Abnormality of α1Adrenergic Receptors in the Frontal Cortex of Epileptic Rats

Abstract

We found that the binding of [³H]prazosin, a selective ligand for α₁‐adrenergic recognition sites, is significantly lower in the frontal cortex of the genetically epilepsy‐prone rats (GEPRs), as compared with normal Sprague‐Dawley rats. Scatchard analysis reveals a decrease in the B_max of [³H]prazosin binding with no change in the apparent K_D, suggesting that there are fewer α₁‐adrenergic recognition sites in the frontal cortex of the GEPR. This abnormality is associated with a reduced capacity of norepinephrine (NE) to stimulate [³H]inositol monophosphate ([³H]IP₁) formation in frontal cortex slices prelabeled with [³H]inositol. No significant differences in [³H]prazosin binding as well as NE‐stimulated [³H]IP₁ formation have been observed in other brain regions including hippocampus, corpus striatum, and inferior colliculus. These results indicate that a deficit in the α₁‐adrenergic receptor system in the frontal cortex may play a role in the seizure process in the GEPR.