TRANSIENT ELEVATION OF AMYGDALA-ALPHA-2 ADRENERGIC-RECEPTOR BINDING-SITES DURING THE EARLY STAGES OF AMYGDALA KINDLING

Enhanced noradrenergic neurotransmission retards but does not prevent the development of kindling. We previously reported that locus coeruleus (LC) α2 adrenergic receptor binding sites are transiently elevated during the early stages of kindling development. Since the firing activity of LC noradrenergic neurons is partially regulated via an α2 receptorsmediated recurrent inhibition, the transient elevation in LC α2 receptors could decrease LC activity and consequently facilitate the development of kindling. Transient elevation of α2 receptor binding sites during early stages of kindling may also occur on noradrenergic axon terminals projecting to forebrain sites. Using in vitro neurotransmitter autoradiography techniques, we investigated this hypothesis by measuring specific [3H]idazoxan binding in 5 different areas of rat forebrain at 2 different stages of kindling development. After 2 class 1 kindled seizures, specific [3H]idazoxan binding was elevated significantly in the amygdala, but not in other forebrain regions. No differences in specific [3H]idazoxan binding were observed in any of the 5 brain regions in rats kindled to a single class 5 kindled motor seizure. Saturation of binding experiments indicated that the increase in amygdala [3H]idazoxan binding, following 2 class 1 kindled motor seizures, was due to an increase in the total number of α2 receptor binding sites without a change in the affinity of the binding sites for [3H]idazoxan. Thus, the transient increase in α2 receptors that occurs in the LC in the early stages of kindling also occurs in the forebrain region in which the kindled seizure originates. © 1990.