Lints, Carlton E.
M.A. (Master of Arts)
Department of Psychology
The first study attempted to increase midbrain beta receptor densities and audiogenic seizure (AGS) susceptibility in DBA/2 mice, at an age when AGS susceptibility normally decreases, by chronic administration of beta antagonists. Although the DBA midbrain contains an increased density of beta receptors compared to seizure resistant mice and beta blockade produces anticonvulsant effects at the age of peak seizure activity, 14 days of chronic beta blockade failed to increase seizure activity in 30-day-old subjects. The receptor binding data are tentative; however, they correspond with the behavioral data in that no increases in either midbrain or telencephalic beta receptors were found. The second study examined the effects of alpha adrenergic antagonists on AGS in 30-day-old DBA mice. Tolazoline, a non-selective alpha antagonist, produced anticonvulsant effects at both low and high doses but produced proconvulsant effects at intermediate doses. Prazosin, an alpha-1 antagonist, produced anticonvulsant effects, while yohimbine, an alpha—2 antagonist, produced proconvulsant effects. These results are consistent with previous studies that found the DBA midbrain contains an increased density of proconvulsant alpha-1 receptors as well as a decreased density of anticonvulsant alpha-2 receptors. This study demonstrated that AGS susceptibility can be manipulated by adrenoceptor mechanisms at an age past the peak of seizure activity.
Stearn, Deborah, "Adrenergic receptors and audiogenic seizures in DBA/2 mice" (1985). Graduate Research Theses & Dissertations. 1018.
Northern Illinois University
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