-Caveat Lector-

 Brain Research Reviews

Duncan, G.E., Sheitman, B.B., & Lieberman, J.A. (1999). An integrated view
of
pathophysiological models of schizophrenia. Brain Research Reviews, 29(2-3),
250-264.

Pathophysiological processes that underlie the profound neuropsychiatric
disturbances in schizophrenia are poorly understood. However, the clinical
course of the disease, and a number of clinical and basic science
observations,
provide direction for formulating pathophysiological models that could be
empirically tested. For example, repeated psychostimulant administration to
healthy subjects can induce psychotic symptoms, and acute stimulant
challenge
in schizophrenia patients can precipitate psychosis. Also, NMDA antagonists
induce positive, negative, and cognitive schizophrenic-like symptoms in
healthy
volunteers and precipitate thought disorder and delusions in schizophrenia
patients. These human studies provide support for the dopamine and NMDA
receptor hypofunction hypotheses of schizophrenia. Well-documented effects
of
NMDA antagonists on dopamine systems provide a basis to integrate the
dopamine
and NMDA receptor hypofunction hypotheses. Furthermore, it has become
apparent
that prominent actions of antipsychotic drugs, especially those with
'atypical'
properties, involve antagonism of behavioral, electrophysiological and brain
metabolic effects produced by administration of NMDA receptor antagonists. A
confluence of clinical and basic science data suggests that an early
developmental insult, potentially involving reduced NMDA receptor function,
could facilitate sensitization of dopamine systems, leading to the formal
onset
of schizophrenia in late adolescence and early adulthood. Although clearly
speculative, this conceptual model is consistent with existing evidence and
suggests lines of future experimental investigation.



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Dr Cameron would have been interested  however and might have discoverred
this some time ago

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