Toth Z, Hollrigel G S, Gorcs T, Soltesz I
Department of Anatomy and Neurobiology, University of California, Irvine, California 92697, USA.
J Neurosci. 1997 Nov 1;17(21):8106-17. doi: 10.1523/JNEUROSCI.17-21-08106.1997.
Whole-cell patch-clamp recordings and immunocytochemical experiments were performed to determine the short- and long-term effects of lateral fluid percussion head injury on the perisomatic inhibitory control of dentate granule cells in the adult rat, with special reference to the development of trauma-induced hyperexcitability. One week after the delivery of a single, moderate (2.0-2.2 atm) mechanical pressure wave to the neocortex, the feed-forward inhibitory control of dentate granule cell discharges was compromised, and the frequency of miniature IPSCs was decreased. Consistent with the electrophysiological data, the number of hilar parvalbumin (PV)- and cholecystokinin (CCK)-positive dentate interneurons supplying the inhibitory innervation of the perisomatic region of granule cells was decreased weeks and months after head injury. The initial injury to the hilar neurons took place instantaneously after the impact and did not require the recruitment of active physiological processes. Furthermore, the decrease in the number of PV- and CCK-positive hilar interneurons was similar to the decrease in the number of the AMPA-type glutamate receptor subunit 2/3-immunoreactive mossy cells, indicating that the pressure wave-transient causes injurious physical stretching and bending of most cells that are large and not tightly packed in a cell layer. These results reveal for the first time that moderate pressure wave-transients, triggered by traumatic head injury episodes, impact the dentate neuronal network in a unique temporal and spatial pattern, resulting in a net decrease in the perisomatic control of granule cell discharges.
采用全细胞膜片钳记录和免疫细胞化学实验，以确定侧方液体冲击性颅脑损伤对成年大鼠齿状颗粒细胞胞体周围抑制性控制的短期和长期影响，特别关注创伤诱导的兴奋性过高的发展。在向新皮层施加单次中度（2.0 - 2.2 atm）机械压力波一周后，齿状颗粒细胞放电的前馈抑制性控制受到损害，微小抑制性突触后电流（mIPSCs）的频率降低。与电生理数据一致，在颅脑损伤数周和数月后，为颗粒细胞胞体周围区域提供抑制性神经支配的海马小白蛋白（PV）和胆囊收缩素（CCK）阳性齿状中间神经元数量减少。海马神经元的初始损伤在冲击后即刻发生，不需要激活生理过程。此外，PV和CCK阳性海马中间神经元数量的减少与AMPA型谷氨酸受体亚基2/3免疫反应性苔藓细胞数量的减少相似，表明压力波瞬变会对大多数体积较大且在细胞层中排列不紧密的细胞造成有害的物理拉伸和弯曲。这些结果首次揭示，创伤性颅脑损伤事件引发的中度压力波瞬变以独特的时间和空间模式影响齿状神经网络，导致颗粒细胞放电的胞体周围控制净减少。
