schizophrenia neurotransmitter explanation Flashcards
what was the orginal dopamine hypothesis
- increased D2 receptor activity in mesolimbic pathway leads to increased dopamine so positive symptoms
- decreased D1 receptor activity in the mesocortical pathway leads to decrease in dopamine so negative symptoms
how does PCP
blocks the NMDA recptor (glutamate) and effects serotonin
both involved in regulation of dopamine
excess serotonin linked to negative symptoms
what happens in the mesolimbic pathway
glutamate normally acts as a BREAK
in schizophrenic
break doesnt work
gluatmate low
low GABA
high levels of dopamine
+ve symptoms
what happens in the mesocortical pathways
glutamate normally acts as an ACCELERATOR
in schizophrenic
accelerator doeesnt work
low levels of glutamate
low levels of dopamine
-ve symptoms
what are the strengths of the dopamine glutamate hypothesis
+ amphetamines produce excess dopamine causing symptoms of psychosis
+ drugs given to patients work by blocking dopamine receptors
+ sufferers of Parkinsons are given levodopa adding dopamine can experience symptoms of Sz
+ genes likely to increase sensitivity to dopamine for found in schizophrenics
+ those with Sz appear to have differences in their brains, gray matter in front and temporal lobes, changes linked to sensitivity to dopamine
+ glutamate hypothesis expamds on dopamine not replacing it, adds to scientific credibility
what are the weaknesses of the dopamine glutamate hypothesis
- PET scans shoe dopamine blocking drugs were not effectove for 10 years or more, if administered early more than 90% repond, more than just dopamine
- reductionist, stressful life events act as triggers producing excess dopamine
- Carlosson mentioned that undergoing scanning puts on pressure and likely to respond differently, lack validity
- Carlosson highlighted NT pathways and interconnections are complicated and need for continuing research, more needs to be found out about GABA and serotonin
- animal studies lack validity, only a human disorder
