Review Flashcards
(28 cards)
When GABAa receptors are activated, they are permeable to which ions?
Cl-
What are monoamines and catecholamines?
-monoamines: epinephrine, norepinephrine, dopamine and serotonin
-catecholamines: epinephrine, norepinephrine, and dopamine
Which serotonin receptor is an LGIC/ionotropic?
-5-HT3
MDMA/ecstasy causes the death of which neuron?
-serotonin (5-HT) in the dorsal raphé
What are some Excitatory Amino Acids neurotransmitters?
-aspertate (Asp)
-cysteate
-homocysteate
-glutamate (Glu)
What is GABA synthesized from and by which enzyme?
-GABA is synthesized from Glutamate in a single step by the enzyme GAD
What are the main inhibitory amino acids?
-GABA
-Glycine
Which type/cluster of schizophrenia symptoms is the most resistant to treatment?
-cognitive
Why were the first MAOI antidepressants dangerous?
-because they prevented the metabolism of tyramine which could lead to high blood pressure (stroke and heart attack)
Which memory system does the hormone progesterone bias female rats to use?
-response learning
Which receptor exists as a dimer before it is occupied by a ligand?
-GABAb
Beta-blockers affect which receptor?
-beta receptors (EPI system)
How is Serotonin synthesized?
-serotonin is directly syntehsized from 5-HTP by the enzyme AADC?
Dopamine has the highest affinity for which reuptake transporter?
-NET
What is the phenomenon where if too many EAA’s are released at once, they may over-excite other neurons and kill them?
-excitotoxicity
What are the 2 co-factors required for the tyrosine hydroxylase enzyme to work most efficiently?
-O2
-BH4
In which area of the brain are noradrenergic neurons’ cell bodies located?
-Locus Ceruleus
What is another name for epinephrine when it is a hormone?
-Adrenaline
What is one of the non-stimulant drugs used to treat ADHD?
-Atomoxetine (SNRI)
What is the name of the inactive form of glutamate and where is it stored?
-Glutamine and it is stored in Glial cell
What are all the positive allosteric modulators?
-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
Where do anxiety pills and sleeping pills bind on GABAa? Which is more dangerous with alcohol?
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.
What is the monoamine hypothesis of depression? Whats wrong about it?
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]
Why do we go back on the rollercoaster despite being scared?
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.
