2- antipsychosis Flashcards
(76 cards)
what is psychosis
mental disorders in which there is a loss of contact with reality, affecting abilities to think feel and act
what are the main clusters of symptoms in schizophrenia
+, -, mood, and disorganized symptoms
memory deficits
what are the 3 biochemical theories of schizophrenia
excess dopamine
reduced serotonin
reduced glutamate or GABA
what is the dopamine hypothesis
that psychotic symptoms are caused by an excess of dopamine
how did they come up with the dopamine hypothesis
drugs that stimulate DA can cause psychotic symptoms
how do first gen antipsychotics FGAs work
they block DA receptors as their main target
how do second gen antipsuchotics work
they blcok serotonin receptors
how did they come up with the reduced serotonin theory
LSD are serotonin agonists
how did they come up with the reduced glutamate or GABA hypothesis
PCP, glu receptor inhibitor, induced +and- symptoms of schizo
what is the mesolimbic/mesocortical system
structures that mediate memory, learning, affect and thought organization
what happens when the mesolimbic/mesocortical system is disturbed
psychotic Symptoms
what does DA do in the tuberoinfuncibular system
effects secretion of some pituitary hormones, like prolactive and growth hormones
what is the nigrostriatal system
pathway thought to be involved in parkinson’s life symptoms after using t neuroleptic drugs, like tardive dyskinesias
what do D1 dopamine receptors do
stimulate Gs pathway
target for antipsychotics, but it may not be clinically relevant
what do D2 dopamine receptors do
Gi pathway (inhibit AC) and couple with other effector systems
what happens when you block the D2 receptor
clinical antipsychotic potency
reduce positive symptoms
what happens with 5-HT2A antagonist
improves + and - symptoms
how does 5-HT2A reduce positive symptoms
positive symptoms by reducing excitation of glutamate neurons in the prefrontal cortex
how does 5-HT2A reduce - symptoms
5-HT2A antagonism releases DA in the prefrontal cortex
what happens when there is an increase in DA in the prefrontal cortex (antagonize 5-HT2A)
may improve negative, cognitive and affective symptoms of schizophrenia
what do 5-HT1A receptors act as for DA release
accelerators
what do 5-HT2A receptors act as for DA release
brakes
what does 5-HT1A agonism do
increases DA release and decreases glutamate release in prefrontal cortex
what does 5-HT2A antagonism stimulate
DA release in nigrostriatal pathway, the increase DA competes with drug at D2 and less receptors binding to drug
