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phgy 209 > Nerve/Synapse - Lecture 6 > Flashcards

Nerve/Synapse - Lecture 6 Flashcards

1
Q

what type of ion channel not found on dendrites

A

voltage-gated ion channels

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2
Q

why neurons evolved to have many EPSPs necessary to fire an AP

A

to be able to process information received from multiple neurons (different inputs)

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3
Q

why fact that many EPSPs necessary for neuron to fire AP is advantageous for sensations/sensory abilities

A

neurons can unify different perceptions (ex auditory and visual)

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4
Q

Structure of NMDA receptor and what activates them

A

Same structure as AMPA receptors and activated by glutamate

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5
Q

First key property of NMDA receptors

A

At resting memb. potential, pore is blocked by Mg2+ and depolarization of memb. expels Mg 2+ , enabling pore to conduct

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6
Q

Second key property of NMDA receptors

A

Open pore is highly permeable to Ca 2+ as well as monovalent cations

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7
Q

What is necessary for NMDA to release its Mg 2+ and become permeable to calcium

A

Glutamate must bind when memb. is already depolarized (-50 mV ex.)

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8
Q

Concentration of calcium outside cell vs inside

A

out : 0.5 mmol/L in : very little

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9
Q

calcium property for cells/what it serves for

A

signaling molecule/messenger

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10
Q

T/F : if memb not depolarized, glutamate wont bind NMDA

A

F : will bind it but NMDA wont open

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11
Q

T/F : if memb. depolarized, glutamate only binds NMDA

A

F : always binds both but will OPEN NMDA if memb. depolarized

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12
Q

NMDA ‘detects’ what 2 things

A

1) That glutamate is released (synaptic cleft)

2) Cell is already depolarized

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13
Q

2 other a.a that bind NMDA

A

glycine and D-serine

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14
Q

What is synaptic plasticity

A

Process involving NMDA receptors by which highly ACTIVE excitatory synapses become stronger (STRONGER = LARGER EPSPs)

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15
Q

What is LTP

A

long-term potentiation -> model of synaptic plasticity (synaptic plasticity that can be shown experimentally)

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16
Q

3 steps in experiment for LTP

A
  1. Control = 1 AP and measure little EPSP
  2. Induction = Burst of APs and measure higher depolarization
  3. LTP = 1 AP and measure higher EPSP
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17
Q

Proportion of neurons using glutamate

A

3/4 of neurons

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18
Q

Phenomenon name for glutamate toxicity and what receptors it involves

A

Excitotoxicity . Involves calcium flux through NMDA receptors

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19
Q

Steps of excitotoxicity

A

1) Lots of glutamate released near neuron
2) AMPA and NMDA receptors hugely activated all over neuron
3) High concentration of calcium in neuron
4) In any cell, conc. of calcium stays high and is known to be bad so cell commits suicide.

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20
Q

2 diseases situations that can lead to excitotoxciity

A

1) Severe epileptic seizure - lot of glutamate released

2) Stroke : neurons die from not getting oxygen and release all their glutamate to nearby regions

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21
Q

During induction step of long-term potentiation, which ions enter cell/why

A

burst of APs = more and more glutamate released so sodium enters cell (AMPA) and then other glutamate released will bind to NMDA and calcium will enter (because of depolarization)

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22
Q

LTP range of time it could work

A

Can work for days

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23
Q

what process is related to LTP and how

A

Memorization because involves synapses getting stronger in a process that ressembles LTP experiment

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24
Q

What is the substance responsible for LTP / that LTP couldn’t happen without

A

calcium

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25
Q

Why calcium makes synapse stronger

A

biochemical events in the cell that make it produce more AMPA receptors

26
Q

excitotoxicity can contribute/cause to what 2 diseases

A

Stroke and in some neurodegenerative diseases

27
Q

Main inhibitory neurotransmitter in the brain and abreviation + its receptor’s name

A

GABA : gamma-aminobutyric acid

Receptor is GABAa receptor

28
Q

What type of receptor GABAa is and what it is permeable to

A

ionotropic receptor. becomes permeable to chloride

29
Q

How many GABA molecules can bind GABAa receptor and consequence

A

2 (on image) -> hyperpolarization of membrane

30
Q

Concentration of chloride in/out neurons

A

Generally, concentration of Cl- higher outside of neuron

31
Q

What does it mean when a substance ‘potentiates’ a particular receptor. What does it do exactly

A

when it binds it, increases its effect by making it more receptive to its original neurotransmitter/substance

32
Q

3 types of drugs that potentiate GABAa receptor + what it means and what it does

A

benzodiazepines, barbiturates and ethanol : make GABAa more receptive to GABA when they bind it and the IPSP from one GABA receptor is higher

33
Q

where excitatory inputs (EPSP) are generally located

A

on dendritic spines

34
Q

where inhibitory inpus (IPSP) are generally located and why

A

on or near the cell soma because inhibitory effect is maximal there

35
Q

What is synaptic integration

A

Constant decision of firing APs or not by a neuron based on sum of EPSPs and IPSPs reaching the initial segment

36
Q

What happens to EPSP as it spreads to the initial segment and why

A

Dissipates because dendrites don’t have voltage-gated ion (sodium) channels

37
Q

What particularities of the APs are determined by the sum/balance of EPSPs/IPSPs and why

A

pattern and frequency of APs because they can be different depending on timing and synchronicity of EPSPs/IPSPs

38
Q

What are metabotropic receptors

A

Neurotransmitter receptors that are not ionotropic (no ion channel) and that change biochemical activities/properties in the cell

39
Q

other name for metabotropic receptors

A

G-protein coupled receptors (GPCRs)

40
Q

Different receptors found on glutamate synapses (3)

A

Ionotropic receptors (1.AMPA and 2.NMDA) and metabotropic glutamate receptors (3.mGluR’s)

41
Q

Name of the chemical signal that mGluRs send in postsynaptic neuron and what region is it sent into

A

Second messenger. Postsynaptic spine

42
Q

What happens to mGluRs for them to initiate a sequence of biochemical events in the cell

A

When are bound by glutamate, they change their shape from an inactive shape to an active shape

43
Q

What second messengers do (and 3 exemples)

A

Activate a range of cellular proteins (ex. Ion channels, Protein kinases, Transcription factors)

44
Q

How second messengers can act on ion channels

A

Open/activate a closed ion channel

45
Q

How second messengers can act on protein kinases

A

Activate them so they can phosphorylate ion channels or other enzymes

46
Q

How second messengers can act on transcription factors

A

Activate them so they can regulate (probably enhance) gene expression

47
Q

2 things synapse does (short-term vs long-term)

A
  1. Short-term : Change electrical properties of the membrane/cell
  2. Long-term : Change biochemical properties inside the cell (which can last from seconds to weeks …)
48
Q

Ionotropic receptors activated by glutamate and GABA (respectively)

A

Glutamate : AMPA, NMDA (binds but activates it if cell is depolarized)
GABA : GABA A receptors

49
Q

Metabotropic receptors activated by glutamate and GABA (respectively)

A

Glutamate : mGluRs

GABA : GABA B receptors

50
Q

Neuromodulator what it is and what it’s involved in

A

Type of neurotransmitter that interact mainly or only with metabotropic receptors.
Involved in modulating global neutral states, influencing alertness, attention and mood. Not involved in fast flow of neuronal information.

51
Q

Exemples of neuromodulators (4)

A

Dopamine, Serotonin, Norepinephrine, Neuropeptides such as endorphins

52
Q

Synapses exist where there are _______ neurotransmitters for metabotropic that are activated.

A

only

53
Q

Each neuromodulator has its specific _________

A

receptor

54
Q

Where are neurons (where do they originate) that release neuromodulators and where do their axons go

A

In small brainstem and midbrain nuclei. Their axons spread diffusely throughout the brain

55
Q

How neurons for neuromodulators (their cell bodies) are organized

A

In clusters

56
Q

Dopamine neurons, in what regions of the brain they originate

A

Substantia nigra (SN) and Ventral tegmental area (VTA) in the midbrain

57
Q

Norepinephrine neurons how many and where they start

A

20 000, in brain stem

58
Q

What neuromodulators (neuromodulator transmission) are affected by antidepressants + ex. of antidepressant

A

ex. Prozac. Serotonergic transmission (serotonine)

59
Q

what neuromodulators (neuromodulator transmission) are affected by amphetamines, cocaine and other STIMULANTS

A

dopamine, norepinephrine (transmission)

60
Q

good mood has been associated with _____ levels of _________ (which neuromodulator)

A

high levels of serotonine

61
Q

addiction has been related to _______ levels of _______ (which neuromodulator)

A

high levels of dopamine

62
Q

Exemples of drugs (2) that can cause addiction (affect dopamine transmission)

A

Nicotine, Cocaine

phgy 209 (17 decks)

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