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Updated: Aug 14, 2026

Generation and On-Demand Initiation of Acute Ictal Activity in Rodent and Human Tissue
Published on: January 19, 2019
Brain thyrotropin-releasing hormone content varies through amygdaloid kindling development according to
P de Gortari1, P Joseph-Bravo, J Monroy-Ruiz
1Instituto de Biotecnología of Universidad Nacional Autónoma de México, Mexico.
Purpose:
Thyrotropin-releasing hormone (TRH), present in extra hypothalamic brain areas, has been proposed to have neuromodulatory functions and to be susceptible to change by electrical stimulation paradigms. We measured TRH concentrations of several brain areas during kindling development before its establishment and determined whether the changes detected in TRH levels were related to the behavioral stages of kindling, the number of stimulations required to reach these stages and, with the electrophysiological parameters characteristic of this paradigm (amygdaloid afterdischarge (AD) frequency, duration, and propagation).
Methods:
Male Wistar rats were implanted stereotaxically with indwelling bipolar electrodes in the basolateral nucleus of the amygdala and with two stainless-steel electrodes epidurally in frontal cortex. Amygdaloid kindling was induced by daily electrical stimulation; AD frequency and duration were recorded and analyzed throughout the development of kindling. TRH was extracted from several regions and quantified by radioimmunoassay (RIA).
Results:
Modifications in TRH concentrations were detected, depending on the region assayed, from stage II of kindling. A positive correlation was noted between the levels of TRH and the frequency and propagation of AD, but not with the number of stimulations. The rate of change in TRH concentration in relation to AD frequency or duration was highest in frontal cortex followed by hippocampus and amygdala.
Conclusions:
A graded response was noted in the increase in TRH concentration dependent on the increase of AD frequency and propagation. The rate of response correlated with the region's epileptogenic susceptibility.
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