Down-Regulation of Synaptotagmin 1 in Cortex, Hippocampus, and Cerebellum after Experimental Subarachnoid Hemorrhage

  1. Wen-Hui Xu2
  1. 1Department of Neurosurgery, The First Affiliated Hospital of Soochow University, Suzhou, Jiangsu Province, China
  2. 2Department of Neurosurgery, Yixing People’s Hospital, Yixing, Jiangsu Province, China
  1. Address correspondence to Zhong Wang, MD or Wen-Hui Xu, MD, Department of Neurosurgery, The First Affiliated Hospital of Soochow University, 188 Shizi Street, Suzhou 215006, P.R.China; phone: +86-13771908806; fax: +86-512-67780165; e mail: nju_neurosurgery{at}163.com

Abstract

Synapses are formed by the coordinated assembly and tight attachment of pre- and postsynaptic specializations. Synaptotagmin 1 (Syt 1) has been proven to be an important factor for synapse function and behavioral cognition. The current research was aimed to investigate the expression of Syt 1 in the brain after an experimental subarachnoid hemorrhage (SAH) in rats. A total of 42 rats were randomly divided into seven groups: normal group; control group; day 1, day 3, day 5, day 7 and day 14 groups. Day 1, day 3, day 5, day 7, and day 14 groups were all SAH groups in which the rats were killed on day 1, 3, 5, 7, and 14, respectively. The rat SAH model was induced by injection of 0.3 ml of fresh arterial, non-heparinized blood into the prechiasmatic cistern for 20 sec. Immunostaining and immunoblotting were performed to detect the expression of the Syt 1 protein. The expressions of the Syt 1 protein decreased remarkably in SAH groups compared to the control group. The down-regulated expression of Syt 1 was detected after SAH and the low ebb was on days 1–3. The immunohistochemical staining demonstrated the expression of Syt 1 to be present mainly in the neurons of the cortex, hippocampus, and cerebellum. Our results indicated that Syt 1 expression is down-regulated in the brain after experimental SAH. These finding suggests that the decreased Syt 1 expression may facilitate the development of cognitive dysfunction after SAH.

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