Lack of Change in Neurochemical Markers During the Postepileptic Phase of Intrahippocampal Tetanus Toxin Syndrome in Rats

Abstract

The chronic epileptic syndrome induced by injecting tetanus toxin into rat hippocampus causes functional changes that essentially are permanent, outlasting the period of active seizures by at least 1 year. These long-term changes have been characterized by an impaired performance on a range of behavioral tasks, which in turn have been associated with a physiologic depression of hippocampal evoked responses but not with any discernible histopathology. In the present study, we examined the hippocampi of rats in the postseizure phase of the tetanus toxin model and observed no significant changes in the concentration of neurochemical markers for six neurotransmitters. Therefore, the long-term reduction in hippocampal excitability cannot be attributed to any major loss of afferents or hippocampal neurons using aspartate, acetylcholine, gamma-aminobutyric acid (GABA), glutamate, norepinephrine (NE), or serotonin as their transmitters.

Differential and Time-Dependent Changes in Gene Expression for Type II Calcium/Calmodulin-Dependent Protein Kinase, 67 kDa Glutamic Acid Decarboxylase, and Glutamate Receptor Subunits in Tetanus Toxin-Induced Focal Epilepsy

“…Subsequently, therefore, injections in excess of 13 ng TT were used. The higher dosage for inducing seizures in the motor cortex in comparison with hippocampus and parietal cortex (Brener et al, 1990;Francis et al, 1990) is consistent with other investigations (Mellanby et al, 1977).…”