Hippocampal
thyrotropin-releasing hormone (TRH) release was examined after
seizures were induced by electroconvulsive shock (ECS). Rat hippocampal slices taken 12, 24, or 48 h after 3 days of alternate-day ECS treatment or
sham-ECS treatment were stimulated with
potassium with or without
calcium in a superfusion system containing in-line
charcoal adsorbent to concentrate TRH. Released TRH and tissue TRH were measured by radioimmunoassay. The TRH content of hippocampal slices was increased fivefold over
sham-ECS levels 12, 24, and 48 h after ECS, but this was not associated with an increase in basal TRH release.
Potassium-stimulated TRH release was significantly elevated over basal release 12, 24, and 48 h after ECS.
Potassium-stimulated
calcium-dependent TRH release increased linearly after ECS, reaching its highest level 48 h after seizure. Thus, although enhanced
calcium-dependent TRH release was associated with elevated tissue levels, this relationship was not proportional in that tissue TRH was elevated to the same extent at all times after ECS, whereas
potassium-evoked
calcium-dependent TRH release increased gradually over time after seizure. These results suggest that postictal elevations in TRH are associated with an enhanced capacity for release that develops as a result of a time-dependent shift of TRH from a storage compartment ot a readily releasable pool. The observed elevation in stimulated TRH release may be relevant to seizure-induced modulation of
TRH receptors in vivo.