[Effect of scorpion venom on the release of GABA in hippocampus of epileptic rats induced by kainic acid].
Jiang Cl, Zhang Wq
Abstract
Jiang Cl, Zhang Wq
Abstract
In the present study, the effect of scorpion venom (SV) on epileptic susceptibility and its neurochemical mechanisms were investigated. After SV or normal saline (NS) administration for three weeks in epileptic rats, epileptic seizures were much more decreased in kainic acid (KA) + SV group than those of KA + NS group. GABA immunocytochemistry showed that both (gamma-aminobutyric acid immunoreactivity (GABA-IR) density and the number of GABA positive neurons were markedly decreased in the ventral hippocampus, especially in hilus of KA + NS group as compared with NS + NS group. However, in the group treated with SV for three weeks, the number of GABA positive neurons and the density of GABA-IR were greater increased than those of both KA + NS group and the NS + NS group. The number of GABA positive neurons and the density of GABA-IR were unchanged in the dorsal hippocampus of all the four groups. The above results suggest that SV may selectively prevent loss of GABAergic interneurons in the ventral hippocampus of rats susceptible to epileptic seizures and increase the release of GABA as an antiepileptic mechanism.
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In the present study, the effect of scorpion venom (SV) on epileptic susceptibility and its neurochemical mechanisms were investigated. After SV or normal saline (NS) administration for three weeks in epileptic rats, epileptic seizures were much more decreased in kainic acid (KA) + SV group than those of KA + NS group. GABA immunocytochemistry showed that both (gamma-aminobutyric acid immunoreactivity (GABA-IR) density and the number of GABA positive neurons were markedly decreased in the ventral hippocampus, especially in hilus of KA + NS group as compared with NS + NS group. However, in the group treated with SV for three weeks, the number of GABA positive neurons and the density of GABA-IR were greater increased than those of both KA + NS group and the NS + NS group. The number of GABA positive neurons and the density of GABA-IR were unchanged in the dorsal hippocampus of all the four groups. The above results suggest that SV may selectively prevent loss of GABAergic interneurons in the ventral hippocampus of rats susceptible to epileptic seizures and increase the release of GABA as an antiepileptic mechanism.
Key concepts: Kainic acid, Hippocampus, GABAergic, Internal medicine, Endocrinology, Chemistry, gamma-Aminobutyric acid, Neurochemical