B2W2 Flashcards

1
Q

Information flow from dendrite to pre synaptic terminal

A

dendrite, soma, axon, nerve terminal, presynaptic terminal

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2
Q

Action potentials are found ….?

A

in the axon, within a neuron

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3
Q

Graded potentials are found …?

A

between neurons, synaptic potentials are graded (IPSPs and EPSPs)

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4
Q

Vrev for EPSP

A

0 mV

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5
Q

Vrev for IPSP

A

-71 mV

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6
Q

End plate potential location, transmitter, receptor, ions, effect and quantal content

A

NMJ, ACh, nicotinic AChR, (Na, K), depolarization, 100

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7
Q

EPSP location, transmitter, receptor, ions, effect, and quantal content

A

CNS, Glutamate, ionotropic voltage gated channels, (Na, K), depolarization, 1

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8
Q

IPSP location, transmitter, ions, effect, channel, quantal content

A

CNS, GABA (Brain), glycine (spinal chord), ionotropic voltage gated channels, (Cl-), hyperpolarization, 1

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9
Q

Glutamate ionotropic receptors have what kind of configuration

A

tetramers, different from ACh, seratonin, and GABA which are pentamers

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10
Q

AMPA receptors

A

point to point transmission, permeant to Na (in) , K (out), more likely to be active at -40 mV on the post synaptic membrane

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11
Q

NMDA receptors

A

has slower kinetics due to influx of Na,K AND Ca, needing both glutamate and depolarization of the cell to activate

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12
Q

Activation of NMDA receptors

A

Mg 2+ is released through depolarization of a cell, making it need both glutamate and depolarization to activate

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13
Q

Which receptors receive EPSP’s

A

AMPA, NMDA, and kainate

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14
Q

Quantal content v quantal size

A

Quantal content is the number of vesicles fusing to the presynaptic membrane, while quantal size is the amount of neurotransmitters in a vesicle

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15
Q

Facilitation v depression of EPSP

A

increases in quantal content v reduction in quantal content, requires a high frequency v low frequency, strongest when there is low ability for vesicle fusion v strongest when there is a high quantal content

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16
Q

Myasthenia Gravis v Lambert Eaton’s Disease in regards to membrane they affect

A

MG- autoimmune attack and affects AChR on the post synaptic membrane
LE- autoimmune attack and affects the Ca channels on the presynaptic membrane

17
Q

LTP mechanism of memory formation

A

LTP has high frequency stimulation leading to higher Ca+ levels, due to the activation of AMPA and NMDA receptors, leading to calmodulin kinase and PKC activation and increase in AMPA receptors on the post synaptic membrane and increase in quantal content

18
Q

LTD mechanism of memory loss

A

LTD has low frequency stimulation leading to moderate levels of Ca and increase in protein phosphatase activity

19
Q

Main inhibitory neurotransmitter in the brain v spinal chord

A

brain - GABA
spinal chord - glycine

20
Q

How do IPSP’s cause hyperpolarization

A

shunting with depolarizations - EPSP brings in Na into the cell while IPSP bring in Cl to equilibrate

21
Q

Benzodiazepines affect on GABA channels

A

increases the frequency of GABA channels opening

22
Q

Barbiturates affect on GABA channels

A

increases the duration of GABA channels opening

23
Q

Top 5 most prescribed Benzodiazepines:

A
  1. Xanax (alprazolam)
  2. Ativan (lorazepam)
  3. Klonopin (clonazepam)
  4. Valium (Diazepam)
  5. Restoril (Temazepam)
24
Q

Dense core vesicle release v small molecule vesicle release

A

Dense: takes longer, needs more Ca, need high frequency stimulation

Small: rapid release due to location to the terminal, less Ca needed

25
Ionotropic v Metabotropic receptors
ion: voltage gated ion channels leading to muscle contraction, uses glutamate, ACh, serotonin, ATP, uses (Na,K) for excitatory and (cl) for inhibitory Meta: GPCRs, slow using cascades, lead to hyperpolarization when in cardiac myocytes, can be excitatory, inhibitory or modularly with use of peptides, opioids, NE, epi, serotonin, dopamine, glutamate, Ach, GABA
26
Neuromodulation of long depolarizations
Using NE you can reduce adaptation periods, and then restore adaptive depolarizations with washout of NE
27
Neuromodulations of short depolarizations
decrease after hyperpolarization's by inhibiting slow Ca+ dependent K channels and then restore using washout
28
Phasic
frequent spiking of depolarizations followed by period of adaptation
29
Tonic
frequent spiking of depolarizations due to neuromodulation, leading to an increase of frequency
30
Divergent neurotransmitter
There is one neurotransmitter which is able to affect many receptors and elicit multiple different responses (ex. NE)
31
Convergent neurotransmitter
There are multiple neurotransmitters which are acting on the same channel/receptor leading to multiple signals converging !
32
Basic relay steps for synapse (general)
action potential travels down axon, Na channels open at the presynaptic terminal, voltage gated Ca channels open at presynaptic terminal, rise in Ca triggers vesicle fusion, followed by neurotransmitter release across the presynaptic cleft and into the postsynaptic cell, followed by neurotransmitter breakdown (diffusion, breakdown, reuptake)