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NE2 > Chemical Messengers > Flashcards

Chemical Messengers Flashcards

1
Q

Location and fx of ACh

A

Pons/Midbrain. Wakefulness/Motor control

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2
Q

Location and fx of GABA

A

Higher CNS. Motor inhibitory, motor constrol, consciousness.

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3
Q

Location and fx of Glycine

A

Spinal cord & lower CNS. General inhibition.

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4
Q

Location and fx of Purines

A

Wide-spread. Adenosine=sleep. ATP=multiple.

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5
Q

Location and fx of Opiods

A

Basal ganglia, hypothalamus, pons/medulla. Analgesia/mood/affect.

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6
Q

Location and fx of endocannabinoids

A

Basal ganglia, cortex, spinal cord. Neuroprotection/mood/nociception

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7
Q

Location and fx of EAA

A

WIdespread. Major excitatory NT.

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8
Q

ACh receptors

A

Ionotropic: Nicotinic
Metabotropic: muscarinic

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9
Q

GABA receptors

A

Ionotropic: GABAa
Metabotropic: GABAb

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10
Q

Glycine receptors

A

Ionotropic: GlyR
Metabotropic: None

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11
Q

Purine receptors

A

Ionotropic: P2X
Metabotropic: P1 (A); P2Y

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12
Q

Opioid receptors

A

Ionotropic: none
Metabotropic: Mu, Delta, Kappa

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13
Q

Endocannabinoid receptors

A

Ionotropic: None
Metabotropic: CB-1

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14
Q

EAA receptors

A

Ionotropic: AMPA, Kainate, NMDA
Metabotropic: 3 groups of metabotropic. One is Gq, other 2 are Gi.

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15
Q

ACh synthesis

A

Chocoline+Acetate -> ACh -> into a vesicle via vesicular ACh transporter protein (VAchT)

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16
Q

ACh ionotropic receptors fx

A

Nicotinic
Located at NMJ, central synapses
A subunit change can create a channel that lers more Ca2+ in.

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17
Q

ACH metabotropic receptors (3 subtypes) fx

A

M1: increase IP3/DAG. Increase Ca2+ w/ Gq

M4: presynaptic autoreceptor; striatum of basal ganglia; Decrease cAMP w/ Gi

M5: increase IP3/DAG; cerebrovasculature; striatum basal ganglia

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18
Q

GABA synthesis

A

Glutamate -> glutamate decarboxylase (GAD) -> GABA -> vesicular GABA trasporter protein (VGAT) -> GABA inside a vesicle

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19
Q

Removal of GAT at the pre synaptic terminal

A

Uses GAT-1. GABA is directly repackaged into a vesicle as is.

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20
Q

Removal of GAT on glial cells

A

Uses GAT 2. GABA is converted into glutamine then sent back into the presynaptic terminal as glutamine.

21
Q

Ionotropic receptors of GABA fx. What enters?

A

GABAa

GABA binds to a receptor and induces a conformational change, allowing Cl- to enter causing an IPSP.

22
Q

What modulates GABAa?

A

Benzos
EtOH
Steroids
All potentiate Cl- influx, leading to hyperpolarization. Harder to get a response.

23
Q

Glycine synthesis

A

NONE. As is.

24
Q

Removal of glycine

A

Utilizes GAT proteins. Same as GABA.

25
Q

Glycine receptors fx. Modulators of this?

A

Only ionotropic, GlyR. Gly binds to receptor and Cl- enters to cause IPSP. ETOH and anesthetics are potentiators of this. Strychnine blocks it and leads to an INHIBITION of motor control.

26
Q

Metabotropic receptors of GABA location & fx

A

Located pre and postsynaptically. At PRE, gives rise to NT. At POST, gives rise to inhibition.

The Gi/Go protein-coupled activates a K+ channel and inhibits Ca2+ channel.

27
Q

Ionotropic Purine receptors location and fx

A

P1 (aka A receptors)
ligand=adenosine
Pre-synaptically: inhibition NT release
Post-synaptically: sleep induction, general inhibition of neural fx

P2X
ligand=ATP

28
Q

Metabotropic Purine receptors fx

A

P2Y
Ligand=ATP, UDP, UTP, UDP
Gi/Gq coupled

Learning and memory; co-release w/ EAA; locomotor modifcation

29
Q

Opioid synthesis. There are 4.

A

ENdorphins (proopiomelanocortinin)

ENkephalins (Proenkaphalin; Tyr-gly-gly-phe-X; X=Met or Leu)

Dynophorins (prodynorphin; 3 molecules of Leu-enkephalin)

Nociceptin (orphanin FQ)

30
Q

Removal of opioids

A

Enzyme destruction with enkephalinase. More general destruction with aminopeptidase.

31
Q

Mu Receptors for Opioids

A

Metabotropic.
Increase K+ efflux, leads to hyperpolarization.
Analgesia, resp. depression, euphoria, constipation, sedation.

32
Q

Kappa and Delta receptors for opioids fx

A

Metabotropic
Decrease Ca2+ influx and reduce depol, keeping further from threshold.

Kappa= analgesia, dysphoria, diuresis, miosis
Delta= analgesia
33
Q

Endocannabinoids have 5 distributions with different functions. What are they?

A 
Basal ganglia: mood, motor performance
Spinal cord: nociception modulation
Cortex: neuroprotection
Hippocampus: Memory formation
Hypothalamus: hunger
34
Q

Synthesis of endocannabinoids. Multiple processes.

A

Made in the presynaptic terminal. Comes from arachidonic acid. Anandamide and 2-AG are synthesized in different pathways.

35
Q

Anandamide pathway vs 2-AG pathway

A

Anandamide: Derived from NAPE
2-AG: Derived from PIP2. Note: 2-AG is major source for arachidonic acid in the brain. The pharmacologic mutation of 2-AG has wide-reaching fx.

36
Q

Cannabinoid receptors CB-1

A

Found on presynaptic terminals. Reduces EAA and GABA release via a Gi-coupled protein. Binds anandamide and 2-AG with equal affinity. Seizures are related to decreased GABA.

37
Q

Cannabinoid receptors CB-2

A

found on microglia, are anti-inflammatory, and appear in response to injury. Binds 2-AG better than anandamide.

38
Q

Uniform vs nonuniform distribution of CB-1

A

Nonuniform is associated w/ specific neuronal types.

Uniform: striatum, thalamus, hypothalamus, cerebellum, lower brain stem

Uniform: Cortex, amygdala, hippocampus

39
Q

Degradation of AEA, 2-AG, and both

A

AEA w/ fatty acid amide hydrolase (FAAH): Mutations here related to increased pain resistance.

2-AG w/ monoacylglycerol lipase (MAGL)

Both via cyclooxygenase and lipoxygenase

40
Q

How do we synthesize glutamate? where is aspartate used?

A

alpha-ketoglutarate.

Asp is the NT in the visual cortex and pyramidal cells.

41
Q

Hallmarks of NMDA receptor

A

Ionotropic EAA.
Channel is blocked by Mg2+
Glycine is needed
When EAA binds, must move Mg2+ out of the way, then Ca2+ enters and produces a long latency EPSP. PCP blocks this channel even when it’s open.

42
Q

Hallmarks of non-NMDA receptor

A

Ionotropic EAA.
2 types: AMPA and Kainate
Both lead to Na+ influx. Kainate also has Ca2+ influx.

43
Q

AMPA vs. Kainate receptors

A

Ionotropic EAA.
AMPA: Na+ influx. Benzos prevent this excitatory response.
Kainate: Na+ and Ca2+ influx

44
Q

Fx of NMDA vs. non-NMDA EAA receptors

A

NMDA: short & long term memory, synaptic plasticity

non-NMDA: sensory afferent, upper motor neurons

45
Q

Group 1 Metabotropic EAA receptors

A

mGlu1
mGlu5
Gq
Increase Ip3/DAG and increase Ca2+

46
Q

Group 2 Metabotropic EAA receptors

A

mGlu2
mGlu3
Gi
Decrease cAMP

47
Q

Group 3 Metabotropic EAA receptors

A

mGlu4,6,7,8
Gi
Decrease CAMP

48
Q

Fx of Nitric Oxide (NO)

A

Memory
Vasodilation
Macrophages make NO

Toxic to neurons in high concentration. 1/2 life of 5 seconds lends itself to instability.

49
Q

How could too much EAA be bad?

A

Related to NO!

EAA binds to postsynaptic terminal and Ca2+ comes in. Ca2+ binds with calcineurin, activating NOS. NOS converts arginine to NO. NO leaves the cell and travels back to presynaptic terminal b/c it is very lipid-soluble.

NE2 (12 decks)

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