Ping Granule on pentylenetetrazol induced epileptic rats on amino acid neurotransmitter receptors in hippocampus of_0.docVIP
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Ping Granule on pentylenetetrazol induced epileptic rats on amino acid neurotransmitter receptors in hippocampus of_0
PAGE \* MERGEFORMAT 11
Ping Granule on pentylenetetrazol induced epileptic rats on amino acid neurotransmitter receptors in hippocampus of
Of: Tian Rong, ZHANG Shiqing, Shi Zhenggang, Mu Baolong
[Abstract] Objective Analysis by immunohistochemistry Ping Granule on pentylenetetrazole (PTZ) induced epileptic rat hippocampus amino acid neurotransmitter receptors, and to explore the mechanism of its antiepileptic effect. Methods 60, 28 days old The Wistar rats were randomly divided into normal control group (A group), model group (B group), phenobarbital group (C group) and Ping Granule small (D), middle (E), large (F group) groups. In addition to the normal control group, other groups of chronic intraperitoneal injection of PTZ seizure model copied by immunohistochemistry and microscopic image analysis of each group were detected in hippocampus CA1, CA3 of glutamate by body (NMDAR1) and γ-aminobutyric acid receptor (GABA-AR @ 1) positive cells in the immune response (n), positive cell area ratio (Aa%) and positive cells integral absorbance (IA). Results and A group, B in hippocampal CA1, CA3 and other parts of NMDAR1 in the n, Aa% increase, IA increased (P lt;0.01), compared with B group, C group and D, E, F group NMDAR1 in different parts of the n, Aa% are decreased to varying degrees, IA also has different levels decreased (P lt;0.05). with the A group, B in hippocampal CA1, CA3 and other parts of GABA-AR @ 1 to n, Aa% decline, IA decreased (P lt;0.01), and B group, C, D, E, F group different parts of the GABA-AR @ 1 of the n, Aa% increase in varying degrees, IA also increased to varying degrees (P lt;0.05). Conclusion The role of antiepileptic Ping Granule mechanism may be through inhibition of excitatory neurotransmitter receptors NMDAR1 activity and expression, and activation of the inhibitory neurotransmitter GABA-AR @ 1 receptor activity and expression, thereby reducing the excitability of the cerebral cortex, the effective suppression of epilepsy th
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