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Food Chem Toxicol. 2003 Nov;41(11):1617-23.

Effects of sodium valproate on synaptic plasticity in the CA1 region of rat hippocampus.

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  • 1School of Life Science, University of Science and Technology of China, Hefei, Anhui, 230027, PR China.


Sodium valproate (VPA) is currently one of the major anticonvulsant drug in clinical use and has a wide spectrum of antiepileptic activity. Previous studies have reported that VPA impairs long-term potentiation (LTP). In the present study, we used two forms of synaptic plasticity, LTP and long-term depression (LTD) of field excitatory postsynaptic potential (fEPSP) to investigate the effects of VPA on synaptic plasticity in rat hippocampal slices. Paired-pulse facilitation (PPF) and field EPSP were recorded in the CA1 area of hippocampal slices exposed to VPA. The results showed that: (1) three different concentrations of VPA (0.6, 1 and 5 mM) all induced a significant impairment of PPF at 20-150 ms inter-pulse intervals (IPI) (P<0.05). (2) acute VPA exposure (0.6 mM) inhibited the induction of LTP (Control: 171 +/- 20%, n=8; VPA-exposed: 117 +/- 16%, n=9, P<0.01) and LTD (Control: 86 +/- 13%, n=8; VPA-exposed: 98 +/- 8%, n=10, P<0.01); and (3) GABA(A) receptor antagonist picrotoxin (PTX) (10 microM) reversed VPA-induced deficits of LTP (VPA-exposed: 117 +/- 16%, n=9; VPA-exposed+PTX: 153 +/- 20%, n=8, P<0.01). However, PTX had no significant effect on impairment of LTD (VPA-exposed: 98 +/- 8%, n=10; VPA-exposed+PTX: 97 +/- 3%, n=8, P>0.05). These results suggested that VPA impaired LTP and LTD. Furthermore, VPA-induced impairment of LTP could be correlated with the enhancement of inhibitory neurotransmission mediated by gamma-aminobutyric acid (GABA) receptor.

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