Abstract
Chronic developmental lead (Pb) exposure to the rat has been reported to impair the long-term potentiation (LTP) in area CA1 and DG of the hippocampus. The present study was performed to investigate the effects of chronic Pb exposure on homosynaptic short-term depression (STD) and long-term depression (LTD) of population spikes (PS) in area CA1 of the rat hippocampus in vivo. Neonatal Wistar rats were exposed to Pb from parturition to weaning via the milk of dams fed with 0.2% lead acetate solution. The input/output (I/O) function, paired-pulse reaction (PPR), the PS were measured in the area CA1 in response to low frequency stimulation (LFS). The results showed that the homo-STD amplitude of PS depotentiation in Pb-exposed rats (87.48 ± 7.44%, n=14) was less significant than that in control rats (72.34 ± 6.05%, n=18, P < 0.05), and the homo-LTD amplitude of PS depotentiation in Pb-exposed rats (72.80 ± 5.86%, n=14) was even less significant than that in control rats (47.80 ± 5.03%, n=18, P < 0.01). The results suggest that chronic Pb exposure in neonatal rats caused impairments in the STD and LTD of area CA1 of hippocampus.
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