Panatier Aude, Gentles Stephen J, Bourque Charles W, Oliet Stéphane H R
INSERM U378, 33077 Bordeaux, France.
J Physiol. 2006 Jun 15;573(Pt 3):711-21. doi: 10.1113/jphysiol.2006.109447. Epub 2006 Apr 13.
Activity-dependent long-term synaptic changes were investigated at glutamatergic synapses in the supraoptic nucleus (SON) of the rat hypothalamus. In acute hypothalamic slices, high frequency stimulation (HFS) of afferent fibres caused long-term potentiation (LTP) of the amplitude of AMPA receptor-mediated excitatory postsynaptic currents (EPSCs) recorded with the whole-cell patch-clamp technique. LTP was also obtained in response to membrane depolarization paired with mild afferent stimulation. On the other hand, stimulating the inputs at 5 Hz for 3 min at resting membrane potential caused long-term depression (LTD) of excitatory transmission in the SON. These forms of synaptic plasticity required the activation of NMDA receptors since they were abolished in the presence of D-AP5 or ifenprodil, two selective blockers of these receptors. Analysis of paired-pulse facilitation and trial-to-trial variability indicated that LTP and LTD were not associated with changes in the probability of transmitter release, thereby suggesting that the locus of expression of these phenomena was postsynaptic. Using sharp microelectrode recordings in a hypothalamic explant preparation, we found that HFS also generates LTP at functionally defined glutamatergic synapses formed between the organum vasculosum lamina terminalis and SON neurons. Taken together, our findings indicate that glutamatergic synapses in the SON exhibit activity-dependent long-term synaptic changes similar to those prevailing in other brain areas. Such forms of plasticity could play an important role in the context of physiological responses, like dehydration or lactation, where the activity of presynaptic glutamatergic neurons is strongly increased.
在大鼠下丘脑视上核(SON)的谷氨酸能突触处研究了活动依赖的长期突触变化。在急性下丘脑切片中,用全细胞膜片钳技术记录发现,传入纤维的高频刺激(HFS)引起AMPA受体介导的兴奋性突触后电流(EPSCs)幅度的长期增强(LTP)。膜去极化与轻度传入刺激配对也能诱导出LTP。另一方面,在静息膜电位下以5 Hz刺激输入3分钟会导致视视上丘脑中兴奋性传递的长期抑制(LTD)。这些形式的突触可塑性需要NMDA受体的激活,因为在存在D-AP5或艾芬地尔(这两种该受体的选择性阻滞剂)时它们会被消除。配对脉冲易化和逐次试验变异性分析表明,LTP和LTD与递质释放概率的变化无关,因此表明这些现象的表达位点是突触后。在体外下丘脑制备中使用尖锐微电极记录,我们发现HFS也能在终板血管器与SON神经元之间形成的功能确定的谷氨酸能突触处产生LTP。综上所述,我们的研究结果表明,SON中的谷氨酸能突触表现出与其他脑区普遍存在的类似的活动依赖的长期突触变化。这种形式的可塑性可能在生理反应(如脱水或泌乳)中发挥重要作用,在这些情况下突触前谷氨酸能神经元的活动会强烈增加。