NEUROPHYSIOLOGY AND PHARMACOLOGY OF LONG-TERM POTENTIATION IN THE RAT SYMPATHETIC-GANGLION
NEUROPHYSIOLOGY AND PHARMACOLOGY OF LONG-TERM POTENTIATION IN THE RAT SYMPATHETIC-GANGLION
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DOI：
10.1113/jphysiol.1985.sp015599
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发表时间：
1985-01-01
影响因子：
5.5
通讯作者：
MCAFEE, DA
中科院分区：
文献类型：
--
作者：
BRIGGS, CA;BROWN, TH;MCAFEE, DA
短暂强直刺激节前神经可引起大鼠上级颈交感神经节烟碱突触传递的持续增强。定量测量强直后增加突触功效揭示了2个不同的时间过程。早期，迅速衰减的组件，称为强直后增强（PTP），有一个衰减时间常数为2-3分钟。最持久的组件，称为长时程增强（LTP）的持续时间是非常依赖于温度，持续时间长得多，在32 ℃。C比在22.degree. C.在32 ℃下进行的实验中，C，LTP在短暂强直刺激后1小时或更长时间内未显示可检测到的衰减。其它实验在22 ℃下进行。C. LTP的诱导依赖于细胞外[Ca ~（2+）]。细胞外[K+]的瞬时升高也产生了突触功效的长期增强，并且这种效应是Ca 2+依赖性的。有效诱导LTP（5-20 Hz，5-20 s）的强直电刺激完全在节前活动的生理范围内。其幅度和时程与刺激的频率和持续时间有关。LTP的发生仅限于强直刺激的节前纤维。通过将节前神经分成2个分支，可以独立测试和调节，证明了这种异突触或全身效应的缺乏。毒蕈碱或烟碱受体的生理激活显然在引起神经节LTP中不起重要作用，神经节LTP表达为烟碱传递的增强。毒蕈碱拮抗剂（2 μ M-阿托品）不阻断LTP。即使在强直刺激期间存在高浓度的烟碱拮抗剂（3 mM-六烃季铵），节前刺激也能诱导LTP。胆碱能激动剂（100-1000 μ M-卡巴胆碱）的浴敷不能代替激发LTP的强直刺激。肾上腺素能受体的激活不起重要作用。也不是β-肾上腺素能拮抗剂（10 μ M-索托洛尔或1 μ M普萘洛尔）或α-肾上腺素能拮抗剂（1 μ M-酚妥拉明）对LTP的幅度或持续时间没有任何显著影响。神经节LTP是一种钙离子和温度依赖性过程，可以独立于烟碱、毒蕈碱或肾上腺素能受体的激活而产生。
Brief tetanic stimulation of the preganglionic nerve induced a persistent potentiation of nicotinic synaptic transmission in the rat superior cervical sympathetic ganglion. Quantitative measurements of the post-tetanic increase in synaptic efficacy revealed 2 distinct time courses. The early, rapidly decaying component, termed post-tetanic potentiation (PTP), had a decay time constant of 2-3 min. The duration of the most persistent component, called long-term potentiation (LTP), was extremely temperature dependent, lasting much longer at 32.degree. C than at 22.degree. C. In half of the experiments performed at 32.degree. C, LTP showed no detectable decay over the course of 1 h or more after a brief tetanic stimulation. Other experiments were conducted at 22.degree. C. The induction of LTP was dependent on the extracellular [Ca2+]. Transient elevation of the extracellular [K+] also produced a long-term enhancement of synaptic efficacy and this effect was Ca2+ dependent. The tetani that were effective in inducing LTP (5-20 Hz for 5-20 s) were well within the physiological range of preganglionic activity. The magnitude and time course were related to frequency and duration of stimulation. The occurrence of LTP was restricted to those preganglionic fibers that were tetanically stimulated. This lack of heterosynaptic or generalized effects was demonstrated by splitting the preganglionic nerve into 2 branches that could be independently tested and conditioned. Physiological activation of muscarinic or nicotinic receptors apparently does not play an essential role in causing ganglionic LTP, which is expressed as an enhancement of nicotinic transmission. A muscarinic antagonist (2 .mu.M-atropine) did not block LTP. Preganglionic stimulation induced LTP even when a high concentration of a nicotinic antagonist (3 mM-hexamethonium) was present during the tetanic stimulation. Bath application of a cholinergic agonist (100-1000 .mu.M-carbachol) could not substitute for tetanic stimulation in provoking LTP. Activation of adrenergic receptors does not play an essential role. Neither a .beta.-adrenergic antagonist (10 .mu.M-sotolol or 1 .mu.M propranolol) nor an .alpha.-adrenergic antagonist (1 .mu.M-phentolamine) had any significant effect on the magnitude or duration of LTP. Ganglionic LTP is a Ca2+- and temperature-dependent process that can be created independently of the activation of nicotinic, muscarinic or adrenergic receptors.