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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
Glycine receptors fx. Modulators of this?
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
Metabotropic receptors of GABA location & fx
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
Ionotropic Purine receptors location and fx
P1 (aka A receptors) ligand=adenosine Pre-synaptically: inhibition NT release Post-synaptically: sleep induction, general inhibition of neural fx P2X ligand=ATP
28
Metabotropic Purine receptors fx
P2Y Ligand=ATP, UDP, UTP, UDP Gi/Gq coupled Learning and memory; co-release w/ EAA; locomotor modifcation
29
Opioid synthesis. There are 4.
ENdorphins (proopiomelanocortinin) ENkephalins (Proenkaphalin; Tyr-gly-gly-phe-X; X=Met or Leu) Dynophorins (prodynorphin; 3 molecules of Leu-enkephalin) Nociceptin (orphanin FQ)
30
Removal of opioids
Enzyme destruction with enkephalinase. More general destruction with aminopeptidase.
31
Mu Receptors for Opioids
Metabotropic. Increase K+ efflux, leads to hyperpolarization. Analgesia, resp. depression, euphoria, constipation, sedation.
32
Kappa and Delta receptors for opioids fx
Metabotropic Decrease Ca2+ influx and reduce depol, keeping further from threshold. ``` Kappa= analgesia, dysphoria, diuresis, miosis Delta= analgesia ```
33
Endocannabinoids have 5 distributions with different functions. What are they?
``` Basal ganglia: mood, motor performance Spinal cord: nociception modulation Cortex: neuroprotection Hippocampus: Memory formation Hypothalamus: hunger ```
34
Synthesis of endocannabinoids. Multiple processes.
Made in the presynaptic terminal. Comes from arachidonic acid. Anandamide and 2-AG are synthesized in different pathways.
35
Anandamide pathway vs 2-AG pathway
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
Cannabinoid receptors CB-1
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
Cannabinoid receptors CB-2
found on microglia, are anti-inflammatory, and appear in response to injury. Binds 2-AG better than anandamide.
38
Uniform vs nonuniform distribution of CB-1
Nonuniform is associated w/ specific neuronal types. Uniform: striatum, thalamus, hypothalamus, cerebellum, lower brain stem Uniform: Cortex, amygdala, hippocampus
39
Degradation of AEA, 2-AG, and both
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
How do we synthesize glutamate? where is aspartate used?
alpha-ketoglutarate. | Asp is the NT in the visual cortex and pyramidal cells.
41
Hallmarks of NMDA receptor
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
Hallmarks of non-NMDA receptor
Ionotropic EAA. 2 types: AMPA and Kainate Both lead to Na+ influx. Kainate also has Ca2+ influx.
43
AMPA vs. Kainate receptors
Ionotropic EAA. AMPA: Na+ influx. Benzos prevent this excitatory response. Kainate: Na+ and Ca2+ influx
44
Fx of NMDA vs. non-NMDA EAA receptors
NMDA: short & long term memory, synaptic plasticity | non-NMDA: sensory afferent, upper motor neurons
45
Group 1 Metabotropic EAA receptors
mGlu1 mGlu5 Gq Increase Ip3/DAG and increase Ca2+
46
Group 2 Metabotropic EAA receptors
mGlu2 mGlu3 Gi Decrease cAMP
47
Group 3 Metabotropic EAA receptors
mGlu4,6,7,8 Gi Decrease CAMP
48
Fx of Nitric Oxide (NO)
Memory Vasodilation Macrophages make NO Toxic to neurons in high concentration. 1/2 life of 5 seconds lends itself to instability.
49
How could too much EAA be bad?
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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