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Objective To evaluate the effect of morphine on synaptic long-term potentiation (LTP) in the spinal dorsal horn evoked by electric stimulation of sciatic nerve in rats. Methods Twenty-seven healthy male SD rats aged 60-90 d weighing 180-200 g were randomly divided into 4 groups: group Ⅰ control (group C, n=7), group Ⅱ morphine (group M, n=7), group Ⅲ naloxone (group N, n=6), and group Ⅳ morphine + naloxone (group MN, n=7). The animals were anesthetized with intraperitoneal 10% urethane 1 g/kg, intubated and then mechanically ventilated. The bipolar insulated stainless steel recording electrode (impedance 0.5-1 MΩ, diameter 0.1 mm) was inserted into the left side of the spinal dorsal horn at T13-L1 to stimulate the left side of the sciatic nerve. Single square pulses (15 V, 0.5 ms, 1/60 Hz for 30 min) was applied to evoke spinal field potentials. Normal saline 10 μl, morphine 10 μl (15 μg/μl), naloxone 10 μl (2.5 μg/μl), and the mixture 10 μl of naloxone 5 μl (2.5 μg/μl) and morphine 5 μl (15 μg/μl) was gradually instilled over 2 rain in the 4 groups respectively. Five minutes later, high-frequency and intensity tetanic stimulation (30-40 V, 0.5 ms, 100 Hz, given in 4 trains of 1-s duration at 10-s intervals) was used to induce LTP. Then single square stimuli (15 V, 5 ms, 1/60 Hz) were applied to the sciatic nerve for 210 min. The amplitude and latency period of the field potential were recorded 30 min before tetanic stimulation, and 0-30, 35-60, 65-120 and 125-210 min after titanic stimulation. Results Compared with group C, the amplitude of the field potential was significantly decreased and the latency period prolonged in group M and MN, but there was no significant difference in the above indices between group N and C. Compared with group M, the amplitude of the field potential was significantly increased and the latency period shortened in group MN. Compared with those 30 min before the tetanic stimulation, the amplitude of the field potential was significantly increased and latency period shorted at the time points after the tetanie stimulation in group C and N, the amplitude of the field potential was significantly decreased and latency period prolonged at the time points after the tetanie stimulation in group M, and the amplitude of the field potential was significantly increased 0-30 and 35-60 min after the tetanic stimulation and latency period shortened 0-30 min after the tetanie stimulation, the amplitude of the field potential was significantly decreased and latency period prolonged 65-120 and 125-210 min after the tetanic stimulation in group MN. Conclusion Morphine can inhibit synaptic LTP in the spinal dorsal horn evoked by electric stimulation of sciatic nerve in rats, and it may be one of the mechanisms of the central sensitization inhibition.
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Objective To investigate the effects of Oxytocin(OT) on hippocampal long-term potentiation(LTP) and FOS protein expression induced by peripheral stimulation.Methods Single stimulation pulses were delivered to the left sciatic nerves to evoke the field excitatory postsynaptic potentials (fEPSPs) in the right hippocampal CA1. Tetanic stimulation was used to induce hippocampal LTP. Different groups of rat were given NS,OT,Oxytocin antagonist-Atosiban + OT before tetanic stimulation,into lateral ventricle(LV) respectively. Expression of FOS protein was compared among the groups by histopathological and immunohistochemistry. Results Single stimulation evoked fEPSPs in hippocampal CA1,which average latency was (171.9?33.1)ms and average amplitude was (25.7?8.4)?V. Tetanic stimulation induced hippocampal LTP and increased the expression of FOS protein. Intracerebroventricular injection of OT inhibited hippocampal LTP and decreased the expression of FOS protein. This effect of OT was blocked by the pretreatment with Atosiban. Conclusion The results suggested that OT may play an inhibitory role in leaning and memory of rats and the effect is mediated by OT receptor.
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Objective To study the effects of acute weak vagus nerve stimulation on hippocampal CA1 unit discharges and field potentials of normal and epileptiform discharging rats.Methods The experiments were performed with 55 male Sprague-Dawley rats weighing 180～250 g,SPF grade.Animals were divided into normal(n=45)and regularly epileptiform discharging(n=10)groups.The normal rat group:Separate the left neck vagus nerve and ligate the peripheral end.Acute weak electrical stimulation(10 Hz,0.5 ms,1.5～5.0 V,15～20 unit /train)were administered to the left neck vagus nerve central end.20 trains were performed with a regular interval of 5 min.Record the unit discharges of right hippocampal CA1 and field potentials of bilateral hippocampal CA1.The epileptiform discharging group:Gelatin spongia was put onto the left cortex to induce epileptiform discharges.After 30 min stable regularly discharging,continue the procedure in the first group.Results Cyclical theta oscillation(about 3～6.5 Hz)appeared in bilateral hippocampal CA1 of normal rats after the stimulation(strain m=5～7,38/45,84.4%).With oscillation,there is unit discharging.It has two kinds:theta-on(n=30)and theta-off(n=5).The sharp wave amplitude was inhibited while the sharp wave interval increased following the acute weak vagus nerve stimulation(n=10)in epileptiform discharging rats.Theta oscillation was induced during the sharp wave.With oscillation,there is tonic unit discharging(n=10).The number of action potential spikes positively correlate with the sharp wave intervals(P
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BACKGROUND: Central oxytocin (OT) may be a neurotransmitter or neuromodulator and play an important role in learning and memory, sexual behaviour, pain modulation and opiate tolerance and dependence. To research the interactions between oxytocinergic and opioidergic system in hippocampus has some significance.OBJECTIVE: To investigate the effects of OT administered intracerebroventricularly on evoked discharge of left dorsal hippocampal CA1 neurons in rats and the possible interactions between oxytocinergic and opioidergic system.DESIGN: A randomised controlled study.SETTING: Department of Physiology of Guangdong Medical College; Department of Physiology and Pathology of Medical College of Wuhan University.MATERIALS: The study was conducted in the Physiology Department of Medical College of Wuhan University from September 2002 to September 2003. A total of 36 male Sprague-Dawley rats were selected and randomly divided into six groups: control (NS), OT groups (0.2 mg/L, 2 mg/L and 20 mg/L), [d (CH2)5-OVT]+OT (2 mg/L), naloxone+OT (2 mg/L), with 6 rats in each group.METHODS: Single-unit recording was performed with glass microelectrode. The glass microelectrode was inserted by a micromanipulator into hippocampal CA1. The electrical activity was amplified by a microelectrode amplifier and then recorded by the biological experimental system,monitored at the same time with oscilloscope. When recording the neural discharge, electrical stimulation of the sciatic nerves was performed once 5minutes through a double stainless electrode. 5 μL oxytocin in dosage of 0.2, 2 and 20 mg/L were injected slowly into lateral ventricle via microlitre syringe. [d(CH2)5-OVT]+OT (2 mg/L) group: 2.5 μL [d(CH2)5-OVT](80 mg/L) was injected into lateral ventricle and then 2.5 μL oxytocin (2 mg/L). Naloxone+OT (2 mg/L) group: 2.5 μL naloxone (400 mg/L) was injected into lateral ventricle and then 2.5 μL oxytocin (2 mg/L). According to frequency of discharge, effect of oxytocin at various dosages on discharge induced by neurons in hippocampal CA1 area and [d (CH2)5-OVT]and naloxone on oxytocin was assayed. MAIN OUTCOME MEASURE: Changes of discharge frequency after stimulation.RESULTS: Data of totally 36 rats were entered the final analysis. ① OT (0.2 mg/L, 2 mg/L and 20 mg/L) administered by intracerebroventricularly could decrease the evoked discharge of hippocampal CA1 neurons in a dose-dependent manner. ② The inhibitory effects of OT (2 mg/L) could be blocked by pretreated intracerebroventricularly injection of [d (CH2)5-OVT](80 mg/L, 2.5 μL). ③ Intracerebroventricular injection of naloxone (400 mg/L, 2.5 μL) could attenuate the effects of OT (2 mg/L) significantly.CONCLUSION: OT can inhibit the electrical activities of hippocampal CA1 neurons to external electrical signal through activating the oxytocin receptor. Moreover, central opioid receptor is involving in the inhibitory effects of OT.