Fifková E, Van Harreveld A
J Neurocytol. 1977 Apr;6(2):211-30. doi: 10.1007/BF01261506.
Stimulation of the perforant path induces a long-lasting increase in the area of dendritic spines, which are sites of termination of the stimulated pathway in the distal third of the dentate molecular layer. No enlarged spines were found in the proximal third of the dentate molecular layer, where the commissural afferents terminate. Following a single tetanic stimulus of 30 sec duration at 30/sec, spines became significantly larger by 15%, 38%, 35% and 23% within poststimulation intervals of 2-6 min, 10-60 min, 4-8 h, and 23 h, respectively. Axon terminals decreased their area by 15% within the 2-6 min interval and the vesicle density was decreased by 19% within the 10-60 min interval. Both changes were reversible and terminals resumed their prestimulation condition at longer intervals (greater than 4 h). The initial enlargement of spines was interpreted as being due to a glutamate-induced increase in the sodium permeability of the spine membrane, whereas for the long-lasting enlargement an increase in protein synthesis was postulated. The long-lasting enlargement of dendritic spines in the dentate molecular layer following a short train of stimuli delivered to the perforant path, supports the postulate which links such a change to the mechanism of long-lasting postactivation potentiation observed in this pathway.
刺激穿通通路会导致树突棘的面积出现持久增加，树突棘是受刺激通路在齿状分子层远端三分之一处的终止位点。在联合传入纤维终止的齿状分子层近端三分之一处未发现增大的树突棘。在以30次/秒的频率进行30秒的单次强直刺激后，在刺激后2 - 6分钟、10 - 60分钟、4 - 8小时和23小时的间隔内，树突棘分别显著增大了15%、38%、35%和23%。轴突终末在2 - 6分钟的间隔内面积减小了15%，囊泡密度在10 - 60分钟的间隔内降低了19%。这两种变化都是可逆的，并且在更长的间隔时间（大于4小时）时终末恢复到刺激前的状态。树突棘最初的增大被解释为是由于谷氨酸诱导树突棘膜钠通透性增加所致，而对于持久的增大则推测是蛋白质合成增加所致。向穿通通路施加短串刺激后，齿状分子层中树突棘的持久增大，支持了将这种变化与该通路中观察到的持久激活后增强机制联系起来的假设。
