Action of Mitochondrial Substrates on Neuronal Excitability in Rat Substantia Gelatinosa Neurons.
10.11620/IJOB.2017.42.2.055
- Author:
Hae In LEE
1
;
Sang Woo CHUN
Author Information
1. Department of Dental Hygiene, Gwangyang Health Science University, Gwangyang 57764, Korea.
- Publication Type:Original Article
- Keywords:
Malate;
Membrane excitability;
Reactive oxygen species;
SG neurons
- MeSH:
Animals;
Calcium;
Electron Transport Complex I;
Glutamic Acid;
Membrane Potentials;
Membranes;
Mitochondria;
Mitochondrial Proton-Translocating ATPases;
N-Methylaspartate;
Neurons*;
Oligomycins;
Rats*;
Reactive Oxygen Species;
Receptors, AMPA;
Receptors, Glutamate;
Receptors, Metabotropic Glutamate;
Spinal Cord Dorsal Horn;
Substantia Gelatinosa*;
Synaptic Transmission;
Tetrodotoxin
- From:International Journal of Oral Biology
2017;42(2):55-61
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
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 group I 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.
