{'fraction_non_alphanumeric': 0.030570652173913044, 'fraction_numerical': 0.01358695652173913, 'mean_word_length': 5.635135135135135, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Biochemical and radiohistochemical analyses of alpha-2 adrenergic receptors in the kindling model of epilepsy.

Biochemical and radiohistochemical methods were used to study alterations in alpha-2 adrenergic receptors in the kindling model of epilepsy. The radioligands used for antagonist and agonist binding were [3H]idazoxan and [3H]p-aminoclonidine, respectively. Radioligand binding to membranes isolated from eight brain regions disclosed a small (14%) but statistically significant reduction in [3H]idazoxan binding in a single area, amygdala-pyriform-entorhinal cortex. This was confirmed by a larger (25%) reduction (P less than .02) in agonist binding in the same region. These reductions were present in animals sacrificed 1 day, but not 2 weeks, after the last kindled seizure. Quantitative radiohistochemical studies identified a bilaterally symmetric reduction of approximately 20% of [3H]p-aminoclonidine binding in the pyriform cortex and the central, medial and lateral amygdaloid nuclei. No significant differences were detected in nine other structures. We propose that the reduction in alpha-2 receptor binding contributes in part to the reduced sensitivity of pyriform cortex neurons of kindled animals to the inhibitory effects of alpha 2 agonists. The reduced alpha-2-receptor binding may also underlie a transient attenuation of alpha-2 receptor-mediated neuro-transmission and thereby constitute one mechanism contributing to kindling development.