Last Questions Flashcards
What is the effect of second messengers?
Cause a series of chain reaction within the cell, with the goal of doing something, but usually the goal is to make ATP to do something (like a channel)
Give an example of a 2nd messenger and the proteins it activates.
cAMP it’s used anime and protein neurotransmitter, Calmodium: it works with Ca, acts like a second messenger
Which NT’s act through metabotropic R’s?
DA, NE, E, opiates, 5-HT (serotonin)
affine what kind of receptor and how it works
adenosine receptor antagonist, AR turns off transmitter release so caffeine keeps it going, respiratory centers in medulla = faster breathing, broad stimulatory effect (monoamine neurons DA,NE,5-HT)
adderall how it works
a formation of amphetamine, diffuses into synaptic ending or transported with DA
Adderall two classes of effects
Two classes of effects- causes enhanced release of catecholamine transmitters with and without APs
Blocking reuptake of catecholamines and interfering with molecular processes that inactivate the catecholamines = broad stimulatory effect
What is the Ach pathway
basal forebrain, hippocampus, cerebellum
What is the two DA pathways
mesolimbocortical and mesostriatal
what is the mesolimbocortical DA pathway
mesolimbocortical (ventral tegmental area to nucleus accumbens, cortex, hippocampus)
what is the mesostriatal DA pathway
mesostriatal (substantia nigra to striatum)
What are the two NE pathways
Local coerculus to hippocampus, basal ganglia, and cortex
Lateral tegmental area to spinal cord cerebellum
what is the serotonin pathway
raphe nuclei to hippocampus, spinal cord, cerebellum
explain AMPA-R
Most common excitatory receptor, glutamate AMPA-R activation opens Na+/K+ channel, depolarizes and EPSP
cocaine reception
blocks DA transporter and 5-HT reuptake (therefore euphoria), Na+ channel blocker local anesthetic, high doses can cause heart failure because APs in heart are inhibited
Nicotinic Ach-R
lets Na+ flow in, receptor everywhere, depolarizing effect, lasts a long time
GABAa reception
activation opens Cl- channel which can hyperpolarize (IPSP) or buffer at resting potential (inhibition)
NDMA reception
relatively little change in voltage from Ca2+ but Ca2+ then activates kinases which produce a variety of postsynaptic effects from activating additional receptors to sending messages to nucleus
Where are cannabinoid receptors located and what kind are they
Receptors in hippocampus, cerebral cortex
G protein coupled metabotropic receptors (often on GABA axon terminals, thereby modify GABA release)
what do cannabinoid receptors cause
anandamide changes in memory function, reduced sensitivity to pain, pleasurable effects associated with raising DA release in nucleus accumbens
