OPIOID ACTIONS ON SINGLE NUCLEUS RAPHE MAGNUS NEURONS FROM RAT AND GUINEA-PIG INVITRO
OPIOID ACTIONS ON SINGLE NUCLEUS RAPHE MAGNUS NEURONS FROM RAT AND GUINEA-PIG INVITRO
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DOI：
10.1113/jphysiol.1990.sp018185
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发表时间：
1990-08-01
影响因子：
5.5
通讯作者：
OSBORNE, PB
中科院分区：
文献类型：
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作者：
PAN, ZZ;WILLIAMS, JT;OSBORNE, PB
1. 对大鼠（n = 128）和豚鼠（n = 115）的中缝大核（NRM）神经元进行细胞内记录。在每个细胞中发现两种类型的细胞，原发性细胞（大鼠103，豚鼠27）和继发性细胞（大鼠25，豚鼠88）。2. 原代细胞的输入电阻为186。9米。（n = 9）大鼠和255 .+-。50米。（n = 11）。每个人的动作电位持续时间约为1.5 ms。突触电位由局灶电刺激引起，包括。-氨基丁酸（GABA）和兴奋性氨基酸成分。3. 吗啡、[Met5]脑啡肽（ME）和[D-Ala2， N-Me-Phe4， Gly5-ol]脑啡肽（DAMGO）可使gaba介导的突触电位幅度最大降低50-65%，而对兴奋性氨基酸介导的突触电位影响不大。这些类阿片对大鼠和豚鼠原代细胞静息膜电位和输入阻抗均无影响。4. 次级细胞动作电位持续时间短（< 1 ms），输入电阻为354 +-。47 M.OMEGA。大鼠（n = 6）和290。40 M.OMEGA。豚鼠（n = 15）。在这组细胞中观察到的突触电位仅由兴奋性氨基酸受体激活介导。5. 在大鼠的24个神经元和豚鼠的84个神经元中，ME超极化和/或消除了自发放电。在-60毫伏的向外电流下产生的ME，在比-92 .+-更负的电位下极性反转。大鼠3 mV （n = 6）和-98。2 mV豚鼠（n = 18）。当外部钾离子浓度增加时，阿片电流的逆转电位向负电位较小的方向移动，这与能斯特方程预测的结果一致。6. 两种细胞的形态可区分，原代细胞呈椭圆形（29倍）。18 .mu。M代表老鼠；36个同学。19 .mu。（在豚鼠中），有两到四个粗的锥形树突，在50亩范围内分枝。细胞体的M。次生细胞一般为圆形或卵圆形（约24倍）。13 .mu。M代表老鼠；27个同学。17 .mu。（在豚鼠中）有2到5个细而不变细的树突。7. 结果表明，阿片类药物通过突触前抑制gaba介导的抑制性输入来增加NRM神经元群的活性。这可能是阿片类药物调节内源性疼痛调节系统中NRM下行抑制的机制之一。
1. Intracellular recordings were made from neurons of the nucleus raphe magnus (NRM) from rat (n = 128) and guinea-pig (n = 115). Two types of cells were found in each, primary (103 in rat, 27 in guinea pig) and secondary cells (25 in rat, 88 in guinea-pig). 2. Primary cells had input resistances of 186 .+-. 9 M .OMEGA. (n = 9) in rat and 255 .+-. 50 M .OMEGA. (n = 11) in guinea-pig. The action potential in each was about 1.5 ms in duration. Synaptic potentials were evoked by focal electrical stimulation and consisted of both .gamma.-aminobutyric acid (GABA) and excitatory amino acid components. 3. Morphine, [Met5]enkephalin (ME) and [D-Ala2, N-Me-Phe4, Gly5-ol]enkephalin (DAMGO) depressed the amplitude of the GABA-mediated synaptic potential by a maximum of 50-65% and had little effect on the excitatory amino acid-mediated synaptic potential. There was no effect of these opioids on the resting membrane potential or input resistance of primary cells in rat or guinea-pig. 4. Secondary cells had short duration action potentials (< 1 ms) and an input resistance of 354 .+-. 47 M.OMEGA. in rat (n = 6) and 290 .+-. 40 M.OMEGA. in guinea-pig (n = 15). The synaptic potential observed in the cells of this group was mediated by activation of only excitatory amino acid receptors. 5. ME hyperpolarized and/or abolished this spontaneous firing in sixteen out of twenty-four neurons in the secondary group from rat and eighty out of eight-four neurons from guinea-pig. ME induced at outward current at -60 mV that reversed polarity at potentials more negative than -92 .+-. 3 mV in rat (n = 6) and -98 .+-. 2 mV in guinea-pig (n = 18). The reversal potential of the opioid current was shifted to less negative potentials when the external potassium concentration was increased, as predicted by the Nernst equation. 6. The morphology of the two types of cells were distinguishable in that primary cells were oval (29 .times. 18 .mu.m in rat; 36 .times. 19 .mu.m in guinea-pig) with two to four thick tapering dendrites that branched within 50 .mu.m of the cell body. Secondary cells were generally round or oval (about 24 .times. 13 .mu.m in rat; 27 .times. 17 .mu.m in guinea-pig) with two to five thin non-tapering dendrites. 7. The results suggest that opioids increase the activity of a population of NRM neurons by presynaptic depression of GABA-mediated inhibitory input. This could be one of the mechanisms by which opioids modulate the descending inhibition from NRM in the endogenous pain-modulating system.