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Alterations in TRH receptors in temporal lobe of schizophrenics: A quantitative autoradiographic study
Author(s) -
Lexow Nedra,
Joyce Jeffery N.,
Kim Soo Jin,
Phillips Jennifer,
Casanova Manuel F.,
Bird Edward D.,
Kleinman Joel E.,
Winokur Andrew
Publication year - 1994
Publication title -
synapse
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.809
H-Index - 106
eISSN - 1098-2396
pISSN - 0887-4476
DOI - 10.1002/syn.890180407
Subject(s) - amygdala , temporal lobe , schizophrenia (object oriented programming) , hippocampus , supramarginal gyrus , neuroscience , receptor , medicine , human brain , psychology , endocrinology , epilepsy , psychiatry , functional magnetic resonance imaging
We utilized quantitative autoradiography to determine the distribution of receptors for thyrotropin‐releasing hormone (TRH) throughout the human temporal lobe and to examine the distribution of these receptors in discrete subregions of the temporal lobe from patients diagnosed premortem with schizophrenia. When compared to non‐neurologic controls, schizophrenic patients demonstrated an increase of 51% in the concentration of TRH receptors in the molecular layer of the dentate gyrus. Within nuclei of the schizophrenic amygdala, marked decreases were found in the central (44%), medial (38%), cortical (36%), accessory cortical (52%), lateral (54%), and medial basal (22%) nuclei. We also examined postmortem brain samples from patients with Huntington's disease, amyotrophic lateral sclerosis, and Alzheimer's disease for alterations in the distribution of TRH receptors. No significant differences from non‐neuropsychiatric controls were noted within the hippocampus in any of these disease states; however, slight alterations were noted in the central and medial basal amygdala in Huntington's disease and in the cortical amygdala in Alzheimer's disease. These disease‐specific findings suggest that TRH may play a role in the neurochemical dysfunction of schizophrenia. © 1994 Wiley‐Liss, Inc.