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Reserpine and tetrabenazine reduced the survival time of mice infused with leptazol. This effect was antagonized by pretreatment with iproniazid. The survival time of iproniazid-treated mice was prolonged by 5-hydroxytryptophan but not by 3:4-dihydroxyphenylalanine. These findings suggest a relation between leptazol sensitivity and brain levels of 5-hydroxytryptamine.
The occurrence of audiogenic seizures in mice has been used as the basis of a method for measuring the antagonism between sodium thiopentone and bemegride or leptazol. Thiopentone in doses of 8 and 16 mg./kg. protected all the mice against the occurrence of audiogenic seizures. Bemegride and leptazol were administered in doses having molecular concentrations which bore a simple relationship to the doses of thiopentone. Bemegride was four times as powerful as leptazol in antagonizing the protective effect of thiopentone, and comparison of their regression lines showed that both analeptics acted in the same way. The antagonistic effect of bemegride occurred with doses less than its normal convulsant dose, but the doses of leptazol needed to antagonize thiopentone were within the convulsant range, and it increased the severity of any audiogenic seizures.
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To test Gellhorn's hypothesis that electroconvulsive shock reinstates extinguished responses, a conditioned "anxiety" response was established and then extinguished in rats. A series of treatments did not restore the extinguished "anxiety" response; in fact, control animals showed appreciable spontaneous recovery of the "anxiety" response while treated animals did not.
In striking contrast to the seizure patterns of other animals, the electroshock seizure of the sloth consists of weak extension followed by tonic flexion and terminal clonus. A similar pattern is seen with direct spinal cord stimulation. Strychnine produces a pure flexor convulsion. In the spinal sloth, painful stimulation of one foot causes extension at some joints of that limb and strong flexion at all joints of the contralateral limb.
Inbred mice susceptible to audiogenic seizures were found to develop resistance to the protective effects of chlorpromazine and its analogs. It is proposed that the use of such inbred mice provides a unique new tool for studying drug mechanism and drug resistance.
Evidence which indicates a positive relationship between susceptibility to audiogenic seizure and dilute coat color in mice is presented, and a possible mechanism for this relationship is discussed.
Tetanus toxin injected into the cortex produces convulsions, neurological disability, and a strychnine-like discharging focus, appearing after a minimal latency of 2 days and lasting more than a month. Such a focus, apparently caused by a blockade of inhibitory synapses, does not demonstrate any major damage in microscopic studies.