d-Sulpiride inhibits oral behaviour elicited from the nucleus accumbens of freely moving rats

Prinssen, Eric; Heeren, D. J.; Cools, Alexander R.

doi:10.1016/0361-9230(95)02056-x

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Dysfunction Of the Frontal Corticostriatal Circuits1

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2006

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“…The present results are consistent with findings that MAM-E15 exposed offspring show higher susceptibility for chronic haloperidol-induced orofacial dyskinesias (Johansson 1990). Given that the striatal retogions innervated by the frontal cortex (i.e., medial and ventral striatum) mediate oral dyskinesias (Cools et al 1995;Hamid et al 1998;Prinssen et al 1996), the more potent effect of PCP on oral movements in the MAM-E17 animals is consistent with a hypo-function of the glutamatergic frontal corticostriatal pathway (Tamminga 1998). …”

Section: Dysfunction Of the Frontal Corticostriatal Circuitssupporting

confidence: 91%

A Neurobehavioral Systems Analysis of Adult Rats Exposed to Methylazoxymethanol Acetate on E17: Implications for the Neuropathology of Schizophrenia

Moore

Jentsch

Ghajarnia

et al. 2006

Biological Psychiatry

324

405

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Background-As a test of plausibility for the hypothesis that schizophrenia can result from abnormal brain, especially cerebral cortical, development, these studies examined whether, in the rat, disruption of brain development initiated on embryonic day (E) 17, using the methylating agent methylazoxymethanol acetate (MAM), leads to a schizophrenia-relevant pattern of neural and behavioral pathology. Specifically, we tested whether this manipulation leads to disruptions of frontal and limbic corticostriatal circuit function, while producing schizophrenia-like, regiondependent reductions in gray matter in cortex and thalamus.

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