Objective Concentration of extracellular calcium ([Ca2+]o) in the central nervous system decreases substantially in different conditions. It results in facilitating neuronal excitability. The goal of this study is ...
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Objective Concentration of extracellular calcium ([Ca2+]o) in the central nervous system decreases substantially in different conditions. It results in facilitating neuronal excitability. The goal of this study is to examine the mechanisms of enhanced neuronal excitation in low [Ca2+]o in order to provide new clues to treat the hyperexcitability diseases in clinic. Methods Whole-cell patch-clamp technique and neuron culture were used in the study. Results The firing threshold of cultured hippocampal neurons decreased markedly in low [Ca2+]o saline. Unexpectedly, apamine and isoprenaline, antagonists of medium afterhyperpolarization (mAHP) and slow AHP (sAHP) respectively, had no statistic significant effect on excitability of neurons. TTX at a low concentration was sufficient to inhibit/Nap, which blocked the increase of firing frequency in low [Ca2+]o. It also reduced the number of spikes in normal [Ca2+]o. Conclusion These results suggest that in cultured hippocampal neurons, modulation of spiking threshold but not AHP may cause the increased excitability in low [Ca2+]o.
Objective To observe the effects of y-aminobutyric acid (GABA) on the electric activities of pain-excited neurons (PEN) in nucleus accumbens (NAc) in central nervous system (CNS) of morphine-dependent rats. Me...
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Objective To observe the effects of y-aminobutyric acid (GABA) on the electric activities of pain-excited neurons (PEN) in nucleus accumbens (NAc) in central nervous system (CNS) of morphine-dependent rats. Methods After GABA or the GABAA-receptor antagonist, bicuculline (Bic), was injected into cerebral ventricles or NAc, right sciatic nerve was stimulated by electrical pulses, which was considered as traumatic pain stimulation. Extracellular recordings methods were used to record the electric activities of PEN in NAc. Results When GABA was injected into intracerebroventricle (ICV) as well as NAc, it could decrease the pain-evoked discharge frequency and prolong the latency of PEN. Bic could interdict the above effects of GABA on the electric activities of PEN. Conclusion Exogenous GABA might have an inhibitory effect on the central pain adjustment. Furthermore, GABA and GABAA receptor participate and mediate the traumatic information transmission process in CNS.
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