کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
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2587550 | 1130933 | 2007 | 7 صفحه PDF | دانلود رایگان |
The present study aims at evaluating the impairment of LTP and depotentiation (DP) of LTP induced by acute lead exposure, and the effects of peripheral carbachol (CCh) application on LTP/DP of acute and chronic lead-exposed rats in dentate gyrus in vivo. Rats (80–100 days) were acutely exposed to lead by intraperitoneal injection of 0.2% lead acetate (PbAc) solution (1.5 mg/100 g) and/or CCh (1 μg/100 g). Rats were chronically exposed to lead from parturition through adulthood (80–100 days) by the drinking of 0.2% PbAc solution and/or CCh (1 μg/100 g) chronic intraperitoneal injection one week. The input–output (I/O) function, paired-pulse reaction (PPR), excitatory postsynaptic potential (EPSP) and population spike (PS) amplitude were measured in response to stimulation applied to the lateral perforant path. Results showed that: first, acute lead exposure significantly depressed the amplitudes of LTP/DP of both EPSP slope and PS amplitude. Second, CCh significantly increased the amplitudes of both EPSP LTP/DP and PS LTP of acute Pb-exposed rats. After CCh treatment, the magnitudes of EPSP LTP/DP and PS LTP of acute Pb-exposed rats showed no significant difference with controls. Third, Chronic CCh application also reversed chronic Pb-induced impairment of PS LTP and EPSP DP of LTP. As CCh does not cross blood-brain barrier in healthy animals, the data suggest that CCh may traverse BBB in Pb-exposed animals and cure Pb-induced dysfunction of learning and memory.
Journal: Food and Chemical Toxicology - Volume 45, Issue 3, March 2007, Pages 412–418