大麻素受体对大鼠海马中 ATP 诱导的 LTP 的调制。
Modulation of ATP-induced LTP by cannabinoid receptors in rat hippocampus.
机构信息
Department of Cellular Membranology, Bogomoletz Institute of Physiology, Kiev, Ukraine.
出版信息
Purinergic Signal. 2012 Dec;8(4):705-13. doi: 10.1007/s11302-012-9296-5. Epub 2012 Mar 28.
Cannabinoids exert powerful action on various forms of synaptic plasticity. These retrograde messengers modulate GABA and glutamate release from presynaptic terminals by acting on presynaptic CB1 receptors. In particular, they inhibit long-term potentiation (LTP) elicited by electrical stimulation of excitatory pathways in rat hippocampus. Recently, LTP of the field excitatory postsynaptic potential (fEPSP) induced by exogenous ATP has been thoroughly explored. The present study demonstrates that cannabinoids inhibit ATP-induced LTP in hippocampal slices of rat. Administration of 10 μM of ATP led to strong inhibition of fEPSPs in CA1/CA3 hippocampal synapses. Within 40 min after ATP removal from bath solution, robust LTP was observed (fEPSP amplitude comprised 130.1 ± 3.8% of control, n = 10). This LTP never appeared when ATP was applied in addition to cannabinoid receptor agonist WIN55,212-2 (100 nM). Selective CB1 receptor antagonist, AM251 (500 nM), completely abolished this effect of WIN55,212-2. Our data indicate that like canonical LTP elicited by electrical stimulation, ATP-induced LTP is under control of CB1 receptors.
大麻素对各种形式的突触可塑性发挥强大作用。这些逆行信使通过作用于突触前 CB1 受体来调节 GABA 和谷氨酸从突触前末梢的释放。特别是，它们抑制了大鼠海马兴奋性通路电刺激引起的长时程增强（LTP）。最近，已彻底研究了由外源性 ATP 诱导的场兴奋性突触后电位（fEPSP）的 LTP。本研究表明，大麻素抑制大鼠海马切片中 ATP 诱导的 LTP。给予 10 μM 的 ATP 可导致 CA1/CA3 海马突触中的 fEPSP 强烈抑制。在从浴液中去除 ATP 后 40 分钟内，观察到强烈的 LTP（fEPSP 幅度占对照的 130.1±3.8%，n=10）。当 ATP 与大麻素受体激动剂 WIN55,212-2（100 nM）一起应用时，这种 LTP 从未出现过。选择性 CB1 受体拮抗剂 AM251（500 nM）完全消除了 WIN55,212-2 的这种作用。我们的数据表明，与电刺激引起的典型 LTP 一样，ATP 诱导的 LTP 受 CB1 受体的控制。
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