Abstract

The hypothesis tested in this study was that a unilateral irritative focal epileptic lesion in the temporal lobe results in hyposexuality. Focal epilepsy was produced in male cats by unilateral injection of aluminum hydroxide into either the basolateral amygdala (temporal lobe group) or anterior sigmoid gyrus (motor cortex group). Weekly sex testing trials with estrous females were conducted prior to and after aluminum hydroxide injection, and mating performance scores were compared with those of normal, unoperated cats (normal control group). All animals receiving aluminum hydroxide developed electroencephalographic and behavioral manifestations of epilepsy; i.e., interictal EEG spiking and partial or generalized seizures. Cats in the temporal lobe group exhibited a dramatic and complete suppression of sexual behavior at periods from 6 to 26 weeks after aluminum hydroxide injection. The duration of the hyposexuality varied between individual animals and returned to normal as suddenly as the onset occurred, despite the use of AEDs to prevent or control generalized seizure activity. Interictal EEG epileptiform spiking in the amygdala preceded the onset of hyposexuality by 1-12 weeks. By contrast, cats in the motor cortex and normal control groups showed no sign of sexual dysfunction throughout the experimental period, independent of seizure activity and/or antiepileptic drug (AED) treatment. These data support the hypothesis that hyposexuality occurs as a result of epileptiform activity in the temporal lobe, but not in the motor cortex. The precise mechanisms by which this occurs are unknown, but are likely to involve abnormally high-frequency neuronal activity in temporal lobe structures known to connect with and/or to regulate hypothalamic nuclei that organize male sexual behavior toward receptive females.

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