Knight, R. T., Scabini, D. & Woods, D. L. (1989) Prefrontal cortex gating of auditory transmission in humans. Brain Research, 504(2), 338-342.
"inhibitory and excitatory prefrontal control of distributed neural activity in posterior brain regions."
I came to this article to find this... Prefrontal cortex has inhibitory and excitatory control over the posterior brain regions.
I know there is research somewhere else looking directly at the kaput head of psychotics. Unfortunately, my head doesn't allow me to go directly into these research... not until my psychotic model is done and lit review zum ended (Do you understand what it means?) Sign
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"There is extensive literature supporting an abnormality in prefrontal function in schizophrenics. Findings of altered dorsolateral prefrontal function include evidence from both cerebral blood flow (Weinberg, Berman & Zec, 1986; Weinberg, Berman, Suddath & Torrey, 1992) and post-mortem studies (Akbarian et al., 1995, 1996). Thus, schizophrenia may represent a ``non-lesion'' model of prefrontal dysfunction in humans. Schizophrenics are also reported to have a deficit in inhibitory control of auditory processing. Freedman and colleagues developed and ERP auditory gating paradigm to study inhibitory control in schizophrenics. In normals, presentation of a pair of clicks results in a decrease in amplitude of the evoked response to the second stimulus in the pair. This response suppression occurs in a latency range of 30±65 msec and has been referred to as the P50 gating paradigm in the schizophrenia literature. This finding has been disputed by some authors (Kathman & Engel, 1990), but this may be due in part to dierences in recording parameters and state of alertness (Boutros, Zouridakis & Overall, 1991a; Boutros, Overall & Zouridakis, 1991b; Smith, Boutros & Schwarzkopf, 1994; Grith, Hoer, Adler & Zerbe, 1995). Freedman, Adler, Waldo, Pachtman and Franks (1983) reported that the second stimulus in a pair of auditory pulses did not habituate in schizophrenics. This electrophysiological findings supported the longstanding proposal that schizophrenics
fail to properly filter extraneous inputs (McGhie & Chapman, 1961; Venables, 1964).
This auditory gating deficit is reliably seen in a signi®cant percentage of nonpsychotic relatives of schizophrenics and has been proposed to be a neurophysiologicl trait for schizophrenia. Phenotypic segregation of schizophrenics and first order relatives using the auditory gating paradigm has been employed in recent genetic studies. This research has isolated a putative schizophrenia gene localized to a region of chromosome 15q 13±14 which controls alpha 7 nicotinic receptor expression (Freedman et al., 1997). Thus, the neural network controlling the P50 gating deficit is of both theoretical and clinical relevance. We examined auditory gating in patients with dorsolateral prefrontal damage and in age-matched controls (see Fig. 3). An initial study has shown that controls have normal suppression of the second stimulus in an auditory pulse pair. Prefrontal patients showed evidence of an inhibitory failure in the auditory gating paradigm in both ears. As can be seen in Fig. 3, prefrontal patients showed problems with suppression of the second stimulus in both ears with the defect more apparent in the ear contralateral to prefrontal damage
(Knight, Finkbeiner & Lawler, in preparation). This failure to suppress is observed for both an early latency component generated in auditory cortex (P35) and a later component (P50) thought to arise in the thalamus. The data suggests that prefrontal cortex dysfunction may underlie or contribute to the auditory gating deficit in schizophrenics."