. 2010 Dec 3;37(2):306–315. doi: 10.1093/schbul/sbq142

Table 1.

TRN Findings Related to The Neurobiology of Schizophrenia

Type of Study	Species	Main Findings
Genetic	Rodents (mice)	TRN neurons had high expression of a gene associated with schizophrenia, disrupted in schizophrenia, DISC-1, in the developing mouse brain, when the connections within the thalamocortical system take shape⁶³
Pharmacological	Rodents (rats)	PCP impaired rats’ extradimensional attentional shifting, which is known to be defective in schizophrenics, caused a decrease in the expression of Zif-268 and parvalbumin in the infralimbic cortex and the TRN⁵⁴
Pharmacological	Rodents (rats)	PCP administration, which can induce psychosis in healthy humans, resulted in metabolic hypofunction within the prefrontal cortex, the auditory system, and TRN of rats, which was reversed by the coadministration of typical (haloperidol) or atypical (clozapine) antipsychotics with PCP⁵⁸^,⁵⁹
Pharmacological	Rodents (rats)	NMDA antagonists, including PCP, ketamine, and MK801, induced lesions in posterior cingulate and retrosplenial cortices of rats following injections in the anterior thalamus. These lesions were prevented by administering haloperidol and clozapine⁶⁰^–⁶²
Electrophysiological	Rodents (rats)	Auditory gating, which is defective in schizophrenics, was established in TRN neurons with single-cell recordings in anesthetized rats. Amphetamine, a dopamine agonist which can induce psychosis, disrupted the TRN-mediated auditory gating, while haloperidol reversed this deficit²
Electrophysiological	Humans	Two sleep hd-EEG studies reported a marked deficits in sleep spindles, EEG oscillations generated by the TRN, in schizophrenics compared with healthy and psychiatric controls⁷¹^,⁷²

Note: EEG, electroencephalogram; hd-EEG, high-density electroencephalogram; NMDA, N-Methyl-D-aspartic acid; PCP, phencyclidine; TRN, thalamic reticular nucleus.