

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10
Q

what is an IPSP?

A
  • inhibitory postsynaptic potential
  • bringing cell further away from threshold potential
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11
Q

how can IPSPs hyperpolarize the membrane?

A

by increasing membrane permeability to K+ or Cl- because they want to move closer to their membrane potential (potassium will want to leave and chloride will want to enter, but making it more negative. both go down concentration gradient)

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12
Q

what is chlorides equilibrium potential?

A

-70mV

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13
Q

do all cells have active transport of Cl- into the cell?

A

no. SOME cells(neurons) have ACTIVE transport of Cl- into OR out of the cell

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14
Q

how would neurons do depolarize(EPSP) using chloride?

A

depolarize by exporting Cl- to ECF

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15
Q

what will passive diffusion of Cl- depend on?

A

its equilibrium potential relative to membrane potential (varies across types of neurons)

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16
Q

what does free movement of Cl- in the membrane do?

A

serves to stabilize membrane potential to help counter leak of other ions and decrease the likelihood of reaching threshold (an IPSP that ‘stabilizes’ the membrane potential like a break pedal/limit change in membrane potential)

17
Q

what is the notion of synaptic delay?

A

the generation of the electrical signals, the chemical conversion to neurotransmitters actually being released and binding as well as regenerating that electrical signal in the postsynaptic neuron and it all takes time
- all these processes have to happen at every synapse

  • the total sum of all those processes
  • typically 0.5-1 msec for 1 synapse
18
Q

what is determined by the sum of the synaptic delays?

A

total reaction time

19
Q

as long as there is neurotransmitter within that synaptic cleft and its bound to these ion channels, these ion channels are?

A

going to remain active

20
Q

if the unbound neurotransmitters are removed from the cleft, the number of occupied receptors will?

A

decrease

21
Q

is there an equilibrium between a neurotransmitter that is bound to its receptor relative to the amount that is unbound?

A

yes

22
Q

how do we remove the neurotransmitter in the synaptic cleft?

A

we degrade/remove the unbound neurotransmitter that’s floating in that synaptic cleft which will putt the equilibrium potential more towards the unbound form by degrading more towards the unbound form by degrading those unbound neurotransmitters

23
Q

what is are the 3 mechanisms that are used to remove the unbound neurotransmitter?

A
  1. reuptake
  2. diffuse away from the receptor site and the cleft
  3. enzymatically transformed into inactive substances (and eventually recycles into the presynaptic axon terminal)
24
Q

what is a reuptake?

A

unbound neurotransmitters are actively transported back into the presynaptic axon terminal

25
Q

true or false: one single neuron that is taking thousands of inputs and that is activating a postsynaptic neuron is going to either induce and EPSP, an IPSP, and all of the input, all of the EPSP and IPSP gets integrated at the postsynaptic neuron

A

true

26
Q

what does the sum of the IPSP and the EPSP equal?

A

overall synaptic potential
- GPSP (Grand Postsynaptic Potential)

27
Q

what is temporal summation?

A

when the same neuron has activated twice so it generated two EPSP and they summate on top of one other (A+A)

28
Q

what is spatial summation?

A

multiple inputs from different locations on a neuron combine to produce a larger, potentially action-potential-generating signal (A+B).

  • when graded potential from two different neurons, summate.
29
Q

what is temporal summation and spatial summation equal to?

A

spatiotemporal summation

30
Q

what happens when an excitatory neuron fires and an inhibitory neuron fires at the same time?

A

they spatially summit
- they essentially cancel each other out

31
Q

what is presynaptic inhibition?

A

you are inhibiting a neuron just before the synapse occurs, preventing it from activating its postsynaptic neuron.
ex. if a IPSP neuron B is attached to an EPSP neuron A which is attached to a neuron C, the A will cancel out the B before it can affect C
- if B is stronger than A, then A will only weaken it not cancel it

32
Q

what is presynaptic facilitation?

A

you are facilitating a neuron just before the synapse occurs, enhancing the release of neurotransmitter to its postsynaptic neuron.
ex. if a EPSP neuron B is attached to an EPSP neuron A which is attached to a neuron C, the A will increase the affect of the B onto C

33
Q

if the level of neurotransmitter released by ‘A’ is increased because of ‘B’ what is this?

A

presynaptic facilitation
opposite = presynaptic inhibition

KINE2011: Human Physiology (29 decks)

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