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Kindling-associated SV2A expression in hilar GABAergic interneurons of the mouse dentate gyrus

► PTZ kindling significantly elevated SV2A expression in the hippocampal dentate gyrus. ► PTZ kindling-associated SV2A expression specifically occurred in the hilar GABAergic, but not glutamatergic, neurons. ► SV2A expression in the stratum lucidum or the pyramidal cell layer of the CA3 field was un...

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Published in:Neuroscience letters 2012-02, Vol.510 (2), p.93-98
Main Authors: Ohno, Yukihiro, Okumura, Takahiro, Terada, Ryo, Ishihara, Shizuka, Serikawa, Tadao, Sasa, Masashi
Format: Article
Language:English
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Summary:► PTZ kindling significantly elevated SV2A expression in the hippocampal dentate gyrus. ► PTZ kindling-associated SV2A expression specifically occurred in the hilar GABAergic, but not glutamatergic, neurons. ► SV2A expression in the stratum lucidum or the pyramidal cell layer of the CA3 field was unaltered by the kindling. ► SV2A seems to be involved in a compensatory or prophylactic mechanism against kindling epileptogenesis. Immunohistochemical studies were performed to analyze the expressional changes in hippocampal synaptic vesicle protein 2A (SV2A) following pentylenetetrazole (PTZ) kindling. Repeated treatments of mice with sub-convulsive PTZ (40mg/kg, i.p.) for 15 days progressively enhanced seizure susceptibility and induced clonic convulsions in most animals examined. Topographical analysis of hippocampal SV2A-immunoreactivity revealed that SV2A was densely expressed in the hilar region of the dentate gyrus, stratum lucidum of the CA3 field and around the periphery of CA3 pyramidal neurons. PTZ kindling region-specifically increased SV2A expression in the dentate hilus without affecting that in the stratum lucidum or the pyramidal cell layer of the CA3 field. Confocal laser microscopic analysis using PTZ-kindled mice illustrated that most SV2A was co-expressed with glutamic acid decarboxylase 67 in the cell bodies and dendrites of hilar interneurons. However, SV2A-immunoreactivity was negligibly observed in the hilar glutamatergic nerve terminals (mossy fibers) probed with the anti-vesicular glutamate transporter 1 antibody. The present study suggests that SV2A specifically regulates hilar GABAergic neurotransmission in the kindled hippocampus probably as a compensatory or prophylactic mechanism against kindling epileptogenesis.
ISSN:0304-3940
1872-7972
DOI:10.1016/j.neulet.2012.01.009