TY - JOUR
T1 - Alterations in TRH receptors in temporal lobe of schizophrenics
T2 - A quantitative autoradiographic study
AU - Lexow, Nedra
AU - Joyce, Jeffery N.
AU - Kim, Soo Jin
AU - Phillips, Jennifer
AU - Casanova, Manuel F.
AU - Bird, Edward D.
AU - Kleinman, Joel E.
AU - Winokur, Andrew
PY - 1994/12
Y1 - 1994/12
N2 - 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.
AB - 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.
KW - Alzheimer's disease Amyotrophic lateral sclerosis
KW - Amygdala
KW - Hippocampus
KW - Huntington's disease
KW - Thyrotropin‐releasing hormone
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U2 - 10.1002/syn.890180407
DO - 10.1002/syn.890180407
M3 - Article
C2 - 7886624
AN - SCOPUS:0027970634
SN - 0887-4476
VL - 18
SP - 315
EP - 327
JO - Synapse
JF - Synapse
IS - 4
ER -