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58432
Treaments
Description
Biological (Depression & Schizophrenia) Mind Map on Treaments, created by n.c.wetmore on 26/04/2013.
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biological
depression & schizophrenia
biological
depression & schizophrenia
Mind Map by
n.c.wetmore
, updated more than 1 year ago
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n.c.wetmore
over 11 years ago
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Resource summary
Treaments
Antipsychotic Drugs and Dopamine
Chlorpromazine relieves positive symptoms of schizo for most patients
antipsychotic/neuroleptic drugs in 2 chemical families
phenothiazines including chlorpromazine
butyrophenones include haloperiodol
behavioural benefits of these drugs develop gradually over month+
symptoms generally return after cessation of treatment
block dopamine synapses
inspired dopamine hypothesis of schizophrenia
holds schizo results from excess activity at dopamine synapses in certain brain areas
concentration of dopamine in brain no higher than normal, turnover is elevated especially in basal ganglia
KUMAKURA ET AL 2007
neurons release dopamine at faster than average rate and synthesise more to replace molecules that they do not reabsorb
elevated dopamine release also occurs in people showing first symptoms of schizo
HOWS ET AL 2009
support for dopamine hypothesis comes from fact late, repeated use of amphetamine, methamphetamine
or cocaine induces substance induced psychotic disorder
characterised by hallucinations and delusions (positive symptoms)
each drug increases prolongs activity at dopamine synapses
LSD produced psychotic symptoms best known for effects on serotonin synapses but also stimulates dopamine synapses
researchers set out to measure number of dopamine receptors occupies given moment
used radioactively labeled drug, IBZM that binds to dopamine type D2 receptors
because IBZM binds only to receptors that dopamine didn't already bind, measuring radioactivity counts number of vacant dop receptors
used second drug AMPT to block all synthesis of dopamine and again used IBZM to count number of vacant D2 receptors
because AMPT had revenged production of dopamine, all D2 receptors should be vacant so researchers got a count of the total
they subtracted first count of second count, yielding number of D2 receptors occupied by dopamine at first count
first: IBZM binds to D3 receptors not already attached to dopamine
second: IBZM binds to all D2 receptors because AMPT eliminated production of dopamine
second count minus first equals number of D2 receptors bound to dopamine at first count
researchers found people with schizo had twice as many D2 receptors occupied as normal
Role of Glutamate
glutamate hypothesis of schizo
problem relates in part to deficient activity at glutamate synapses, especially in prefrontal cortex
many brain areas dopamine inhibits glutamate release or glutamate stimulates neurons that inhibit dopamine release
increased dopamine would produce same effects as decreased glutamate
antipsychotic effects of drugs block dopamine compatible with either excess dopamine hypothesis or deficient glutamate hypothesis
schizo assoc with lower than normal release of glutamate and fewer than normal receptors in prefrontal cortex and hippo
similar in those high at risk for developing schizo due to family background
support for glutamate hyp of schizoi from effects of phencyclidine (PCP)
inhibits NMDA glutamate receptors
low doses produces intoxication and slurred speech
high doses produces both negative and positive symptoms of schizo including hallucination though disorder, loss of emotions and memory loss
PCP and ketamine produce little if any psychotic response in preadolescents
just as symptoms of schizo usually begin emerge well after puberty, so do psychotic effects of PCP and ket
LSD, coke and amphetamine produce temp schizo symptoms in anyone and effects aren't much worse with this with history of schizo
PCP produces severe effects for someone recoveringg form schizo
administer glutamate itself?
strokes kill neurones by overstimulating glutamate synapses
too risky
drugs stimulating particular kinds of metabotropic glutamate receptors have shown promise in treating schizo
PATIL ET AL 2007
New Drugs
brian had several dopamine pathways with diff functions
drugs that block dopamine synapses produce benefits by acting on neurones in mesolimbocortical system
set of neurons that project from midbrain tegmentum to the limbic system
drug also blocks dopamine neurons in mesostriatal system projects to basal ganglia
effect on basal ganglia produces tardive dyskinesia
characterised by tremors and involuntary movement that develop gradually to varying degrees among different patients
once tardive dyskinesia emerges, can last long after someone quits the drug
KIRIAKAKIS ET AL 1998
second-generation antipsychotics alleviate schizo without producing movement problems
most common is clozapine, risperidone, apripipazole
more effective than older drugs at treating negative symptoms of schizo and now used more widely
other side effects like weight game and impairment of immune system
don't improve quality of life much more than older drugs
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