Amphetamine and Ammonshorn-sclerosis

Abstract

IN a previous communication¹ I reported the tendency for repetitive carbon-monoxide seizures in guinea pigs to produce ‘eosinophilic ischæmia’ relatively selectively in CA2 pyramidal cells of the hippocampus, and made passing mention of amphetamine's sparing effect on the coincident ‘collapse’ of synaptic entities within the adjacent end-bulb of the mossy fibre system. Since then I have completed the neurohistological survey of 11 guinea pigs, of 400–600 g in weight, in which 10 mg amphetamine was always injected intramuscularly 0.5–4 h before exposures to carbon monoxide hypoxia and was still producing motor activation (notably in the form of compulsive gnawing) at the times of exposure. Of 5 of these animals which had 6, 5, 4, 3, and 3 full seizures, respectively, only 2 displayed ischæmia in CA2, and then only in mild degree—so that cell-soma pathology also had apparently been very appreciably spared at end-bulb levels. The remaining 6 animals, despite at least 5 exposures each, produced not even a modified seizure, and no CA2 ischæmia whatever. In 3 of these 6 it is possible that incipient coma was interrupted prematurely at every exposure; but in the other 3 the depth of pre-coma normally characterized by a full four-legged running seizure in opisthotonus was undoubtedly reached each time —so that these 3 were presumably either seizure-resistant by constitution or seizure-suppressed by the drug. (Acetazolamide, in lieu of amphetamine in a similar smaller series of experiments, tended to suppress seizures but not to diminish CA2 pathology.)