Anticonvulsant A1 receptor-mediated adenosine action on neuronal networks in the brainstem-spinal cord of newborn rats
Anticonvulsant A1 receptor-mediated adenosine action on neuronal networks in the brainstem-spinal cord of newborn rats
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DOI：
10.1016/s0306-4522(99)00544-8
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发表时间：
2000-01-01
期刊：
影响因子：
3.3
通讯作者：
Ballanyi, K
中科院分区：
文献类型：
--
作者：
Brockhaus, J;Ballanyi, K
腹侧呼吸组神经元的膜电位以及吸气相关的颅（舌下）和脊髓（C-1-Th-4）神经活动进行了分析，在脑干脊髓制备从新生大鼠。阻断Cl-介导的抑制荷包牡丹碱（加士的宁）既不影响节律性去极化，也不影响尖峰放电的30腹侧呼吸组细胞中的23。在其他7个神经元中，抑制性突触后电位的阻断诱发了明显的去极化和棘波放电，这是同步的神经节样脊神经活动。呼吸舌下神经活动持续横断脊髓交界处后，而脊髓节律被阻断。横断后，中度荷包牡丹碱诱发的舌下神经活动的神经纤维样扰动被取消和节律性腹侧呼吸组神经元活动不受干扰，而癫痫样放电持续在脊神经。腺苷或A（1）腺苷受体激动剂2-氯-N-6-环戊基腺苷可逆转扰动腹侧呼吸群神经元的小亚群的神经元样活动和去极化。A（2）受体激动剂CGS 21860无影响。在对照组中，腺苷、2-氯-N-6-环戊基腺苷或CGS 21860也不改变吸气神经活动和膜电位波动（35个细胞中的29个）。在其他六个细胞中，腺苷引起超极化（
Membrane potential of ventral respiratory group neurons as well as inspiratory-related cranial (hypoglossal) and spinal (C-1-Th-4) nerve activities were analysed in brainstem-spinal cord preparations from neonatal rats. Block of Cl--mediated inhibition with bicuculline (plus strychnine) affected neither rhythmic depolarizations nor spike discharge in 23 of 30 ventral respiratory group cells. In the other seven neurons, block of inhibitory postsynaptic potentials evoked pronounced depolarizations and spike discharge that was synchronous with seizure-like spinal nerve activity. Respiratory hypoglossal nerve activity persisted after transection at the spinomedullary junction, whereas spinal rhythm was blocked. After transection, the moderate bicuculline-evoked seizure-like perturbation of hypoglossal nerve activity was abolished and rhythmic ventral respiratory group neuron activity was not disturbed, whereas epileptiform discharge persisted in spinal nerves. The seizure-like nerve activity and depolarization of the minor subpopulation of perturbed ventral respiratory group neurons were reversed by either adenosine or the A(1) adenosine receptor agonist 2-chloro-N-6-cyclopentyladenosine. The A(2) receptor agonist CGS 21860 had no effect, In control preparations, inspiratory nerve activity and membrane potential fluctuations (29 of 35 cells) were nor changed by adenosine, 2-chloro-N-6-cyclopentyladenosine or CGS 21860. In the other six cells, adenosine evoked a hyperpolarization (