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Aim To investigate the role of collybistin in the regulation of pain transmission. Methods The distribution of collybistin in spinal cord was observed by immunohistochemical staining. The role of collybis¬tin in pain transmission was evaluated by behavioral experiments. The effect of collybistin on inhibitory synap¬tic transmission was studied by electrophysiological ex¬periments. Results Collybistin was distributed in spi¬nal cord neurons; ShRNA-collybistin induced pain sen-sitization of intact mice ( P < 0. 05 ) . Overexpression of collybistin in spinal cord significantly alleviated pain sensitization induced by peripheral nerve injury ( P <0. 05 ) . ShRNA-collybistin also significantly reduced the amplitudes and frequencies of miniature inhibitory postsynaptic currents (mlPSCs) in superficial neurons of spinal cord dorsal horn (P <0. 05) . Overexpression of collybistin in spinal cord could reverse the effects of peripheral nerve injury on mlPSCs (P <0. 05). Con¬clusions Collybistin is involved in pain sensitization induced by peripheral nerve injury in mice.
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@#Objective To explore the physiological characteristics of synaptic transmission of anterior horn early development in thorac-ic spinal cord mediated byα-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors in rats. Methods 36 Wistar rats were divided into embryonic 17 days group (E17, n=12), embryonic 20 days group (E20, n=12) and postnatal 7 days group (P7, n=12). Immuno-fluorescent staining of calmodulin-dependent protein kinaseⅡ(CaMKⅡ) was used to test the distribution of AMPA receptors. Multi-elec-trode array technique (MED-64 system) was used to test the changes of field excitatory post-synaptic potential (fEPSP) of synaptic transmis-sion mediated by AMPA receptor. Results There was small amount of CaMKⅡ-positive neurons existing in gray matter of spinal cord at E17, CaMKⅡ-positive neurons migrated to the center, and the number of neurons became more and more in E20 and P7 rats. The number of evoked fEPSP gradually increased in rats from E17 to P7, and could be blocked by 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX). The range of synaptic connection in spinal cord gray matter significantly reduced (P<0.001). Conclusion AMPA receptors participate in the early development of spinal cord in rats and act as the main excitatory receptor of functional synaptic connection in neural network of ventricornu.
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0.05).However,there was no significant difference in the AMPAR-mediated basal synaptic transmission on hippocampal CA1 between those at the later period(6 weeks) of epilepsy induced by pilocarpine and controls,while LTP was inhibited(P
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Aim To investigate the antagonistic action o f total saponins of panaxnotoginseng(PNS) on cardiac hypertrophy and its nervous mechanism.Methods (1)cardiac hypertrophy of rats due to pressure overload was induced by constricting of abdominal aorta. There were five groups in the experiments. The rats in Group A(control group)were sham operated . Group B was aorta-constricted group.The rats in Group C,D,E were given ip PNS 50,100,150 mg?kg?d -1 for three weeks respectively. Three weeks later, We measured the heart-weight(HW),left ventricular weight(LVW), the ratio of HW/BW,LVW/BW (LVI) and the cardiomyocyte diameters(MD) after dyeing by HE color.(2)The effects of PNS on the fast excitatory postsynaptic potential(f-EPSP),membrane depolarization induced by application of acetylcholine (ACh),membrane potential and membrane resistance of the isolated Stellate ganglion(SG)of the rats were investigated by means of intracellular recording techniques. Results (1)HW/BW, LVI and MD of Group E were significantly lower than that of Group B(P0.05).(2)At the concentration of 0.10 ～0.16 g?L -1, PNS reversibly depressed the amplitude of f-EPSP, but the ACh depolarization,membrane potential and membrane resistance were not significantly altered by PNS. Conclusion PNS can prevent cardiac hypertrophy due to pressure overload in rats and this action may underline its inhibitory action on presyn aptic effect of regulating calcium influx.
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AIM To investigate the effects of several 5-hydroxytryptamine(5-HT) subtype receptor antagonists on late slow excitatory postsynaptic potential(LS-EPSP) of the neurons of guinea pig inferior mesenteric ganglion(IMG). METHODS Intracellular recordings were made from neurons of the isolated guinea pig IMG. RESULTS Cyproheptadine and BRL 24924 suppressed LS-EPSP of 5-HT sensitive neurons reversibly, while mianserin, MDL 72222 and spiperone showed no significant effect. Continuous superfusion of IMG with MCPP suppressed LS-EPSP of 5-HT sensitive neurons by 5-HT 1P receptor desensitizated. CONCLUSION LS-EPSP of 5-HT sensitive neuron is mediated by 5-HT 1P subtype receptor.