发育期铅、铝共同暴露与单独铝暴露引起的大鼠海马突触可塑性损伤的差异

THE DIFFERENCE OF DAMAGE OF SYNAPTIC PLASTICITY BETWEEN ALUMINIUM EXPOSURE AND ALUMINIUM-LEAD EXPOSURE IN DENTATE GYRUS OF POSTLACTATIONAL RATS

铝近年来被认为是一种神经毒,可以引起动物和人认知及行为的损伤。应用在位电生理技术发现慢性0.2%氯化铝暴露(从出生到成年)损伤了大鼠海马齿状回归一化群峰电位(PS)的长时程增强(LTP),明显降低了兴奋性突触后电位(fEPSP)LTP的去长时程增强(DP)和归一化PS LTP的DP幅度,而对fEPSP的LTP影响不大。铅是人们公认的神经毒,能造成中毒者智力、认知和行为的损伤。铅、铝作为常见的环境毒,在我们周围并存。探讨了发育期的铅、铝共同暴露和单独铝暴露所造成的突触可塑性损伤的差异。结果表明,发育期的铅、铝共同暴露明显比单独铝暴露引起的归一化PS LTP和PS LTP 的DP的损伤要严重,并引起了fEPSP 的LTP损伤。

Aluminum (Al) is thought as a neurotoxic agent recently, which induces abnormality of neurobehavior and cognition in animals and human beings. The neurotoxicity of lead was known from ancient time, which causes intelligence, neurobehavioral and cognitive defect. The effects of chronic 0.2% AlCl3 exposure on synaptic plasticity of LTP and DP of LTP and the difference of the impairment of synaptic plasticity between Al-exposed and Al and Lead (Pb) exposure (0.3% PbAc) in postlactational rat dentate gyrus (DG) were studied by eletrophysiological technique in vivo. There was no significant difference of the I/O of both fEPSP slope and PS amplitude (P>0.05) between control and Al-exposed rats, which means that chronic 0.2% AlCl3 exposure had no effect on baseline synaptic transmission evoked by single-shock and failed to influence synchronous firing of many dentate granule cells. Both of the I/O of fEPSP slope and PS amplitude had significant difference (P< 0.05) between Al-exposed and Al+Pb-exposed rats, which means that chronic Al and Pb postlactational exposure affected baseline synaptic transmission evoked by single-shock and attenuated synchronous firing of many dentate granule cells. There was no significant difference of EPSP-Spike plot among control, Al and Al+Pb group which indicates depression in granule cell excitability to synaptic input by Al or Al and Pb applying. The average peak facilitation was 181.1±15.9% in control (n=8), 189.6±10.5% in Al-exposed (n= 7), and 129.6±15.0% in Al+Pb-exposed (n=6) rats. There were no significant differences of the facilitation period duration and the peak facilitation between control and Al-exposed rats(P>0.05), which were significant depressed in Al+Pb-exposed rats(P<0.05). There was no significant change of fEPSP LTP amplitude between control and Al-exposed rats (P> 0.05), which significant reduced to 123.3±5.8% by Al+Pb exposure(P<0.05). After LFS, fEPSP LTP of control rats depressed from 140.6±15.6% to 122.1±4.5%,a DP of 18.5%; fEPSP LTP of Al-exposed rats depressed from 134.9±7.4% to 120.0±1.7%, a DP of 14.9%; fEPSP LTP of Al+Pb-exposed rats depressed from 123.3±5.8% to 110.8±7.0%, a DP of 12.5%. The results demonstrated that chronic 0.2% Al exposure had no effects on fEPSP LTP,but DP of fEPSP LTP was impaired; Developmental Al and Pb exposure induced impairment of fEPSP LTP and reduced the amplitude of DP of fEPSP LTP to 12.5%. Normalized PS LTP was 146.7±3.6% in controls(n=8), which was significant reduced to 126.5±3.6%(n=7, P<0.05)by chronic Al applying. After Al and Pb exposure, it was more depressed (105.0±1.1%, n=6, P<0.05). After LFS,normalized PS LTP of controls was depressed from 146.7±3.6% to 127.1±1.7%,and DP of 19.6%; LFS reduced normalized PS LTP of Al-exposed rats from 126.5±3.6% to 115.2±1.3%, DP of 11.3%; and from 105.0±1.1% to 104.6±1.4%, a DP of 0.4% in Al+Pb-exposed rats. The results showed that chronic Al exposure induced impairment of normalized PS LTP and DP, it was more serious in developmental Al and Pb exposed rats.