Action of Mitochondrial Substrates on Neuronal Excitability in Rat Substantia Gelatinosa Neurons
(주)코리아스칼라
- 최초 등록일
- 2023.04.03
- 최종 저작일
- 2017.06
- 7페이지/ 어도비 PDF
- 가격 4,000원
* 본 문서는 배포용으로 복사 및 편집이 불가합니다.
서지정보
ㆍ발행기관 : 대한구강생물학회
ㆍ수록지정보 : International Journal of Oral Biology / 42권 / 2호
ㆍ저자명 : Hae In Lee, Sang Woo Chun
영어 초록
Recent studies indicate that mitochondria are an important source of reactive oxygen species (ROS) in the spinal dorsal horn. In our previous study, application of malate, a mitochondrial electron transport complex I substrate, induced a membrane depolarization, which was inhibited by pretreatment with ROS scavengers. In the present study, we used patch clamp recording in the substantia geletinosa (SG) neurons of spinal slices, to investigate the cellular mechanism of mitochondrial ROS on neuronal excitability. DNQX (an AMPA receptor antagonist) and AP5 (an NMDA receptor antagonist) decreased the malate-induced depolarization. In an external calcium free solution and addition of tetrodotoxin (TTX) for blockade of synaptic transmission, the malateinduced depolarization remained unchanged. In the presence of DNQX, AP5 and AP3 (a groupⅠ metabotropic glutamate receptor (mGluR) antagonist), glutamate depolarized the membrane potential, which was suppressed by PBN. However, oligomycin (a mitochondrial ATP synthase inhibitor) or PPADS (a P2 receptor inhibitor) did not affect the substrates-induced depolarization. These results suggest that mitochondrial substrate-induced ROS in SG neuron directly acts on the postsynaptic neuron, therefore increasing the ion influx via glutamate receptors.
참고 자료
없음
"International Journal of Oral Biology"의 다른 논문