Abnormality of α1Adrenergic Receptors in the Frontal Cortex of Epileptic Rats

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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 Bmax of [3H]prazosin binding with no change in the apparent KD, 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.

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