The Modulation Effect Of Endocannabinoids 2-AG On Lipopolysaccharide Enduced The Current Of Potassium Ion Channel And L-Type Calcium Channel On Rat Caudate Nucleus Neurons

Objective Neurodegenerative diseases are familial and sporadic conditions characterized by the progressive dysfunction of the nervous system, and now it is not completely cured. Inflammation is one of the pathogenic factors, can make the microglia and astrocytes activation, proliferation, influences the degenerative changes in the structure and function of neuron. The hyperpolarization of potassium channels can extend the action potential of neurons, and affect the neurotransmitters. The L-type calcium channel can lead to an elevated intracellular calcium ion concentration, mitochondrial dysfunction, neurotransmitter release, that cause neural degenerative changes. Endocannabinoids is a kind of synthesis in the body, has the anti-inflammatory effects of lipid material, previous studies have shown that endocannabinoids can inhibit the activity of Caspase-3 to decrease the lipopolysaccharide of caudate nucleus neurons damage, so as to achieve anti-inflammatory, protect the neurons. This study was to explore the mechanism of protective effect of endocannabinoids 2-AG and AEA on lipopolysaccharide injury of rat caudate nucleus neurons potassium ion channel, L-type calcium channel electrical characteristics, to offer a new theoretical basis for treatment of neurodegenerative diseases.Methods Using whole-cell patch clamp recording the electrical characteristics of IA, IK, L-type calcium channel of LPS on primary cultured rat caudate nucleus neurons, and the mechanismof of protective effect of endocannabinoids 2-AG, AEA on it.Results(1) LPS can inhibit the I-V current of IA; 2-AG can completely inhibit this effect by CB1 receptors; LPS can not influence the activation and deactivation of IA.(2) The concentration of the AEA can not affect LPS on IA.(3) LPS can inhibit IK current density, but there is no effect of the 2-AG; LPS can not influence the activation and deactivation of IK.(4) LPS can enhance L- Ca2+ current density, 2-AG can restrain this enhancement effect, but not by CB1 and CB2 receptors; LPS can not impact on L-Ca2+ activation and deactivation.Conclusion(1)Endocannabinoids 2-AG can be completely through the CB1 receptor affect the inhibition effect of LPS to caudate nucleus IA ion channel.(2) Endocannabinoids 2-AG can affect the enhancement effect of LPS to caudate nucleus L-type calcium channel, but not by CB1 and CB2 receptors.