Pharmacology of CNS NTs Flashcards
Ionotropic NTs
Fast LGICs that go point to point and can be modified by local circuit presynaptic reg
Metabotropic NTs
Slow, GPCR coupled that are diffuse so go to multiple Rs for global effects
Off-Target Effects of NTs
CNS transmitters/Rs are also present in periphery
3 Glutamate Drugs (and major point)
No drugs to increase its signaling
Felbamate blocks NMDA Rs as an anti-convulsant
Phenylcyclindine (PCP) and ketamine occlude NMDA channel, can be hallucinogenic
NMDA R (4)
Implicated in learning/LPP
Increases Ca influx as well as Na
Requires Gly or Ser as coagonist
Ligand and voltage gated
4 GABA Drugs
Valproate - increase levels of GABA: anti-convulsant
Benzodiazepines/barbituates: enhance GABAa function: anti-seizure
Baclofen: GABAb agonist: reduce spasticity
Glycine (3)
Inhibitory, especially at SC
No useful drugs
AD Treatment
AChE Inhibitors
SN and VTA
DA neurons that project to striatum or n. accumbens (reward), respectively
2 NE Anti-Depressants
Desipramine - selective NE uptake inhibitor
Phenelzine - MAO inhibitor
3 Clinical Conditions Relating to 5-HT
Migraines
Too much: anxiety
Too little: depression
4 5-HT Drugs
Fluoxetine: selective 5-HT uptake inhibitor (anti-depression)
Buspirone: partial agonist, anxiolytic
Sumatriptan: agonist, anti-migraine
LSD - 5-HT2a agonist, psychadelic
ATP
Stored in small synaptic vesicles and coreleased w/ NT. Can either activate P2 Rs or be hydrolyzed to adenosine
Adenosine
Released from non-vesicular cytoplasmic stores or formed by ATP, activate P1 Rs
P1 R
Involved in sedative properties (& other shit) of adenosine. Caffeine blocks
