Lecture 16 + 17 Flashcards

1
Q

What types of neurons should be mapped if examining excitatory nervous system circuits? (2)

A

Glutamatergic and cholinergic

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2
Q

What types of neurons should be mapped if examining inhibitory nervous system circuits? (2)

A

GABAergic and glycinergic

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3
Q

What is the Allan mouse brain atlas?

A

Genome-wide atlas of gene expression in mouse brain created using in situ hybridization

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4
Q

What is the role of ACh in neuromuscular junctions?

A

Generation of post-synaptic depolarization activates pentameric ionotropic cys-loop channels

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5
Q

Cholinergic neuron gene marker

A

Choline acetyltransferase (ChAT)

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6
Q

Where is ACh secreted from in the CNS?

A

Axonal swellings (varicosities)

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7
Q

Define volume transmission

A

Axonal swelling secretion and diffusion of neurotransmitters into extracellular environment

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8
Q

What function do pre-synaptic nAChR’s have?

A

Boost neurotransmission

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9
Q

AMPA/Kainate receptor blocker

A

CNQX

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10
Q

What is a muscarinic receptor?

A

Receptor which can be activated by fungal toxin muscarine

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11
Q

What is the role of the G_q -> phospholipase C (PLC) -> protein kinase C (PKC) pathway?

A

Drives post-synaptic excitation in hippocampus through increased cytoplasmic Ca2+ and PKC activation

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12
Q

mAChR activation leads to inhibition of what K+ channels? (2)

A

M-type K_v channels

Ca2+ activated SK channels

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13
Q

How do M1/M3 mAChRs inhibit M-type K_v channels?

A

PIP2 is required for M-type K_v channel activity. mAChR activation results in decrease in PIP2.

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14
Q

What is the effect of M1/M3 mAChR activation on pyramidal neurons?

A

Increased excitability

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15
Q

What two neurological functions are pyramidal neurons important for?

A

Attention and memory formation

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16
Q

How can volume transmittion of ACh cause pre- and post-synaptic inhibitory effects?

A

M2/M4 mAChRs inhibit pre-synaptic Ca2+ channels and activate post-synaptic K+ channels

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17
Q

M2/M4 mAChR blocker

A

Atropine

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18
Q

What are the effects of atropine? (2)

A
  1. M2/M4 blocking

2. Enhanced ACh secretion in cerebral cortex

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19
Q

Why does atropine result in increased ACh secretion?

A
  1. Attenuated M2/M4 mAChRs
  2. Loss of active G_O complex
  3. Loss of pre-synaptic Ca_v2 channel inhibition
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20
Q

What do cholinergic pathways in the brain modulate?

A

Neural circuits involved in attention and memory formation

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21
Q

Degeneration of what neurons are associated with Alzheimer’s disease?

A

Cholinergic neurons

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22
Q

List 3 iGluRs

A
  1. NMDA receptors
  2. AMPA receptors
  3. Kainate receptors
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23
Q

What is NMDA selective for, and what process are they involved with?

A

Ca2+ selective, Mg2+ block

Involved with synaptic plasticity

24
Q

What is AMPA selective for, and what process are they involved with?

A

Non-selective

Predominant drivers of EPSP

25
Q

Gene marker for glutamatergic neurons

A

Vesicular glutamate transporter (VGLUT) aka solute carrier family 17

26
Q

What are pyramidal neurons? (3)

A
  1. Pyramidally shaped soma
  2. Complex dendritic structure (numerous excitatory/inibitory imputs)
  3. Single axon that fires as consequence of synaptic integration
27
Q

What two brain areas have been focused in research on plasticity relating to learning and memory?

A

Hippocampus

Dentate gyrus

28
Q

Post-synaptic potentiation at glutamatergic synapses involves:

A

Voltage dependent removal of NMDA receptor Mg2+ block

29
Q

How is the NMDA receptor Mg2+ block removed?

A

Ca2+-dependent activation of calmodulin kinase II (CaMKII)

30
Q

Sustained long-term changes in synaptic strength involves:

A

Nuclear signalling by Ca_V1 (L-type) voltage-gated calcium channels

31
Q

What does glutamate activate in the CNS?

A

Slow metabotropic GPCRs (G_q, G_i/G_o)

32
Q

How does glutamate activate G_q?

A

mGluRs 1 and 5

33
Q

How does glutamate activate G_i/G_o?

A

mGluRs 2, 3, 4, 6, 7, and 8

34
Q

mGluRs 1 and 5 increase post-synaptic excitability by: (2)

A
  1. Reducing M-type K+ channel activity

2. Reducing Ca2+ sensitivity for SK channels

35
Q

What is a role of excitatory glutamatergic circuitry?

A

Carrying of sensory information

36
Q

Convulsions/seizures and cell death following stroke are caused by

A

Excessive glutamatergic excitation

37
Q

Cys-loop ligand-gated chloride channels are activated by

A

GABA and glycine

38
Q

In the cortex and midbrain, what is the pridominant inhibitory transmitter?

A

GABA

39
Q

In the brainstem and spinal cord, what is the predominant inhibitory transmitter?

A

Glycine

40
Q

What is the function of GABA_A receptors?

A

Mediate fast synaptic IPSPs

41
Q

Gene markers for GABAergic neurons (2)

A
  1. Glutamate decarboxylase (GAD)

2. Membrane GABA transporter

42
Q

GABA_A receptor agonists are:

A

Sedatives/anticonvulsants

43
Q

Disruption of GABA_A receptors causes:

A

Excessive activity in excitatory neural circuits (convulsions, seizures)

44
Q

Through what receptor does GABA activate G_i/G_o pathways?

A

GABA-B

45
Q

What two types GABA_B form the functional heterodimer? What are their functions?

A

GABA_B1: detects GABA ligand
GABA_B2: activation of G proteins

46
Q

What is the function of GABA activated GIRK channels?

A

Suppression of post-synaptic excitation (slow inhibition)

47
Q

What are bigenic amines?

A

Small carbon-based molecules with 1+ anime groups (derived from amino acids)

48
Q

Where are the cell bodies for aminergic neurons located (except histamine)?

A

Brain stem ‘nuclei’ (locus coeruleus)

49
Q

What G protein pathways can norepinephrine activate?

A

All of them (G_s, G_q, G_i/G_o)

50
Q

Marker for norephinephrine receptors

A

Dopamine-beta-hydroxylase

51
Q

Which biogenic amine activates ionotropic receptors?

A

Serotonin

52
Q

Marker for serotonin receptors

A

Typtophan hydroxylase 2

53
Q

What G protein pathways can dopamine activate?

A

G_S, G_i/G_o

54
Q

Markers for dopamine (2)receptors

A

Tyrosine hydroxylase

PM dopamine transporter

55
Q

What G protein pathways can histamine activate?

A

All of them

56
Q

Marker for histamine receptors

A

Histidine decarboxylase