Dolleman-Van der Weel M J, Lopes da Silva F H, Witter M P
Graduate School for Neurosciences Amsterdam, Research Institute for Neurosciences, Faculty of Medicine, Department of Anatomy and Embryology, Vrije Universiteit, 1081 BT Amsterdam, The Netherlands.
J Neurosci. 1997 Jul 15;17(14):5640-50. doi: 10.1523/JNEUROSCI.17-14-05640.1997.
The nucleus reuniens thalami (RE) originates dense projections to CA1, forming asymmetrical synapses on spines (50%) and dendrites (50%). The hypothesis that RE input modulates transmission in CA1 through excitation of both pyramidal cells and interneurons was tested using electrophysiological methods in the anesthetized rat. The RE-CA1 afferents were selectively stimulated at their origin; evoked field potentials and unit activity were recorded in CA1. RE-evoked depth profiles showed a prominent negative deflection in the stratum lacunosum-moleculare and a positive one in the stratum radiatum. The lacunosum-moleculare sink-radiatum source configuration is compatible with RE-elicited depolarization of apical dendrites of pyramidal cells. Despite a consistent and robust paired pulse facilitation of RE-evoked field potentials, population spikes in the stratum pyramidale were not detected at any tested condition. This indicates the inability of RE-CA1 input to discharge pyramidal cells. However, stimulation of RE-elicited spiking of extracellularly recorded units in strata oriens/alveus and distal radiatum, indicative of the activation of local interneurons. Thus, RE seems to modulate transmission in CA1 through a (subthreshold) depolarization of pyramidal cells and a suprathreshold excitation of putative inhibitory oriens/alveus and radiatum interneurons. RE-evoked monosynaptic or disynaptic field potentials were associated with stimulation of rostral or caudal RE, respectively. Anatomically, a projection from caudal to rostral RE was demonstrated that can account for the disynaptic RE-CA1 input. Because caudal RE receives input from the hippocampus via the subiculum, we propose the existence of a closed RE-hippocampal circuit that allows RE to modulate the activity in CA1, depending on hippocampal output.
丘脑连合核（RE）发出密集投射至CA1区，在棘突（50%）和树突（50%）上形成不对称突触。采用电生理方法在麻醉大鼠中测试了RE输入通过兴奋锥体细胞和中间神经元来调节CA1区传递的假说。在RE-CA1传入纤维的起始部位进行选择性刺激；记录CA1区诱发的场电位和单位活动。RE诱发的深度剖面图显示，在分子层出现明显的负向偏转，在放射层出现正向偏转。分子层下沉-放射层源配置与RE诱发的锥体细胞顶树突去极化相一致。尽管RE诱发的场电位存在一致且强烈的双脉冲易化现象，但在任何测试条件下，锥体层均未检测到群体峰电位。这表明RE-CA1输入无法使锥体细胞放电。然而，刺激RE可诱发在海马下托/肺泡层和远端放射层细胞外记录的单位产生峰电位，这表明局部中间神经元被激活。因此，RE似乎通过锥体细胞的（阈下）去极化和假定的抑制性海马下托/肺泡层及放射层中间神经元的阈上兴奋来调节CA1区的传递。RE诱发的单突触或双突触场电位分别与刺激嘴侧或尾侧RE相关。在解剖学上，已证实存在从尾侧RE到嘴侧RE的投射，这可以解释双突触RE-CA1输入。由于尾侧RE通过海马下托接受来自海马的输入，我们提出存在一个封闭的RE-海马回路，该回路允许RE根据海马输出调节CA1区的活动。
