[3H] Corticosterone binding in rat superior cervical ganglion.

Binding of [3H]corticosterone was examined in the soluble fraction (100,000 g) from superior cervical ganglia dissected from adrenalectomized and perfused rats. A large binding capacity (2100 fmol/mg protein) was found. However, no binding for [3H]-dexamethasone and [3H]triamcinolone was detected. The binding protein present in the ganglion preparation was characterized by DEAE-cellulose and DNA-cellulose chromatography and by isoelectric focusing. The corticosterone binding protein from the ganglia was found to be different from the cytoplasmic glucocorticoid receptor, but similar to plasma transcortin. A large portion (approximately 75%) of the transcortin-like [3H]corticosterone binding protein was located in the interstitial space between the sheath and the ganglionic cells. However, 25% of the binding protein was retained in the desheathed ganglion even after extensive washing with saline. Our findings indicate that cytoplasmic glucocorticoid receptors are not present in the superior cervical ganglion. It is possible that the transcortin-like protein associated with the desheathed ganglion may be intracellular, as other investigators have suggested similar intracellular presence of a transcortin-like protein in the liver, uterus, and pituitary.

Electroencephalographic correlates of audiogenic seizures during ethanol withdrawal in mice.

C57BL/6Bg mice had silver bead electrodes chronically implanted on the surface of the cortex and had their cortical EEG recorded during audiogenic seizures following ethanol withdrawal. For 7 days, the experimental groups were fed a liquid diet containing 6% v/v ethanol ad lib as the only source of food and water. The control group was fed a similar diet containing an isocaloric amount of sucrose. The cortical EEG's of experimental and control groups before, during, and after treatment were virtually identical. Only the experimental group was susceptible to audiogenic seizures. During audiogenic seizures, the cortical EEG showed no sign of spike waves or paroxysmal activity. This is in contrast to picrotoxin convulsions with these same mice as well as to spontaneous convulsions in animals following ethanol withdrawal. Similar EEG observations have been reported on audiogenic seizures from genetic and acoustically primed susceptibilities. Consequently, we suggest that all audiogenic seizure responses, including those during ethanol withdrawal, are a type of subcortical epilepsy.