The work was carried out to investigate the effects of clonidine on Ach quantal release of presynaptic nerve terminals in guinea pig celiac ganglia in vitro by means of intracellular recording technique. After perfusion of celiac ganglia with clonidine ( 10?mol/L ) for 7 ~10 min, the frequency of spontaneous miniature excitatory postsynaptic potentials ( mEPSP ) which was increased by high K+ (15 mmol/L ) , diminished about 35% with little change in amplitude. Under condition of low Ca2+( 0.5mmol/L )/high Mg2+( 5.5mmol/L ) presynaptic nerve was repetitively stimulated by 200 pulses ( 1 Hz), the failure number of EPSP increased from 82 to 145 in 200 stimuli and the quantal content ( m ) decreased about 62% with little change in quantal size ( q ) under clonidine ( 10?mol/L ) action. It is indicated that clonidine can decrease Ach auantal release from presynaptic nerve terminals without effecting Ach content in vesicles, and is one of the mechanisms for depressant effect of clonidine on synaptic transmission of the sympathetic ganglia.

In experimental teaching of medical physiology for medical students,simulation experiment,which is developed from animal substitute and animal protection,can mimic animal ex-periments by multiple medias,and result in increasing students' study interests,enhancing the teaching effects and decreasing the cost of goods including experiment animals.However,the ratio of simulation experiment to experimental teaching of medical physiology needs to be discussed and determined in future.

Aim To explore the neuroprotective effects of preconditioning with resveratrol on focal cerebral ischemia-reperfusion injury in rats.Methods Forty-five Sprague-Dawley rats were randomly divided into sham group,ischemic-reperfusion group(I/R)and resveratrol preconditioning ischemic-reperfusion group(Res+I/R).Each group had 15 animals.The middle cerebral artery in rats was occluded for 90 min by an intraluminal filament and then reperfused to cause transient focal cerebral ischemia.In the resveratrol preconditioning group,the resveratrol(30 mg?kg-1)was injected intraperitoneally 30 min before ischemia.Twenty-four hours after reperfusion,the infarct volume was shown with 2,3,5-triphenyl tetrazolium chloride(TTC)staining.The spatial learning and memory ability of rats was measured by Morris water maze 72 h after reperfusion.Electrophysiological recordings were conducted to detect the effects of resveratrol on Schaffer collateral-CA1 synaptic transmission in ischemic rats.Results The infarct volume and neurological score in Res+I/R group were lower than I/R group(P

Aim To investigate whether capacitative Ca~(2+) entry involved in excitation-contraction coupling in rat distal colon smooth muscle.Methods Changes of isolated organ's tension were monitored with force-displacement transducer and Powerlab 4/25T recording system.Results Thapsigargin(10 nmol?L~(-1)～1 ?mol?L~(-1))produced slowly developing sustained contractions in isolated distal colon smooth muscle strips of rats.The timed contractile responses to thapsigargin(10 n mol?L~(1)-1 ?mol?L~(-1)) were significantly different.The contractile response to Ca~(2+) reintroduction following incubation of strips in a Ca~(2+)-free Krebs in the presense of thapsigargin was significantly higher than in its absence(99%?28% vs 70%?8%).Contractile responses to Ca~(2+)reintroduction following depletion of sarcoplasmic reticulum Ca~(2+) stores with thapsigargin were attenuated by La~(3+),while unaffected by verapamil.Conclusion Contractile responses to Ca~(2+)reintroduction following depletion of sarcoplasmic reticulum Ca~(2+)stores with thapsigargin,are mediated by capacitative Ca~(2+)entry.The results suggested that CCE provided activator Ca~(2+)for the contraction and participated in excitation-contraction process in rat distal colon smooth muscle.

Besides cyclooxygenase and nitric oxide synthase, another distinct endothelial pathway, endothelium-dependent hyperpolarization factor (EDHF), is involved in relaxation of the vascular smooth muscle cells. EDHF has been demonstrated unequivocally in various blood vessels from different species, including human, and is likely to play an important role in cardiovascular physiology and pharmacology.

Aim To study the effect of total flavones of Rhododendra(TFR)on bioelectricity changes of ventricular myocytes in guinea pigs. Methods Conventional microelectrode technique was used to record action potentials (AP) , resting potentials (RP) and effective refractory period (ERP). Results TFR 25,50 mg?L-1 decreased the action potential duration at 50%,90% repolarization (APD50,APD90) while TFR 100,200,400 mg?L-1 prolonged APD50 and APD90Significantlg. TFR 200,400 mg?L-1markedly decreased action potentials amplitude (APA) and velocity maximum of depolarization (Vmax). TFR 400 mg?L-1decreased resting potential. TFR 200 mg?L-1 prolonged ERP. Conclusion TFR may antagonize Ca2+ inward flow at lower concentration and block K+ inward flow at higher concentration.

Objective To investigate the effects of bisphenol A(BPA)exposure to perinatal on learning and memory behaviour in F1 generation male rats.Methods From the 11th day of gestation to the 7th day of field test was used to detect the locomotion activity,the Morris water maze was employed to measure learning and memory ability and long-term potentiation(LTP)were recorded to detect the synaptic plasticity in hippocampus CA1 with extracellular recording.Results The crossing number of BPA group(70.35±13.56)was much more than control group((29.32±14.12),P＜0.05).The number of standing up and ornament of BPA group((38.52±6.52),(6.26±2.78))were both higher than control group((10.35±8.38),(2.67±1.46),P＜0.05).BPA rats had longer escape latencies to find platform((55.22±5.78)s)than control rats((21.22±2.65)s,P＜0.05).Conditional protocol with high-frequency stimulation evoked a stable LTP in hippocampus CA1 region in control rats((162.13±10.12)%),however the LTP could not be induced with the same conditional protocol in BPA-exposed rats((101.05±7.58)%,P＜0.05).Conclusion Perinatal BPA exposure impaires learning and memory ability in F1 generation male rats related to presynaptic dysfunction.