Effect of seizure activity and calpain inhibitor I on LTP in juvenile hippocampal slices

Abstract

Kainic acid-induced seizure activity in adult rats produces an impairment of long-term potentiation induction in hippocampal slices. As the consequences of seizure activity are different in adult and juvenile rats, we tested the ability of hippocampal slices prepared from kainate-treated juvenile rats to exhibit long-term potentiation. Long-term potentiation was induced by theta-burst stimulation and was not significantly different in slices prepared from control or kainate-injected juvenile rats (16-18 postnatal days). Short-term potentiation, however, was reduced in the kainate-treated juveniles. Calpain inhibitor I has been shown to prevent long-term potentiation formation in adult hippocampal slices, and we evaluated its effect on long-term potentiation in hippocampal slices from juvenile rats. Calpain inhibitor I produced a significant reduction in the degree of long-term potentiation induced by theta-burst stimulation in hippocampal slices prepared from 14-20 postnatal day-old animals. The results are consistent with the notion that, although similar mechanisms participate in the formation of long-term potentiation in juvenile and adult animals, juvenile animals are much more resistant than adult animals to the consequences of seizure activity.

Enhanced hippocampal neurodegeneration after traumatic or kainate excitotoxicity in GFAP-null mice

“…21 The effects of cerebral trauma on synaptic plasticity are LTP-specific. 22 GFAP-KO mice are also abnormal with respect to LTP.…”

Activation of extrasynaptic GABAA receptors inhibits cyclothiazide-induced epileptiform activity in hippocampal CA1 neurons

“…The brain slice is a simple and convenient method that has been widely used in anticonvulsant drug development, and in experimental studies on the neuroprotective roles of these drugs during epilepsy [28][29][30] .…”

Distribution of protein kinase M? and the complete protein kinase C isoform family in rat brain

“…The translocation to the membrane‐particulate compartment of multiple PKC isoforms during LTP induction, for example, may result in divergent signal transduction pathways, perhaps mediated through spatial targeting of the isoforms within neurons. This divergence would be expected for initial LTP induction because it involves a highly complex set of signal transduction events, including the activation of multiple kinases (Klann, 1991, 1993; O'Dell et al, 1991; Frey et al, 1993; Lisman, 1994; Zhuo et al, 1994; Blitzer, et al, 1995; English and Sweatt, 1997), proteases (Cerro et al, 1990; Denny et al, 1990; Fitzpatrick et al, 1992), and macromolecular synthesis (Stanton and Sarvey, 1984; Krug et al, 1984; Frey et al, 1988; Otani et al, 1989, Osten et al, 1996a).…”