Carman H M, Dhillon H S, Zhang D, Geddes J W, Prasad R M
Department of Surgery, University of Kentucky Chandler Medical Center, Lexington, KY 40536-0084, USA.
Brain Res. 1998 Oct 12;808(1):116-9. doi: 10.1016/s0006-8993(98)00824-5.
Levels of PLCgamma, a phospholipase C (PLC) isozyme, were significantly increased in the cytosol in the injured left cortex (LC) at 5, 30 and 120 min after brain injury. In the same site, although levels of membrane PLCgamma did not alter at 5 and 30 min, they were found to be decreased at 2 h after brain injury. In general, the levels of both cytosolic and membrane PLCgamma were unaltered in the contralateral right cortex (RC), ipsilateral left hippocampus (LH) and contralateral right hippocampus (RH) between 5 and 120 min after brain injury. These results suggest that, in addition to well-proposed excitatory neurotransmitter-receptor systems, increased levels of PLCgamma may also contribute to alterations in PIP2 signal transduction pathway, particularly in the greatest injury site (LC) after lateral FP brain injury.
磷脂酶C（PLC）同工酶PLCγ的水平在脑损伤后5分钟、30分钟和120分钟时，损伤的左侧皮质（LC）胞质溶胶中显著升高。在同一部位，虽然膜PLCγ水平在5分钟和30分钟时未发生改变，但在脑损伤后2小时发现其降低。总体而言，在脑损伤后5至120分钟期间，对侧右侧皮质（RC）、同侧左侧海马（LH）和对侧右侧海马（RH）中胞质和膜PLCγ的水平均未改变。这些结果表明，除了已被充分提出的兴奋性神经递质-受体系统外，PLCγ水平的升高也可能导致磷脂酰肌醇-4,5-二磷酸（PIP2）信号转导通路的改变，特别是在侧方液压脑损伤后的最大损伤部位（LC）。
