Methamphetamine Hippocampal Neurons Of Rat Toxicity Mechanism Research

Objective: Methylamphetamine, also known as methamphetamine, it is commonly knownas "ice-drug". Belongs to stimulants of amphetamine-type, Abusers has a strong dependence,Also can damage nerve cells, Decreased learning ability, Decline in memory and motorfunction. In this study, approach is through the acute administration of METH. One by one, todetect the current in rat hippocampal neurons postsynaptic and NMDA-induced. Provide abasis for further study of METH directly contribute to the presynaptic nerve terminals to releaseglutamate.Methods: Take the day of the newborn Wistar rats, Hippocampus will be isolated and cellculture. Cultured neurons can be used for patch clamp experiments in12-15days. Whole-cellmode of Patch-clamp to record currents of excited postsynaptic. Experimental data using thepClamp9.0software package（Axon Instrument，USA）, The Clampfit be used to completethe data analysis and processing. Among them, the Clampex9.0was used to collect data. Gap-free first to get the data when we use whole-cell mode recording the data for neurons, Wait untilthe end of the recorded data processing, format of ASCII output to Origin7.5(Origin Labs,Northampton, MA, USA), Curve fitting and drawing. Statistical methods: Two sets of data werecompared using paired sample t-test. All data were statistically analyzed using SPSS12.0software package (SPSS Inc., Chicago, IL, USA). When P <0.05indicates a significantdifference.Results:1、METH increase the frequency and amplitude of spontaneous excitatorypostsynaptic currents, P <0.001statistically significant.2、METH increased the frequency ofminiature excitatory postsynaptic current, P <0.001statistically significant.3、METH onNMDA-induced currents in hippocampal neurons has no effect.Conclusion: METH increased the frequency and amplitude of the excited postsynapticcurrent in hippocampal neurons, P<0.001statistically significant, METH on NMDA-inducedcurrents in hippocampal neurons has no effect. Neurons presynaptic glutamate quantumincrease of the release, Lead to the increase of neurons excited postsynaptic current frequencyand amplitude. METH increased the release of glutamate form membrane of the synaptic.When the glutamic acid content is too high, Excessive activation of excitatory glutamate receptors, Over-excited neurons, Induced neuron toxicity damage, Ultimately lead to neuronaldeath.