Takahashi M, Ogawa M, Ohta H, Ikeda H
Department of Neuropsychiatry, Kochi Medical School, Japan.
Brain Res. 1992 May 8;579(2):204-10. doi: 10.1016/0006-8993(92)90052-b.
We studied the effects of vasoactive intestinal polypeptide (VIP) on the cholinergic synaptic transmission that was developed between rat sympathetic neurons in culture. Electrophysiological examinations revealed that the amplitude of fast excitatory postsynaptic potential (fast EPSP) was increased by VIP (0.2-0.8 microM) reversibly and dose-dependently, whereas transient nicotinic depolarization evoked by pressure application of acetylcholine (ACh) was not affected by VIP. In most of the cells examined, VIP depolarized membrane potential by a few millivolts with concomitant increases in membrane conductance. Furthermore, the VIP-induced depolarization was suppressed by Co2+ but not by hexamethonium or atropine. Hence it is highly likely that the peptide augmented the amplitude of fast EPSPs by increasing ACh release from the presynaptic cell. These results demonstrate that VIP influences the presynaptic phase of cholinergic synaptic transmission between sympathetic neurons.
我们研究了血管活性肠肽（VIP）对培养的大鼠交感神经元之间形成的胆碱能突触传递的影响。电生理检查显示，VIP（0.2 - 0.8微摩尔）可使快速兴奋性突触后电位（快速EPSP）的幅度可逆且剂量依赖性增加，而通过压力施加乙酰胆碱（ACh）诱发的瞬时烟碱样去极化不受VIP影响。在大多数检测的细胞中，VIP使膜电位去极化几毫伏，同时膜电导增加。此外，VIP诱导的去极化被Co2 +抑制，但不被六甲铵或阿托品抑制。因此，该肽极有可能通过增加突触前细胞释放ACh来增大快速EPSP的幅度。这些结果表明，VIP影响交感神经元之间胆碱能突触传递的突触前阶段。
