Hippocampal calcium-binding protein during commissural kindling-induced epileptogenesis: progressive decline and effects of anticonvulsants.
Changes in hippocampal calcium-binding protein ( CaBP) were examined in rats given kindling stimuli via electrodes chronically implanted in the midline commissural pathway. CaBP levels decreased progressively and were significantly lower (16.6%) than controls after only 10 kindling trials. The maximum fall (33%) was achieved prior to the production of stage 5 motor seizures and additional kindling-induced seizures produced no further decline. Induction of motor seizures with pentylenetetrazol had no effect upon hippocampal CaBP levels. Diazepam treatment during the course of kindling significantly increased the number of stimulation trials required to produce stage 5 motor seizures but did not inhibit the fall in CaBP. Diazepam treatment of fully kindled rats was effective in blocking generalized motor seizures without causing any restoration of the depleted levels of CaBP. Diphenylhydantoin was neither effective during the course of kindling nor in modifying the effect of further stimulations in fully kindled rats. These data indicate that the highly specific decrease in hippocampal CaBP, previously demonstrated to be localized to dentate granule cells and their processes following kindling-induced epilepsy, does not result from the expression of full tonic-clonic (stage 5) motor seizures. The loss of CaBP may be a biochemical factor contributing either to the predisposition of neuronal tissue to seizure activity or to a protective attempt to overcome the deleterious effect of repeated high-frequency stimulation.[1]References
- Hippocampal calcium-binding protein during commissural kindling-induced epileptogenesis: progressive decline and effects of anticonvulsants. Baimbridge, K.G., Miller, J.J. Brain Res. (1984) [Pubmed]
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