Lecture 16 Flashcards Preview

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Flashcards in Lecture 16 Deck (23):
1

Is there a genetic component to schizophrenia?

YES - strong

2

What is the dopamine hypothesis?

Anti-psychotics work as dopamine antagonists
Block dopamine binding at D2 receptor
- Amount of D2 receptor changes how well these drugs work
Means pituitary won't seen any dopamine - ↑prolactin

3

When you're on anti-psychotics, is your HVA ↑↓?

↑dopamine circulating because receptors being blocked by antagonists
↑HVA

4

How does dopamine signaling change in schizophrenia?

MORE dopamine singaling
This is why D2 blockers work - decrease the number of signals getting through - normalize levels

5

How does the brain respond to antipsychotics given for schizophrenia?

↑ # dopamine receptors
Body's natural response to these drugs is to upregulate the receptor

6

What are the major dopamine pathways in the brain? Where does it start/end?

Meso-limbic pathway
Substantia nigra --> forebrain/limbic regions
Nigro-striatal
Substantia nigra --> striatum, connects basal ganglia

7

Are GABA and glycine excitatory or inhibitory NTs?

INHIBITORY

8

Are glutamic and aspartic acid excitatory or inhibitory NTs?

EXCITATORY

9

Describe the GABA/glycine receptor.

Same as ACh - 4 transmem domains, assembles as pentamer
Receptor = channel
BUT is lined with positive charges for ANION selectivity

10

Describe the response when GABA/glycine binds the receptor.

Move Cl- through the receptor pore
Inhibitory response because makes the membrane more negative - harder to reach threshold

11

Where do you find GABA: brain vs spinal cord? Glycine: brain vs spinal cord?

GABA - brain, especially substantia nigra and striatum
Glycine - spinal cord

12

Describe the GABA neuronal pathway. What disease is this pathway linked to?

Cell bodies @ striatum
To substantia nigra
Links basal ganglia (coordination of motor movements)
Degenerates in Huntington's

13

Describe the glycine neuronal pathway. What disease is this pathway linked to?

Act as spinal cord interneurons between motor neurons (think biceps activated while inactivating triceps)
Knocked out by tetanus - spasm result

14

What drug increases the action of GABA?

Benzodiazepine
- Allosteric binding site @ GABA receptor
Prolongs GABA response because ↑s receptor's affinity

15

Describe the 2 main glutamate receptors. What is their major role as excitatory NT receptors in the brain and spinal cord?

GluRs
- Activated by AMPA
- Permeable to Na or Ca
NMDA
- Activated by NMDA
- Permeable to Ca
Role: memory & learning
*Ca and Na are positive so push membrane towards threshold --> depolarization (excitatory role)*

16

What is NMDA?

Agonist of glutamic and asparatic acid

17

Describe the general structure of the glutamate receptors.

TETRAMER assembly (not like ACh)
Clam site = site of conformational change when bind
- Part of LARGE extracell domain

18

Why are glutamate and aspartate potentially neurotoxic? What drug can you use to counter this?

Constant depolarization
Swelling and neuronal death
USE: NMDA antagonists

19

Where in the brain do you find NMDA receptors?

Hippocampus
Outer cortex

20

Describe Huntington's pathology.

Unknown degeneration of GABA neurons --> leads to excess of excitatory NT release --> excessive activation of NMDA pathways

21

What might the NMDA receptor use as a second messenger? Describe its synthesis.

NO
- arginine + NO synthase = NO
Activates guanylyl cylase in neighboring cells to ↑cGMP

22

Where is NO found in the brain?

Cerebellum - granule & basket cells
NOT purkinje

23

How can excess NO cause disease related issues?

NO = free radial
Can nitrosylate proteins with SH groups --> neuropathology