| ADRENAL STEROID MODULATION OF PLASTICITY IN THE AMYGDALA
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| J.A.Caccavo*; B.S.McEwen; C.Pavlides |
| Neuroendocrinology, The Rockefeller Univ., New York, NY,
USA |
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Previously we reported that both chronic immobilization
as well as chronic unpredictable stress produced an enhancement in
long-term potentiation (LTP) in the cortical input to the dorsolateral
amygdala (dLA), in freely behaving animals. However, activation of
glucorticoid receptors (GR) with an in vivo administration of corticosterone
(40mg/kg) produced a suppression in LTP in both the cortical and thalamic
inputs to the dLA, in anesthetized animals. In the present study we
investigated effects of direct administration of corticosterone on
LTP in the cortical input to the basolateral amygdala (BLA), in vitro.
Rats were adrenalectomized (ADX) at least 5d prior to experiments.
Coronal slices of the amygdala were then prepared and incubated with
1mM corticosterone for 20min. Recordings were performed either immediately
or at least 1h following corticosterone administration. High-frequency
stimulation (HFS) consisted of two trains of 100Hz for 1sec. The results,
thus far, indicate that corticosterone produces a slight suppression
of LTP as measured at 40min following tetanization. These effects
were antagonized by the glucocorticoid antagonist RU-486, which produced
a slight enhancement in LTP.
Support Contributed By: Supported by grants MH58911 and MH41256.
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