Locus coeruleus bursts induced by glutamate trigger delayed perforant path spike amplitude potentiation in the dentate gyrus
Locus coeruleus bursts induced by glutamate trigger delayed perforant path spike amplitude potentiation in the dentate gyrus
复制标题
谷氨酸诱导的蓝斑爆发触发齿状回延迟穿通路径尖峰振幅增强
作者：
C. Harley;S. Sara
蓝斑（LC）神经元附近的谷氨酸压射可引起齿状回（DG）中穿通通路（PP）诱发的群体峰电位幅度的短时和长时增强。LC-谷氨酸激活的这些作用类似于直接应用NE在体外或体内产生的那些作用。本研究监测LC神经元的细胞反应，以当地谷氨酸喷射伴随着刺激的PP诱发电位。双筒微量移液器或33 ga cannulaelectrode组件允许LC单元记录和谷氨酸喷射在或接近乌拉坦麻醉大鼠的相同部位。谷氨酸喷射产生的LC活动持续250-400毫秒的爆发，然后由单位活动持续4.6分钟的抑郁症。LC激活产生的最大尖峰增强为158%。超过对照范围的第一个尖峰出现在LC爆发后34 s。全身可乐定诱导的LC单位活动中的可比沉默间期并不伴随着群体峰电位幅度增强。增强的平均持续时间为4.4分钟，除了在四种情况下，反应保持增强的实验期间。增强的持续时间与LC抑制的终止不相关。在谷氨酸诱导的活动抑制后，LC单位恢复到基线速率。增强的发生似乎需要谷氨酸激活达到临界数量的LC神经元，因为小的谷氨酸喷射可以产生局部爆发而不引起增强。长期的变化也与较大的谷氨酸体积（100 nl）。EPSP斜率的增加是短暂的，发生频率较低，比穗幅度的变化，表明EPSP-穗分离。LC活动的爆发和幅度增加之间的延迟DG支持NE作用的模型，其中有快速和缓慢发展的影响NE释放的DG。总之，LC神经元的短暂但强烈的激活在LC爆发后产生持续数分钟至数小时的DG响应的延迟增强。
SummaryGlutamate pressure ejections in the vicinity of locus coeruleus (LC) neurons have been shown to produce both short and long-lasting potentiation of perforant path (PP) evoked population spike amplitude in the dentate gyrus (DG). These effects of LC-glutamate activation resemble those produced by direct application of NE in vitro or in vivo. The present study monitored the cellular response of LC neurons to local glutamate ejections concomitant with stimulation of the PP evoked potential. Double barrel micropipettes or 33 ga cannulaelectrode assemblies permitted LC unit recording and glutamate ejection at or near the same site in urethane anesthetized rats. Glutamate ejections produced a burst of LC activity lasting 250–400 ms and followed by a depression of unit activity lasting 4.6 min. The maximal spike potentiation produced by LC activation was 158%. The first spike to exceed the control range occurred 34 s after the LC burst. Comparable silent intervals in LC unit activity induced by systemic clonidine were not accompanied by population spike amplitude potentiation. The mean duration of potentiation was 4.4 min except in four cases where responses remained potentiated for the duration of the experiment. The duration of potentiation was not correlated with the termination of LC depression. LC units recovered to baseline rates following glutamate induced depression of activity. The occurrence of potentiation appeared to require that glutamate activation reach a critical number of LC neurons since small glutamate ejections could produce a local burst without eliciting potentiation. Long-lasting changes were also related to larger glutamate volumes (100 nl). EPSP slope increases were briefer and occurred less frequently than spike amplitude changes suggesting EPSP-spike dissociation. The delay between the burst of LC activity and amplitude increases in the DG supports a model of NE action in which there are both rapid and slowly developing effects of NE release in the DG. In summary, brief, but intense, activation of LC neurons produces a delayed potentiation of DG responses lasting minutes to hours following the LC burst.