Long-term potentiation induced by nicotine in CA1 region of hippocampal slice is Ca(2+)-dependent.
Jin He, Chunyu Deng, Ruzhu Chen, Xiaonan Zhu, Jianping Yu
Abstract
Jin He, Chunyu Deng, Ruzhu Chen, Xiaonan Zhu, Jianping Yu
Abstract
AIM: To observe the effects of Ca2+ on hippocampal long-term potentiation (LTP) induced by nicotine in CA1 region of rat hippocampal slice. METHODS: Extracellularly recorded population spikes (PS) of the pyramidal cell layer in the hippocampal CA1 region in vitro. RESULTS: Nicotine 1 mumol.L-1 induced LTP in the hippocampal CA1 region. It did not induce LTP in CA1 region when CA2+ was removed from artificial cerebrospinal fluid (ACSF). Nifedipine 1 and 10 mumol.L-1 partly inhibited LTP induced by nicotine, and thapsigargin 1 and 10 mumol.L-1 completely inhibited LTP induced by nicotine. CONCLUSION: LTP induced by nicotine in hippocampal CA1 region is Ca(2+)-dependent. Both Ca2+ influx and Ca2+ release participate in the induction of LTP.
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AIM: To observe the effects of Ca2+ on hippocampal long-term potentiation (LTP) induced by nicotine in CA1 region of rat hippocampal slice. METHODS: Extracellularly recorded population spikes (PS) of the pyramidal cell layer in the hippocampal CA1 region in vitro. RESULTS: Nicotine 1 mumol.L-1 induced LTP in the hippocampal CA1 region. It did not induce LTP in CA1 region when CA2+ was removed from artificial cerebrospinal fluid (ACSF). Nifedipine 1 and 10 mumol.L-1 partly inhibited LTP induced by nicotine, and thapsigargin 1 and 10 mumol.L-1 completely inhibited LTP induced by nicotine. CONCLUSION: LTP induced by nicotine in hippocampal CA1 region is Ca(2+)-dependent. Both Ca2+ influx and Ca2+ release participate in the induction of LTP.
Key concepts: Long-term potentiation, Hippocampal formation, Population spike, Nicotine, Chemistry, Thapsigargin, Population, Hippocampus