Analysis of decreased conductance serotonergic response in Aplysia ink motor neurons.
Analysis of decreased conductance serotonergic response in Aplysia ink motor neurons.
复制标题
海兔墨运动神经元电导血清素能反应降低的分析。
DOI：
10.1152/jn.1985.53.2.590
复制
发表时间：
1985
影响因子：
2.5
通讯作者：
Byrne,JH
中科院分区：
文献类型：
--
作者：
Walsh,JP;Byrne,JH
微压喷射5-羟色胺（5-HT）在L14墨水运动神经元产生兴奋性反应，依赖于应用的网站。喷射5-HT到细胞体上产生缓慢的反应，显示出制剂之间的电压灵敏度的变化。与此相反，喷射5-HT到神经元下的细胞体产生的反应，其幅度始终是一个线性函数的保持电位，逆转附近的预测钾平衡电位。随后的分析集中在这第二个反应。5-HT诱发的神经元放电反应呈线性电流-电压关系（约在200 μ mol/L时发生逆转）。-80 mV），与输入电导的降低有关，并且对细胞外K+浓度的变化敏感。5-羟色胺的应用在人工海水（ASW）含有30 mM K+产生的反应，扭转接近改变能斯特电位的K+。5-HT的反应似乎并不是由于二次激活的interneurons或主要依赖于细胞外的Ca 2+，因为喷射5-HT到细胞沐浴在ASW含有30 mM的CO 2+产生的反应相当，虽然有些衰减，在ASW中观察到的。5-羟色胺反应类似于ASW中产生的神经节灌注后，ASW含有Co 2+，4-氨基吡啶（4-AP），和四乙基铵（TEA）。这表明5-HT敏感电流与Ca 2+激活的快速和延迟整流K+电流是分开的。5-HT反应似乎是由cAMP水平的变化介导的。浴应用磷酸二酯酶抑制剂IBMX（3-异丁基-1-甲基黄嘌呤）或Ro 20-1724，或腺苷酸环化酶激活剂forskolin通过产生与膜电导降低相关的缓慢内向电流来模拟5-HT反应。细胞cAMP代谢的改变调节了对5-HT的反应。神经节暴露于低浓度的Ro 20-1724或毛喉素增强5-HT反应。较高浓度的这些药物在很大程度上阻断了对随后5-HT应用的反应。浴应用的8-溴衍生物的cAMP或cGMP产生了一个缓慢的内向电流与细胞的膜电导降低电压钳位在静息电位。然而，在暴露于8-溴-cAMP后，对5-HT的反应被阻断，而不是8-溴-cGMP。这些结果表明，5-HT产生的电压不依赖性降低稳态钾电导，可能是由cAMP介导的。（摘要截短至400字）
Micropressure ejection of serotonin (5-hydroxytryptamine, 5-HT) produced excitatory responses in the L14 ink motor neurons of Aplysia that depended on the site of application. Ejection of 5-HT onto the cell body produced a slow response that showed variability in voltage sensitivity between preparations. In contrast, ejection of 5-HT onto the neuropil underneath the cell body produced a response whose amplitude was consistently a linear function of the holding potential, reversing near the predicted potassium equilibrium potential. Subsequent analyses focused on this second response. The neuropil response induced by 5-HT had a linear current-voltage relationship (reversing at ca. -80 mV), was associated with a decrease in input conductance, and was sensitive to changes in the concentration of extracellular K+. Serotonin application in artificial seawater (ASW) containing 30 mM K+ produced a response that reversed close to the altered Nernst potential for K+. The 5-HT response did not appear to be due to secondary activation of interneurons or to depend primarily on extracellular Ca2+, since ejection of 5-HT onto cells bathed in ASW containing 30 mM Co2+ produced responses comparable to, although somewhat attenuated from, those observed in ASW. Serotonin responses similar to those produced in ASW were obtained after perfusing the ganglion with ASW containing Co2+, 4-aminopyridine (4-AP), and tetraethylammonium (TEA). This suggests that the 5-HT-sensitive current is separate from the Ca2+-activated, fast, and delayed rectifying K+ currents. The 5-HT response appeared to be mediated by changes in levels of cAMP. Bath application of the phosphodiesterase inhibitors IBMX (3-isobutyl-1-methylxanthine) or Ro 20-1724, or the adenylate cyclase activator forskolin mimicked the 5-HT response by producing a slow inward current associated with a decrease in membrane conductance. Alteration of cellular cAMP metabolism modulated the response to 5-HT. Exposure of the ganglion to low concentrations of either Ro 20-1724 or forskolin potentiated the 5-HT response. Higher concentrations of these agents largely blocked the response to subsequent 5-HT applications. Bath application of the 8-bromo derivative of either cAMP or cGMP produced a slow inward current associated with a decrease in membrane conductance in cells voltage clamped at the resting potential. Responses to 5-HT were blocked, however, after exposure to 8-bromo-cAMP, but not to 8-bromo-cGMP. These results suggest that 5-HT produces a voltage-independent decrease in a steady-state potassium conductance that may be mediated by cAMP.(ABSTRACT TRUNCATED AT 400 WORDS)