PS275 Lecture Notes - Temporal Lobe, Chromosome, Basal Ganglia

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1 Feb 2013
Molecular genetics
it does not appear that the genetic predisposition to s is transmitted by a single gene; several multi
or polygenic models remains viable.
Hunt for s related genes has proven more difficult than expected for several reasons including 1)
lack of preciseness in defining the boundaries of the clinical phenotype 2) absence of biological
tests that confirm diagnostic categorization 3) clinical heterogeneity and the complex nature of s
Alternative strategies for s vulnerability gene identification were and are needed. S research turned
to the endophenotypic strategy . endophentoyupes are characteristics that reflect the actions of
genes predisposing an indiv to a disorder even in the absence of a diagnosable pathology.
Imp cuz indiv endophenotypoe are determined by fewer genes than the more complex s
phenotype. Thus the complexity of genetic analyses would be reduced
Possible role of many specific genes: serotonin type 2A receptor (5—HT2a) gene, dopamine DS
receptor gene, and chromosomal region on chromosome 6,8, 13 and 22. also suggested that G
protein signalling 4 a gene localized to chromosome 1q23 plays a role in s susceptibility
Increasing evidence for an overlap in genetic susceptibility including s and bipolar disorder
Evaluation of the genetic data
s is not complete due to genetics
S is defined by beh: it is a phenotype and thus reflects the influence of both genetics and enviro
Genetics predispose ppl to it and ten you need stress to bring it out
Biochemical factors
best researched factors :dopamine
Dopamine activity
excess dopamine leads to s is based on the fact that drugs used to treat s reduce dopamine activity
but produce side effects remsnling the symp of Parkinson’s disease
Parkinson’s is known to be caused in part by low levels of dopamine in a particular nerve tract of
the brain.
As time went on assumption that excess dopamine led to s was not true cuz the major metabolites
of dopamine homovanillic acid (HVA) was not found in greater amounts in patients with s
Research on the antipsychotics mode of action suggest that the dopamine receptors are a more
likely locus of disorder than the level of dopamine itself
excess dopamine receptors may not be responsible for all the symp of s; in fact they appear to be
related to mainly to positive symp
amphetamines worsen positive symp and lessen negative one. Amtipsyhcotics lessen positive
symmp but there effect on negative symp is less clear; some studies show no benefit while others
show a reduction in negative symp
prefrontal cortex is thought to be esp relevant to the negative symp of s the under activity in this
part of the brain may also be the cause of negative symp in s
antipsychotics do not have major effects on the dopamine neurons in the prefrontal cortex they are
ineffective treatments for negative symp
evaluation of the dopamine theory
dopamine theory isn’t complete theory of s
other neurotransmitters
glutamate a transmitter that is widespread in the human brain may also play a role. Low levels of
this have been found in cerebrospinal fluid of ppl with s
street drug PCP can induce psychotics states including both positive and negative sump in normal
ppl. Interferes with one of glutamates receptors
schizophrenia and the brain: structure and function
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