Effects of samarium chloride on nicotinic transmission in superior cervical ganglia of rats

Ping HE; Ning MO

ABSTRACT

BACKGROUND:

The rare earth elements (Res) have multiple bio-activities and some extent neurotoxicity, Because of their distinct physical and chemical properties. The studies on neuromuscular junction and sympathet ic ganglia have shown that some Res, such as lanthanum(La), gadolinium (Gd),etc, exert considerable effects on synaptic transmission, but the effects and mechanism of Samarium on synaptic transmission are still unknown.

OBJECTIVE:

To investigate the effects and impossible mechanism of Samarium Chloride (SmCl3) on the nicotinic transmission in the isolated sympathetic ganglia, superior cervical ganglion (SCG) of rats.

DESIGN:

Controlled experimental study based on cells.

SETTING:

Department of Pharmacology, Guangxi Medical University. MATERIALS Totally 40 adult Wistar rats (weighing 250-300 g) of either sex, provided by the Experimental Animal Center of Guangxi Medical University, were used in this study. SmCl3 was made by the chlorination of Samarium Oxide with purity 99.5% and relative molecule mass 348.7, presented by Professor Liu Da-yuan, Guangxi Medical University. Acetylcholine chloride (Ach) and carbachol (Carb) were purchased from Sigma.

METHODS:

The experiment was completed at the neuropharmacology lab of the experimental center of Guangxi Medical University from September 2001 to December 2002. After sacrificing animals by acute exsanguination,SCG together with their preganglionic nerve trunks were isolated rapidly,then transferred to the recording chamber, the preganglionic nerve trunk was drawn into a suction electrode for orthodromic stimulation. The ganglia were superfused continuously with a Krebs solution, saturated with 950 mL/L 02 and 5mL/L CO2, pH 7.4±0.05, (34±0.5) ℃.The fiber containing glass microelectrodes filled with 3 mol/L KC1 (30-60 MΩ tip resistance) were used to impaled cells and do intracellular recording. The fast excitatory postsynaptic potentials (FEPSPs) were evoked in SCG neurons by single pulse stimulations (0.2-0.5 Hz, 0.5-1.0 ms, 2-10 V)on preganglionic nerve trunk. The remarkable membrane depolarization would be recorded in SCG neurons by superfusing ganglia with exogenous Ach (0.1 mmol/L) or Carb(0.1 mmol/L) for 30-60 s. The effects of 1×(10-7-10-4) mol/L SmCl3 on FEPSPs, membrane potentials, membrane resistance, exogenous Ach and Carb-induced membrane depolarization of SCG neurons were investigated in this experiment.The effects of SmCl3 on the facilitation of high Ca2+ (10 mmol/L ) on FEPSPs were also be observed, namely, first superfusing the ganglia with high Ca2+ (10 mmol/L)to facilitate FEPSPs, then superfusing the ganglia with Ca2+(10 mmol/L)contained SmCl3. All the drugs were solved in Krebs solution or improved Krebs solution and applied to ganglia by superfusion in known concentration.The bioelectricity difference before and after the drug superfusion were analyzed by paired Student's t test.MAIN OUTCOME MESURES ①Effects of SmCl3 on FEPSPs.②Effects of SmCl3 on membrane potentials and membrane resistances. ③Effects of SmCl3 on exogenous Ach and Carb-induced membrane depolarization. ④Effects of SmCl3 on the facilitation of high Ca2+ (10 mmol/L ) on FEPSPs.

RESULTS:

① 1 ×(10-7-10-4)mol/L SmCl3 could reversibly depressed the FEPSPs of rats SCG neurons [the amplitude inhibitory percentage of FEPSPs of l×10-4, 1×10-5, 1×10-6, 1×107 mol/L SmCl3 was (49.78±13.85)%(n=20),(39.05±4.05)%(n=10),(29.83±9.73)%(n=10)and (16.30±2.16)%(n=10)respectively (P ＜ 0.05-0.01)].1×10-4 mol/L SmCl3 could chang Aps into FEPSPs (n=5).②The membrane depolarization induced by Ach (n=5) and Carb (n=7) were not significantly changed by 1×10-4 mol/L SmCl3(P ＞ 0.05).③The membrane potential and membrane resistance were not significantly altered by 1×(10-7-10-4)mol/L SmCl3(n=67), P ＞ 0.05. ④1×10-4 mol/L SmCl3 could antagonized the facilitation of high Ca2+ (10 mmol/L ) on FEPSPs (n=5), P ＜ 0.01.

CONCLUSION:

SmCl3 can depresses nicotinic transmission in rats sympathetic ganglia by presynaptic mechanisms, perhaps due to its inhibition on Ca2+ influx.