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.
|Number of pages||4|
|Journal||Journal of Neurochemistry|
|Publication status||Published - 1986|
ASJC Scopus subject areas
- Cellular and Molecular Neuroscience