Review

Question 1

When GABAa receptors are activated, they are permeable to which ions?

Answer 1

Cl-

Question 2

What are monoamines and catecholamines?

Answer 2

-monoamines: epinephrine, norepinephrine, dopamine and serotonin
-catecholamines: epinephrine, norepinephrine, and dopamine

Question 3

Which serotonin receptor is an LGIC/ionotropic?

Answer 3

-5-HT3

Question 4

MDMA/ecstasy causes the death of which neuron?

Answer 4

-serotonin (5-HT) in the dorsal raphé

Question 5

What are some Excitatory Amino Acids neurotransmitters?

Answer 5

-aspertate (Asp)
-cysteate
-homocysteate
-glutamate (Glu)

Question 6

What is GABA synthesized from and by which enzyme?

Answer 6

-GABA is synthesized from Glutamate in a single step by the enzyme GAD

Question 7

What are the main inhibitory amino acids?

Answer 7

-GABA
-Glycine

Question 8

Which type/cluster of schizophrenia symptoms is the most resistant to treatment?

Answer 8

-cognitive

Question 9

Why were the first MAOI antidepressants dangerous?

Answer 9

-because they prevented the metabolism of tyramine which could lead to high blood pressure (stroke and heart attack)

Question 10

Which memory system does the hormone progesterone bias female rats to use?

Answer 10

-response learning

Question 11

Which receptor exists as a dimer before it is occupied by a ligand?

Answer 11

-GABAb

Question 12

Beta-blockers affect which receptor?

Answer 12

-beta receptors (EPI system)

Question 13

How is Serotonin synthesized?

Answer 13

-serotonin is directly syntehsized from 5-HTP by the enzyme AADC?

Question 14

Dopamine has the highest affinity for which reuptake transporter?

Answer 14

-NET

Question 15

What is the phenomenon where if too many EAA’s are released at once, they may over-excite other neurons and kill them?

Answer 15

-excitotoxicity

Question 16

What are the 2 co-factors required for the tyrosine hydroxylase enzyme to work most efficiently?

Answer 16

-O2
-BH4

Question 17

In which area of the brain are noradrenergic neurons’ cell bodies located?

Answer 17

-Locus Ceruleus

Question 18

What is another name for epinephrine when it is a hormone?

Answer 18

-Adrenaline

Question 19

What is one of the non-stimulant drugs used to treat ADHD?

Answer 19

-Atomoxetine (SNRI)

Question 20

What is the name of the inactive form of glutamate and where is it stored?

Answer 20

-Glutamine and it is stored in Glial cell

Question 21

What are all the positive allosteric modulators?

Answer 21

-full allosteric modulators (FAM): high potency & efficacy; acts on many GABAa types; most addictive/dangerous (with alcohol [narrow TI]); e.g., Xanax
-selective allosteric modulators (SAM): high potency & efficacy; only binds to selective groups of GABAa; less dangerous with alcohol but still high abuse potential [narrow TI but slightly less]; e.g. Valium
-partial allosteric modulators (PAM): high potency, low efficacy; only act on limited GABAa; less addiction and overdose risk; e.g., Lunesta, Ambien

Question 22

Where do anxiety pills and sleeping pills bind on GABAa? Which is more dangerous with alcohol?

Answer 22

Sleeping pills bind to the barbiturate site, whereas anxiety pills bind to the BDZ site. Both barbiturates and benzodiazepines are very dangerous with alcohol as mixing alcohol with these drugs can lead to overdose and death. But barbiturates are more dangerous when mixed with alcohol because they can open the GABAa by themselves. On the other had, benzodiazepines require GABA to be bound to the active site as well as a benzo being bound to BDZ in order to open the channel.

Question 23

What is the monoamine hypothesis of depression? Whats wrong about it?

Answer 23

Depression is caused due to a deficit of serotonin, norepinephrine, or both in the brain. The evidence supporting this theory is that SSRIs, NSRIs, and SNRIs work in 60-70% of the depressed population. However, these medications take 2-6 weeks after initially taking them for patients to feel better. However, this is only slightly better than placebo with 50-60% effectiveness. Also, ketamine acts directly [within 24h], curing TRD for up to 3-6 months. Suggesting that this theory is wrong. [also the inflammatory hypothesis has a lot of supporting evidence]

Question 24

Why do we go back on the rollercoaster despite being scared?

Answer 24

When we go on a rollercoaster, our brain releases endogenous opioids to reduce the pain signal, but also the endorphins increases DA release in the VTA at the same time, because the VTA has a high rate of Mu receptors (MOR). This is what makes us go back on the rollercoaster despite being scared.

Question 25

What is the neuroinflammatory (cytokine) theory of depression?

Answer 25

-depression is caused by chronic inflammation of the brain [potentially caused by stress or other factors]
-proinflammatory cytokines [released by microglia] are higher in the brain tissue of individuals diagnosed with depression
-stress increases proinflammatory cytokines
-NMDA receptors signal activation of some of these cytokines

Question 26

How are memories made in the brain?

Answer 26

Memory/learning happens in the brain due to long-term potentiation (LTP), and long-term depression (LTD) is the process of unlearning (extinction).
the 5 steps of LTP are:
1. NMDA receptors lose the Mg2+ channel blockers [short-term event behind LTP; during learning]
2. Ca2+ flows into post-synaptic neuron [short-term event behind LTP; during learning]
3. increase in post-synaptic AMPA receptors
4. increase in post-synaptic membrane/synapse
5. increase Glu release

Question 27

How does GHB block memory?

Answer 27

-Glu is released
-there are AMPA and NMDA receptors on the post-synaptic neuron; also GABAb receptors
-GHB binds with high affinity to GABAb receptor –>activating GPCR –> alpha subunit reduces amount of cAMP being produced in neuron –> reduces PKA –> reduces phosphorylation of NMDA receptors [non-functional] [no memories]

Question 28

How does ADHD medication act in the brain?

Answer 28

The nigrostriatal pathway is affected in ADHD. Because the PFC is not fully developed, there is less DA in the PFC [less functional]. Simulants increase DA in PFC, which activates the negative feedback loop and reduces DA in DS (which has too much DA in ADHD individuals). [regulating DA levels]