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Neuroscience > Chapter 6 Events at the Synapse > Flashcards

Chapter 6 Events at the Synapse Flashcards

1
Q

Where do AP get started?

A

axon hillock or sensory receptor

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2
Q

Place where AP reach “the end of the line”

A

presynaptic terminal

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3
Q

what type of gate do AP open at “the end of the line”

A

voltage gated channels

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4
Q

What do these voltage gated channels let in?

A

calcium (when the gates swing open, calcium pours in)

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5
Q

What floats around in the end of an axon?

A

vesicles (neurotransmitter ligands)

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6
Q

What herds the bubbles (vesicles) to the very end of the axon?

A

Calcium (sheep dog)

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7
Q

What happens when the vesicles fuse with the membrane?

A

bubbles pop and spill their guts and ump out their ligand into the synaptic space and release their neurotransmitters

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8
Q

is it a high concentration of the NT that pops and travels through space or low?

A

High concentration

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9
Q

what causes the membrane channel to open?

A

the receptors accept the NT ligand, they bind to the recepter on the membrane and channel and thus they open

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10
Q

What flows into the membrane?

A

the gates open and the ions flow through, one positive ion flows through (most likely a single positive like Na+)

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11
Q

How does the synapse get cleared?

A

mechanisms disassemble any NT that is just floating around, get it ready for the next AP coming down the line.

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12
Q

Duration of strong and weak signals?

A

strong: come quickly
weak: come less frequently

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13
Q

axosomatic

A

axon to soma

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14
Q

axodendritic

A

axon to dendrite

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15
Q

influence of axosomatic and axodendritic

A

both increase or decrease the chances of an AP getting created in the next neuron because they attach to the new neuron before the axon hillock so they influence how likely it is that a new AP will come out

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16
Q

axoaxonic

A

axon from one neuron makes a synapse with another neuron

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17
Q

influence of axoaxonic

A

synapse increases and decreases amount of NT that gets released

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18
Q

EPSP

A

starter signal for the next potential
excitatory (depolarizes) and lets sodium or calcium into cell
facilitation

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19
Q

what is facilitation?

A

when a NT creates an EPSP the post synaptic is facilitated or more likely to create a new AP

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20
Q

IPSP (local potential, grades and doesn’t go very far)

A

inhibitory and post synaptic potential
local potential hyperpolarizes the membrane
can be caused most often by letting chlorine in and potassium out
inhibition

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21
Q

what is inhibition?

A

less likely for AP to happen so less likely to be active

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22
Q

presynaptic faciltation

A

figure 6.6A
want to increase NT from 2 to 3
anything that increases calcium into 2 will increase the amount of NT that are kicked from 2 to 3

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23
Q

what facilitates NT release

A

increase of calcium release

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24
Q

Axoaxonic Connection

A

if 1 releases a ligand that opens more calcium channels on number 2 then number 2 will release more NT to 3

the more calcium channels opened on 2 then more NT is released thus a stronger signal

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25
Q

anti depressant axoaxonic activity

A

increase activity of 1 and increase release of feel good NT from 2

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26
Q

presynaptic inhibition

A

2 is carrying pain (hitting shit) and 2 has a synapse with 3 which takes it further into the nervous system

2 is a pain neuron and 1 is a light touch sensory neuron and when one is active, it releases ligand that prevents calcium channels from opening 2. rubbing CAN help reduce signaling

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27
Q

remember about neurons!!

A

as long as neurons are active they’re reducing calcium

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28
Q

What are neurotransmitters?

A

proteins that bind to receptors

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29
Q

what happens when NT are released into the synaptic cleft?

A

they act immediately on post synaptic receptors and neuromodulators

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30
Q

what do the receptors and neuromodulators do?

A

excite or inhibit depending on receptor they bind to

quick but short lived response. do what they need to do and move for next signal to come

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31
Q

Where are neuromodulators released?

A

not into the synaptic space (released outside of synapse) away from the synapse

32
Q

Where do nerve cells have receptors?

A

on them across the membrane

33
Q

receptors of nerve cells act on?

A

non synaptic receptors

34
Q

neuromodulators can affect what?

A

the number of neurons

35
Q

onset of neuromodulators?

A

slower onset, float away from release, longer to be felt but a LONGER response

36
Q

is it a NT or a NM?

A

same ligand can be either a NT or a NM but depending where the release is and the kind of receptor it binds to

37
Q

Types of synaptic receptors

A

4 different types

38
Q

what is a directly open ion channel?

A

fast acting

receptor bets bound, ions enter immediately, located IN synapse and great for signaling

39
Q

indirectly open channels?

A

ligand, NT doesn’t bind to channel but binds to a different protein and it indirectly opens the door. Either in or out of synapse. it is SLOW

40
Q

intracellular events channel?

A

no gate but there’s an activation of intracellular events (slow acting)
a ligand binds it, goes and flips a switch on a machine (enzyme)

41
Q

ligand gated ion channels?

A

DIRECTLY
a receptor is directly part of the membrane protein that has a gate
fast but short lived (slide 39)

42
Q

G-protein activated channels?

A

INDIRECTLY.
gate but not receptor, ligand binds to receptor, G-protein is activated
tetris piece breaks away to channel and opens door from inside (butler hearing a doorbell)
the ligand binds, G protein gets energized, tetris takes a little longer for this response to occur, door stays open longer
G receptor has receptor for this protein

43
Q

G- Protein Second messenger system?

A

see slide 42
ligand binds to a G protein, tetris piece floats over and turns on machine to make something that can be made in the cell
second messenger sequence

44
Q

where are the messenger sequences?

A

1st is outside the cell and 2nd is from the machine

45
Q

what does an agonist effect?

A

increases the effects of ACH

46
Q

example of an agonist?

A

nicotine

47
Q

what is an exognist?

A

ligands made outside that can enhance or inhibit and bind to receptor

48
Q

what a change in synaptic function….

A

there’s an increase of andognious ligands that facilitate release of NT

49
Q

what is an example of an antagonist?

A

Botox

50
Q

what do antagonists do

A

bind or block the number of NT that get out. the brain can send countless AP, neuron will never release ACH

51
Q

what does Botox do?

A

it inactivates calcium channels, muscle won’t respond

52
Q

what is acetylcholine?

A

causes something to happen and then gets out of the way for something to come

53
Q

where is ACH fast acting?

A

the neuromuscular junction

54
Q

what is the neuromuscular junction?

A

post synaptic has receptor right on it, directly opens the gate. it is FAST

55
Q

is ACH slow anywhere?

A

yes, in the ANS and CNS

56
Q

what happens with ACH in the ANS and CNS?

A

binds to a muscarinic receptor, it’ll be some type of G-protein linked to membrane channel. slow to open but it lasts longer

57
Q

Glutamate

A

in the CNS
excitatory (depolarizes) but can be toxic for brain cells
fast acting, AMPA receptor
slow (NMDA)

58
Q

what is the most prevalent fast acting excitatory NT in CNS

A

glutamate

59
Q

GABA

A

inhibitory
generates an IPSP
fast when binding to a GABAa receptor slow when binding to GABAb receptor

60
Q

what is an amines?

A

slow acting NTs

61
Q

dopamine?

A

influences motor activity, cognition, and behavior. as well as addiction

62
Q

what is norepinepherine

A

can increase our awareness to sensory info coming in

autonomic

63
Q

serotonin?

A

mood and perception of pain, arousal level

64
Q

peptide?

A

endogenousopoids–pain relieving

can turn down perception of pain in pain pathway

65
Q

substance P

A

transmitter or modulator

send signal of pain or enhance route for perception of pain

66
Q

chronic pain?

A

substance P is over active

67
Q

remodeling of post synaptic membranes?

A

can be remodeled to increase or decrease receptiveness

68
Q

down regulate?

A

less receptive to signaling, internalize membrane receptors—pulls them in so they can’t be active or open.

69
Q

inactivate?

A

leaving receptors up but flipping them off internally

70
Q

down regulation reduces?

A

chances of AP or signal in pathway

71
Q

up regulate

A

post synaptic can be regulated

receptor floating in cell and stick it up into membrane

72
Q

activate?

A

unlock gate, allow it to open and let ions flow into ion channel

73
Q

activation does….

A

increases odds of AP

74
Q

Myasthenia Gravis

A

the membrane unfolds itselt
Ach-esterase are more likely to shut it down before it can do anything
Number of receptors go down
ACH is at the neuromuscular junction so muscles

The longer they try to hold the contraction goes down because there aren’t enough ACH and the esterase are eating it up so it’s not getting recycled

Giving drugs to patients that turn off the enzymes that eat up ACH
Shut off esterase it allows for more of a contraction. Makes sure there aren’t strong and long contractions that will hurt her muscles

75
Q

depression?

A

SSRI: anti depressant drug that has a very specific action
Seratonin: NT of anti depression.. The feel better action

There isn’t enough serratonin released or there aren’t enough receptors

Drug approach: in the blue, there are serotonin reuptake transporters… vacuum seroatin out of synapse to get ready for signal
drug shuts off vacuums and lets them bounce around for a prolonged effect of it

SSRI: selective seratonin reuptake inhibitor

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