Egan T M, Henderson G, North R A, Williams J T
J Physiol. 1983 Dec;345:477-88. doi: 10.1113/jphysiol.1983.sp014990.
Intracellular recordings were made from neurones in the nucleus locus coeruleus (l.c.) in slices of rat pons maintained in vitro. Focal electrical stimulation to the slice surface within the region of the l.c. evoked a synaptic depolarization followed by a hyperpolarization. These potentials were graded with stimulus intensity and were abolished in calcium-free and/or high-magnesium solutions. The nature of the hyperpolarizing synaptic potential (i.p.s.p.) was investigated. The i.p.s.p. amplitude decreased as the membrane was artificially made more negative and reversed at -114 mV. This reversal potential shifted to less negative potentials in solutions of elevated potassium ion content as predicted by the Nernst equation. The i.p.s.p. was potentiated in amplitude and its time course was prolonged by desmethylimipramine (DMI). Yohimbine (100 nM) and phentolamine (100 nM) reversibly abolished the i.p.s.p. and did not change the synaptic depolarization. Noradrenaline hyperpolarized all l.c. neurones tested, whether applied by perfusion (1-30 microM) or by pressure ejection from a micropipette placed in the solution near the recording site. The noradrenaline-induced hyperpolarization was accompanied by an increase in conductance and it reversed in polarity at -104 mV. The reversal potential of the noradrenaline hyperpolarization became less negative when the potassium ion content was increased. The noradrenaline-induced hyperpolarization was potentiated by DMI and was antagonized by yohimbine and phentolamine in the same concentrations which blocked the i.p.s.p. The results support the notion that l.c. neurones can release noradrenaline onto the somadendritic membrane of other l.c. neurones and thereby provide local feed-back inhibition.
在体外维持的大鼠脑桥切片中，对蓝斑核（l.c.）中的神经元进行细胞内记录。对l.c.区域内的切片表面进行局部电刺激，诱发突触去极化，随后是超极化。这些电位随刺激强度分级，并在无钙和/或高镁溶液中消失。研究了超极化突触电位（i.p.s.p.）的性质。i.p.s.p.幅度随着膜电位人为地变得更负而降低，并在-114 mV时反转。如能斯特方程所预测，在钾离子含量升高的溶液中，这种反转电位向较不负极性的方向移动。去甲丙咪嗪（DMI）使i.p.s.p.幅度增强，其时程延长。育亨宾（100 nM）和酚妥拉明（100 nM）可逆转地消除i.p.s.p.，且不改变突触去极化。无论通过灌注（1 - 30 microM）还是通过从置于记录部位附近溶液中的微量移液器进行压力喷射施加，去甲肾上腺素都会使所有测试的l.c.神经元超极化。去甲肾上腺素诱导的超极化伴随着电导增加，并在-104 mV时极性反转。当钾离子含量增加时，去甲肾上腺素超极化的反转电位变得较不负极性。去甲肾上腺素诱导的超极化被DMI增强，并被与阻断i.p.s.p相同浓度的育亨宾和酚妥拉明拮抗。结果支持这样的观点，即l.c.神经元可以将去甲肾上腺素释放到其他l.c.神经元的胞体树突膜上，从而提供局部反馈抑制。
