Blasco-Ibáñez J M, Freund T F
Institute of Experimental Medicine, Hungarian Academy of Sciences, Budapest, Hungary.
Eur J Neurosci. 1995 Oct 1;7(10):2170-80. doi: 10.1111/j.1460-9568.1995.tb00638.x.
The synaptic input of interneurons with horizontal dendrites in stratum oriens of the CA1 region was investigated, with particular attention to the portion of synapses originating from local pyramidal cells. Most of these GABAergic interneurons are known to contain somatostatin, and terminate on pyramidal dendrites in conjunction with entorhinal afferents in stratum lacunosum-moleculare. A smaller number of horizontal cells in this layer are immunoreactive for calbindin, and project to the medial septum. Selective ischaemic degeneration was used to label local axon collaterals of CA1 pyramidal cells, and immunostaining for mGluR1 or calbindin to visualise somatostatin- and calbindin-containing horizontal interneurons, respectively, at the stratum oriens-alveus border. The number of degenerating and intact synaptic boutons was counted on mGluR1- as well as on calbindin-positive dendrites and somata, whereas in another group of animals the proportion of GABA-immunoreactive synapses was estimated on calbindin-positive dendrites. On average, > 60% of the total presynaptic elements of both cell types were degenerating, i.e. originated from CA1 pyramidal cells, whereas GABA-positive boutons, which are known to survive ischaemia, are likely to account for a large proportion of non-degenerating boutons. Thus the vast majority of presumed excitatory synapses on somatostatin- and calbindin-containing horizontal neurons derives from local collaterals of CA1 pyramidal cells. The remaining GABA-negative synapses surviving ischaemia may also originate from CA1 pyramidal cells, e.g. from those in the ventral hippocampus, which are rarely damaged by global forebrain ischaemia. Alternative sources may include subcortical afferents known to innervate interneurons, or ipsi- and contralateral CA3 pyramidal cells, which, according to the present results, may account only for a negligible number of synapses on these interneurons types. We conclude that somatostatin-containing neurons at the oriens-alveus border of CA1, which are likely to mediate an inhibitory control of the efficacy and/or plasticity of entorhinal synapses on pyramidal cell dendrites, are driven primarily in a feed-back manner. The source of afferent excitation for calbindin-containing horizontal neurons in this region is very similar, suggesting that the GABAergic hippocamposeptal feed-back is also activated by local pyramidal cell collaterals.
研究了CA1区海马下托中具有水平树突的中间神经元的突触输入，特别关注源自局部锥体细胞的突触部分。已知这些GABA能中间神经元大多含有生长抑素，并与海马分子层中的内嗅传入纤维一起终止于锥体细胞树突上。该层中少量水平细胞对钙结合蛋白呈免疫反应，并投射至内侧隔区。采用选择性缺血性变性来标记CA1锥体细胞的局部轴突侧支，并分别用mGluR1或钙结合蛋白进行免疫染色，以显示海马下托-海马槽边界处含生长抑素和钙结合蛋白的水平中间神经元。在mGluR1阳性以及钙结合蛋白阳性的树突和胞体上计数变性和完整的突触小体数量，而在另一组动物中，估计钙结合蛋白阳性树突上GABA免疫反应性突触的比例。平均而言，两种细胞类型的突触前成分总数中>60%正在发生变性，即源自CA1锥体细胞，而已知能在缺血中存活的GABA阳性突触小体可能占非变性突触小体的很大一部分。因此，绝大多数推测存在于含生长抑素和钙结合蛋白的水平神经元上的兴奋性突触源自CA1锥体细胞的局部侧支。其余在缺血中存活的GABA阴性突触也可能源自CA1锥体细胞，例如源自腹侧海马的锥体细胞，它们很少受到全脑缺血的损伤。其他来源可能包括已知支配中间神经元的皮质下传入纤维，或同侧和对侧CA3锥体细胞，根据目前的结果，它们在这些中间神经元类型上的突触数量可能仅占可忽略不计的比例。我们得出结论，CA1海马下托-海马槽边界处含生长抑素的神经元可能介导对内嗅突触在锥体细胞树突上的效能和/或可塑性抑制性控制，主要以反馈方式被驱动。该区域中含钙结合蛋白的水平神经元的传入兴奋源非常相似，表明GABA能海马-隔区反馈也由局部锥体细胞侧支激活。
