Abstract
The synthetic steroid amidine 3-α-hydroxy-16-imino-5-β-17aza androstan-11-one (R 5135) is known to elicit long-lasting spiking in the cortex in the presence of neocortical damage. R 5135 administered to amygdaloid-kindled and naive rats resulted in regular, high-amplitude spiking in the cortex but only occasionally elicited small-amplitude spikes in the amygdala (AMY) and hippocampus (HPC). Interictal spikes from the AMY of kindled rats were not synchronized with cortical spikes induced by the steroid. Given that R 5135 is known to be a GABA A receptor antagonist, these findings suggest that GABA A receptors in AMY and HPC may have lower affinity for 3α-hydroxysteroids.
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