Alterations in TRH receptors in temporal lobe of schizophrenics: A quantitative autoradiographic study

Abstract

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.

Amygdalar activation alters the hippocampal GABA system: ?Partial? modelling for postmortem changes in schizophrenia

“…Moreover, physiological neuronal population events, as well as abnormal neuronal activity during temporal lobe seizures recorded in the amygdala have been found to precede corresponding events in the hippocampus (Paré et al, 1995;Gotman and Levtova, 1996). Clinically, both imaging (Shenton et al, 1992;Bogerts et al, 1993;Marsh et al, 1994;Lawrie and Abukmeil, 1998) and postmortem (Bogerts et al, 1985;Reynolds et al, 1990;Okada et al, 1991;Lexow et al, 1994) studies have consistently demonstrated concordant changes in both the amygdala and the hippocampus in SZ. Taken together, these observations support the hypothesis that the amygdala could be involved in the induction of hippocampal abnormalities found in SZ brain.…”

Modulation of Signal Transduction Pathways in Senescence-Accelerated Mice P8 Strain: A Useful Tool for Alzheimer’s Disease Research

“…TRH concentration was decreased in the AD hippocampus compared to normal elderly controls (Luo et al, 2002). However, no significant differences from non-neuropsychiatric controls were noted on TRH receptor levels within the hippocampus in AD; just a slight alteration was noted in the cortical amygdala in AD (Lexow et al, 1994).…”