Evaluation of opioid-induced respiratory center inhibition in medulla

膜潜力和抵抗力（Rm）在灵感中得到了衡量（Insp，I-III型）、前激性（Pre-I）和外激性（Exp）在体外肠梗阻性静脉中的神经元（RVLM）在微阿片类受体拮抗剂吗啡和DAGO中的应用（Try-D-Ala-Gly-[N MePhe]-Gly-ol）， κ-阿片类受体拮抗剂U 50488（trans-（±）-3，4-Dichloro-N-methyl-N-[2-]（1-吡咯烷基）-环己基]-苯二乙酰胺甲氟酸酯）或δ-阿片类受体抑制剂DPDPE（{D-pen-D12，5-D1]-enkephalin）。DAGO （1-M）、morphine （10-M） and U50488 （10-M） led to a significant concomitant decrease in burst rate of C4 nerve activity and of Insp neurones。阿片类受体治疗师并不因为I前神经元和大多数神经元的任何明显影响。40%的Insp神经元，是由阿片类受体抑制剂抑制的，显示出超极化和退化的Rm。45%的Insp神经元也显示了超极化和超极化 ... More decreased Rm with opioid receptor agonists在四氯多毒素灌注下被抑制，A simultaneous intracellular recording from Insp neurones and an extracellular recording from Pre-I neurones确认的观察的异常后synaptic Potentials （EPSPs）或抑制后synaptic Potentials synchronized with the corresponding period of Pre-I neurones in Insp neurones during opioid-induced respiratory depression，in inspneurones during opioid-induced respiratory depression，EPSPs是通过刺激反相结合的medulla oblongata，成为在Insp神经元中弯曲的温和曲线。这是一个关于阿片类受体抗插入神经元的预反应的建议。即使在超极化神经元中，EPSPs曲线变得温和，我们建议神经元的存在，这些神经元同时展示了两种前和后合成抑制作用。我们将阿片类受体直接抑制了新生大鼠RVLM中的神经元和分流神经元网络包括在内。阿片类诱导的抑制剂对Insp神经元的作用似乎出现在前合成和后合成位点中。Less（低）

Membrane potential and resistance (Rm) were measured in inspiratory (Insp, type I-III), preinspiratory (Pre-I) and expiratory (Exp) neurones in rostral ventrolateral medulla (RVLM) of the isolated brainstem-spinal cord preparation from newborn rats during bath application of μ-opioid receptor agonists morphine and DAGO (Try-D-Ala-Gly-[N MePhe]-Gly-ol), κ-opioid receptor agonist U50488 (trans-(±)-3, 4-Dichloro-N-methyl-N-[2-(1-pyrrolidiny)-cyclohexyl]-benzeneacetamide methanesulfonate) or δ-opioid receptor agonist DPDPE ({D-penィイD12,5ィエD1]-enkephalin).DAGO (1 μM), morphine (10 μM) and U50488 (10 μM) led to a significant concomitant decrease in burst rate of C4 nerve activity and of Insp neurones. The opioid receptor agonists did not cause any significant effects in Pre-I and most Exp neurones. Forty percent of Insp neurones, which were inhibited with opioid receptor agonists, showed hyperpolarization and decreased Rm. Forth-five percent of Insp neurones also showed hyperpolarization and … More decreased Rm with opioid receptor agonists under tetrodotoxin perfusion.A simultaneous intracellular recording from Insp neurones and an extracellular recording from Pre-I neurones confirmed the observation of excitatory postsynaptic potentials (EPSPs) or inhibitory postsynaptic potentials synchronized with the corresponding period of Pre-I neurones in Insp neurones during opioid-induced respiratory depression.During opioid-induced respiratory depression, EPSPs evoked by stimulation to contralateral medulla oblongata became gentle in curve in Insp neurones. This suggests that opioid receptor agonists exert presynaptic action on Insp neurones. Even in hyperpolarized neurones, the EPSPs curve became gentle, which suggests the presence of neurones that simultaneously exhibit both pre- and postsynaptic inhibitory effects.We conclude that opioid receptor agonists directly inhibit Insp neurones and disturb respiratory networks in the RVLM of newborn rats. The opioid-induced inhibitory action on Insp neurones is appeared to be both the pre- and postsynaptic sites. Less