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Abnormalities in thalamic neurophysiology in schizophrenia: could psychosis be a result of potassium channel
Zoran Vukadinovic1, Ivana Rosenzweig
1Montefiore Medical Center, Albert Einstein College of Medicine, Department of Psychiatry and Behavioral Sciences, 111 E 210th Street, Bronx, NY 10467, USA. zvukadi@gmail.com
Abstract:
Psychosis in schizophrenia is associated with source-monitoring deficits whereby self-initiated behaviors become attributed to outside sources. One of the proposed functions of the thalamus is to adjust sensory responsiveness in accordance with the behavioral contextual cues. The thalamus is markedly affected in schizophrenia, and thalamic dysfunction may here result in reduced ability to adjust sensory responsiveness to ongoing behavior. One of the ways in which the thalamus accomplishes the adjustment of sensory processing is by a neurophysiological shift to post-inhibitory burst firing mode prior to and during certain exploratory actions. Reduced amount of thalamic burst firing may result from increased neuronal excitability secondary to a reported potassium channel dysfunction in schizophrenia. Pharmacological agents that reduce the excitability of thalamic cells and thereby promote burst firing by and large tend to have antipsychotic effects.
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