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Intro to neuro > Lecture 5 > Flashcards

Lecture 5 Flashcards

1
Q

Types of neurotransmitters

A

Amino-acids (smallest but largest concentration)
Amines (mid-size, mid-concentration)
Peptides (largest, lowest concentration)

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2
Q

Transport of enzymes from the cell body to the presynaptic terminal

A

By the kinesin on the microtubulin

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3
Q

Are amino-acids and amines short or long-duration neurotransmitters?

A

short

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4
Q

How are amino-acids and amines mostly inactivated?

A

Largely through reuptake

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5
Q

Where are amino-acids and amines synthetized?

A

Synaptic terminal

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6
Q

Where are peptides synthesized?

A

In the cell-body

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7
Q

How are peptides inactivated?

A

Through breakdown and diffusion

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8
Q

Cytoskeleton

A

Scaffolding within a neuron, dendrites, axon etc.

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9
Q

Tubulin

A

In proximal axon, dendrites and soma

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10
Q

Tau (microtubulin binding protein)

A

In axon

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11
Q

Parts of the cytoskeleton

A

Tubulin, neurofilament, microfilament

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12
Q

Actin

A

In growth cone, heads of the dendritic spines

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13
Q

Anterograde (Orthodrome)

A

From soma to synapse

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14
Q

Retrograde (Antidrome)

A

From synapse to soma

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15
Q

Retrograde tracers

A

Horseradish peroxidase (HRP), Fluoro gold (FG), Cholera toxin (CT), Fast Blue (FB)

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16
Q

Anterograde tracers

A

Phaseolus vulgaris leucoagglutinin (PHA-L)

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17
Q

Tracers

A

Hijack the transport system along the microtubui

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18
Q

How does anterograde tracing work?

A

Inject tracer in an area, tracer is taken up by the cell-body, kinesin transports it

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19
Q

Antibodies in tracing

A

Primary - binds to the protein of interest
Secondary (such as HRP) -binds to the primary antibody

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20
Q

Layer 2-3 of cortex

A

Send information to other cortical areas (ipsi- and contra-laterally)

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21
Q

Layer 5

A

Connect to subcortical structures (such as striatum and colliculus)

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22
Q

Layer 6

A

Projects back to the thalamus

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23
Q

Layer 4

A

Thalamus sends information to this layer

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24
Q

Acetylcholine ion channels

A

Nicotinic receptor

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25
Q

Is acetylcholine part of the diffuse modulatory systems?

A

Yes

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26
Q

Production of acetylcholine depends on 2 enzymes

A
  1. Achetylcholine esterase (ACHE)- recycles Ach
  2. Choline acetyl transferase (CHAT) - makes Ach
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27
Q

How does ChAt build acetylcholine?

A

From Choline + Acetyl CoA

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28
Q

How does ACHE manage the reuptake

A

Breaks down ACH into Choline + acetate

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29
Q

Novichok

A

Organophosphate that blocks ACHE –> No reuptake of Choline –> No making of ACH

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30
Q

Where are ACH receptors most prominent?

A

In the muscles

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31
Q

Symptoms of novichok poisoning

A

First spasms because the first abundance of ACH over activates the muscles –> Then no more ACH production because choline reuptake is not possible, so neuromuscular paralysis

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32
Q

Where are vesicles?

A

In a reserve pool

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33
Q

What connects the individual vesicles to each other?

A

Synapsin

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34
Q

What breaks down the bonds made by the synapsin so that the vesicles become available?

A

CAMK-II (cam kinase II) - calmodulin dependent protein kinase type II

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35
Q

What primes and docks the vesicles in the membrane?

A

SNAPs and SNAREs

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36
Q

Core elements of the SNARE complex

A

Synaptobrevin (in the vesicle membrane)
SNAP-25, Syntaxin (in the presynaptic membrane)

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37
Q

Fusion of the vesicle with the presynaptic membrane?

A

SNARE complexes form vesicle docks; synaptotagmin binds to SNARE complexes; Ca2+ binds to synaptotagmin which leads to the curvature of plasma membrane so membranes come together –> fusion

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38
Q

Synaptotagmin

A

Is a Ca+ sensor, triggers the fusion of the membranes

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39
Q

Clathrin

A

Coats a piece of membrane that will become the retrieved vesicle

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40
Q

Dynamin

A

Pinches the vesicle (the recovered piece of the membrane from the membrane itself)

41
Q

Actin

A

Kinesin transports the pinched off recovered vesicle via the Actin

42
Q

Auxilin

A

Removes the clathrin coat –> retrieved vesicle

43
Q

Where is most of the Acetylcholine made?

A

Medial septal nuclei and in the basal nucleus of Meynert (both in Basal forebrain, communicates with the cortex)

44
Q

In which area is acetylcholine made that communicates with the thalamus?

A

Ponto-mesencephalo-tegmental complex

45
Q

The 2 types of ACh receptors

A

Ion channels (nicotine - gated)
Metabotropic receptors (muscarine)

46
Q

Nicotine ACh receptors (nAChr)

A

Has 5 subunits
Fast and short-acting
When Ach binds gate flips open

47
Q

Ligand-gated receptors

A

ACh, GABA, AMPA, NMDA, Glycine, Kainate, serotonin, and purine receptors

48
Q

Metabotropic receptor characteristics

A

Have no pore, do not let ions in, but have a G-protein coupled in the inside
–> Are slow and long-lasting

49
Q

How do G-protein coupled (metabotropic) receptors work?

A

Neurotransmitter binds to the receptor –> G-protein in the inside gets activated –> Subunit of the G-protein or an intracellular messenger modulate ion channel –> Ion channel opens

50
Q

Metabotropic receptors are …

A

Muscarinic, glutamate, dopamine, GABAb, adrenergic, histamine, serotonin and purine receptors

51
Q

What does ACh do in the brain?

A

Enhances long-term potentiation, learning, working memory, enhances selective attention, involved in the generation of neuronal oscillations

52
Q

ACh’s role outside the brain

A

Transmitter at the neuromuscular junction
Transmitter of the PNS: rest and digest function

53
Q

Alzheimer’s disease

A

Degeneration of ACh nuclei in the basal forebrain

54
Q

Myasthenia Gravis

A

Antibodies against nACh in neuromuscular junction -autoimmune disease (peripheral problem) –> It “eats” your receptors -> Muscle strength decreases

55
Q

Medicating Alzheimer’s disease

A

-ACh esterase blockers: Rivastigmine, Galantamine - temporarily beneficial on attention, concentration and speech performance in patients with mild to moderate dementia (more ACh left)
-NMDA blockade: Memantine - prevents overexcitation of glutamate because of which cells could die

56
Q

Side effects of Alzheimer’s medication

A

Nausea, diarrhea and tiredness

57
Q

MEPP

A

Muscular Endplate Potential - Amplitude of this gets lower in myasthenia gravis

58
Q
  • MG medication
A

-Cholinesterase inhibitors - pyridostigmine: enhance communication between nerve and muscles
-Corticosteroids -prednisone: inhibit immune system–> limiting antibody production. (side effects: bone-thinning, weight-gain, diabetes, infections etc)
-Immunosuppressants: side effects: nausea, vomiting, liverdamage, kidney damage, increased risk of infection

59
Q

inhibitor of nACh receptor

A

Curare- venoms of some snakes
Reversible nACh receptor blockers for anaesthesia

60
Q

Inhibitor of muscarinic ACh receptor blockers

A

atropine: ACh antagonist, leads to pupil dilation, resuscitation

61
Q

Glutamate reuptake

A

By excitatory amino acid transporters via astrocytes

62
Q

Glutamate is made out of

A

Glutamine by glutaminase

63
Q

Packaging protein of Glutamate

A

VGLUT

64
Q

Experiment with human astrocytes in the mouse brain showed that…

A

Astrocytes are involved in learning and memory

65
Q

Glutamate ion channels

A

AMPA, NMDA, and Kainate receptors

66
Q

How do the AMPA receptors work?

A

They have subunits that change when the neurotransmitter binds to the channel (like with nACh receptors). Short and fast effect

67
Q

How do the NMDA receptors work?

A

They can open and close (so Ca2+ and Na+ can flow in), but they are blocked by Mg2+. First depolarization is carried by AMPA. –> NMDA channels have a longer effect in depolarization (Basically depolarization opens the NMDA channel)

68
Q

What does Glutamate do?

A

Mediates fast excitatory transmission (dangerous to modulate it)

69
Q

NMDA receptors are involved in …

A

Short and long-term memory

70
Q

What happens after the blockade of NMDA receptors?

A

hallucinations, other psychosis-like symptoms, and dissociative anaesthesia

71
Q

Is excessive glutamate toxic?

A

Yes, can lead to ischemia and epilepsy

72
Q

What do learning and memory depend on?

A

Long-term potentiation

73
Q

LTP

A

-Is a long-lasting increase in EPSP amplitude
-AMPA and NMDA have to coexist. LTP happens when there is high-frequency transmission (glutamate binds to AMPA and NMDA receptors), strong depolarization, Ca2+ enters the cell

74
Q

How can LTP be studied?

A

With the Morris water-maze

75
Q

Standardized excitation goes up…

A

after LTP, and stays high for a longer time

76
Q

In regard to LTP, if you block NMDA receptors …

A

You have an initial activation, but it is not stored in the memory

77
Q

What ion’s influx is essential for LTP?

A

Ca2+

78
Q

Dendritic spines …

A

Can grow
Actin makes the spines bigger after LTP (and also makes more of them)

79
Q

CaMK II’s role in LTP

A

Triggers synaptotagmins to fuse more AMPA receptors in the membrane

80
Q

If you block CaMK II

A

Impaired place learning
Studied with knockout mice

81
Q

Late LTP

A

Depends on a protein in the cell-body called CREB
New spines

82
Q

Early LTP

A

NMDA, AMPA activation; addition of postsynaptic AMPA receptors after LTP; synaptotagmin mediated

83
Q

Long-term depression

A

Prolonged low-frequency stimulation

84
Q

Neurogenesis

A

Growth of new neurons and connections from stem cells

85
Q

Neurogenesis was found in …

A

Hippocampus
Caudate nucleus

86
Q

GABA receptors are …

A

Inhibitory

87
Q

GABA is made from

A

Glutamate by glutamic acid decarboxylase

88
Q

Excess GABA from the synaptic cleft is taken up …

A

Via the glial cells and GAT cotransporters

89
Q

Gamma-hydroxybutyrate (GHB)

A

Rape drug: excess GABA (inhibition of breakdown) –> more inhibition –> sedative effect

90
Q

Gaba receptor

A

Many, we have to know the ionotropic one

91
Q

Ionotropic GABA receptor

A

Permeable for Cl- –>Inhibits the target cell

92
Q

Agonists of GABA channels

A

Benzodiazepines, barbiturates

93
Q

Antagonists of GABA channels

A

Convulsants: excite the target cell (picrotoxin, bicuculline)

94
Q

Shunting inhibition

A

If you excite a neuron and have an EPSP but simultaneously activate the inhibitory synapse, it prevents the EPSP from leading to action potential

95
Q

What does the GABA system do?

A

Local balance of excitation through GABAergic inhibition
Inhibition prevents overexcitation (epilepsy)
Pulsed inhibition generates neuronal oscillations (important for cognition)
Excessive GABAergic inhibition leads to sedation or narcosis

96
Q

Young GABA receptors lead to

A

Cell depolarization (because after birth way more Cl- is inside than outside)

97
Q

What connect the clathrin to the plasma membrane?

A

Adaptor proteins: AP-2, AP-180

98
Q

What happens in ischemic stroke?

A

Oxygen deficit in brain: no ATP
No glutamate reuptake, continuous depolarization, excessive Ca2+ influx –> cell death

Intro to neuro (9 decks)

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