EXTRACELLULAR K+ IN THE SUPRAOPTIC NUCLEUS OF THE RAT DURING REFLEX BURSTING ACTIVITY BY OXYTOCIN NEURONS
EXTRACELLULAR K+ IN THE SUPRAOPTIC NUCLEUS OF THE RAT DURING REFLEX BURSTING ACTIVITY BY OXYTOCIN NEURONS
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DOI：
10.1113/jphysiol.1991.sp018672
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发表时间：
1991-07-01
影响因子：
5.5
通讯作者：
POULAIN, DA
中科院分区：
文献类型：
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作者：
COLES, JA;POULAIN, DA
1. 我们研究了哺乳大鼠视上核细胞外钾浓度[K+]o 的变化，特别是在参与泌乳反射的催产素神经元强烈放电期间发生的变化。2．将含有基于缬氨霉素的高选择性传感器的双管 K+ 选择性微电极通过暴露的皮层降低到用乌拉坦麻醉的雌性大鼠的视上核（SON）。五只大鼠下丘脑的平均静息 [K+]o 为 2.4 mM，S.D. = 0.3 毫摩尔.3。当参考桶记录来自催产素细胞的细胞外动作电位时，放电反射爆发（4秒，典型最大50Hz）伴随着[K+]0（DELTA[K+]0）平均增加0.22mM（S.E.M.=0.02mM，7只大鼠的8个细胞中的57次爆发）。 [K+]0 的上升在爆发开始前 0.1 秒内开始，并在爆发期间从其最大值开始下降。表明 K+ 空间缓冲的慢场电位无法检测到 (< 50-mu-V)。当电极逐步前进时，DELTA[K+]0 和动作电位的振幅在 20 μm 的距离内急剧下降至约 10%：来自催产素细胞的 K+ 似乎被阻止通过 SON.4 的细胞外空间自由分散。当电极记录加压素细胞的动作电位时，催产素细胞爆发期间的 DELTA[K+]0 非常小：0.021 mM (S.E.M. = 0.005 mM)。在 SON 的其他位点，逆向刺激诱发场电位但无动作电位，DELTA[K+]0 为 0.047 +/- 0.005 mM。我们得出结论，催产素爆发不影响加压素细胞的原因是加压素细胞周围的 [K+]0 上升很少。更不用说，由于除了记录催产素细胞的动作电位之外，[K+]0 的增加非常小，因此它们对同步不连续的催产素细胞中的突发爆发没有显着的贡献。5。来自垂体柄的标准逆向刺激，以 40 Hz 持续 4 秒，同时刺激催产素神经元和加压素神经元，导致 DELTA[K+]0 为 0.17-1.8 mM，差异主要存在于大鼠之间。较大的 DELTA[K+]0 值伴随着高达 1.5 mV 的缓慢负电位，DELTA[K+]0 在 SON 下限处向软脑膜呈梯度下降，并且在蛛网膜下腔中 [K+] 缓慢增加。我们得出结论，在一些大鼠的逆向刺激过程中，一些K+通过神经胶质细胞从SON到蛛网膜下腔被清除。6．逆向刺激期间 SON 所有位点的 DELTA[K+]0 汇总测量平均值是仅催产素神经元放电时观察到的平均值 DELTA[K+]0 的 5.6 倍。我们得出结论，催产素细胞周围的 K+ 清除比加压素细胞周围的 K+ 清除更有效，并且大部分清除是通过避免 SON 其他部分显着增加或慢电位产生的机制实现的。这种清除可能是通过神经胶质细胞的净摄取，或者可能是通过主动转运到毛细血管中实现的。7。众所周知，在哺乳期间，直接面向其他催产素细胞膜或突触末端的膜的催产素细胞膜面积增加，而没有神经胶质突起的介入。考虑到这种几何结构表明，它应该允许无胶质细胞裂隙中的 [K+]0 短暂增加，这可能有助于同步相邻细胞中爆发的开始，但不会允许爆发后期的过度积累。
1. We have investigated changes in extracellular potassium concentration [K+]o in the supraoptic nucleus of lactating rats and in particular those that occur during the intense burst of firing by the oxytocin neurones involved in the milk ejection reflex.2. Double-barrelled K+-selective microelectrodes containing a highly selective sensor based on valinomycin were lowered through the exposed cortex towards the supraoptic nucleus (SON) of female rats anaesthetized with urethane. The mean resting [K+]o in the hypothalami of five rats was 2.4 mM, S.D. = 0.3 mM.3. Where the reference barrel recorded extracellular action potentials from an oxytocin cell, the reflex burst of firing (4 s, typical maximum 50 Hz) was accompanied by a mean increase in [K+]0 (DELTA[K+]0) of 0.22 mM (S.E.M. = 0.02 mM, fifty-seven bursts in eight cells in seven rats). The rise in [K+]0 did not begin more than 0.1 s before the onset of the burst, and began to fall from its maximum during the burst. Slow field potentials, indicative of spatial buffering of K+, were undetectable (< 50-mu-V). When the electrode was advanced in steps, the amplitudes of both DELTA[K+]0 and the action potential declined steeply to about 10% over a distance of 20-mu-m: K+ from oxytocin cells appears to be prevented from dispersing freely through the extracellular space of the SON.4. When the electrode recorded action potentials from a vasopressin cell, DELTA[K+]0 during an oxytocin cell burst was very small: 0.021 mM (S.E.M. = 0.005 mM). At other sites in the SON, where antidromic stimulation evoked a field potential but no action potential, DELTA[K+]0 was 0.047 +/- 0.005 mM. We conclude that the reason oxytocin bursts do not affect vasopressin cells is that [K+]0 rises very little around vasopressin cells. A fortiori, since the increases in [K+]0 were very small except where action potentials from oxytocin cells were recorded, they can make no significant contribution to synchronizing the onsets of bursts in oxytocin cells that are not contiguous.5. A standard antidromic stimulation from the pituitary stalk, at 40 Hz for 4 s, which stimulated both oxytocin neurones and vasopressin neurones, caused a DELTA[K+]0 of 0.17-1.8 mM, the variation being mainly from rat to rat. The larger DELTA[K+]0 values were accompanied by slow negative potentials of up to 1.5 mV, there was a gradient in DELTA[K+]0 decreasing towards the pia at the inferior limit of the SON, and there was a slow increase in [K+] in the subarachnoid space. We conclude that during antidromic stimulation in some rats, some K+ is cleared through glial cells from the SON to the subarachnoid space.6. The mean of pooled measurements of DELTA[K+]0 from all sites in the SON during antidromic stimulation was 5.6 times the mean DELTA[K+]0 observed when only the oxytocin neurones fired. We conclude that K+ is cleared from around oxytocin cells more effectively than from around vasopressin cells, and that most of this clearance is by a mechanism that avoids significant increases in other parts of the SON or the generation of slow potentials. This clearance could be by net uptake by glial cells, or, possibly, by active transport into blood capillaries.7. It is known that during lactation there is an increase in areas of oxytocin cell membrane that directly face membranes of other oxytocin cells or of synaptic terminals without the interposition of glial processes. Consideration of this geometry shows that it should permit brief increases in [K+]0 in the glial-free cleft that might contribute to synchronizing the onset of bursts in adjacent cells, but would not allow an excessive accumulation later in the burst.