ArticleNeurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology2013
Expression of synaptic cell adhesion molecule 1 (SynCAM 1) in different brain regions in a rat subarachnoid hemorrhage model.
Article in Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers, 1 of them a synthesis that pooled it.
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3 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Mechanisms of memory impairment in animal models of nontraumatic intracranial hemorrhage: A systematic review of the literature.Brain hemorrhages · 2022Pooled it
- The blood-brain barrier and the neurovascular unit in subarachnoid hemorrhage: molecular events and potential treatments.Fluids and barriers of the CNS · 2022Review
- Long-term functional consequences and ongoing cerebral inflammation after subarachnoid hemorrhage in the rat.PloS one · 2014Article
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4 authors.
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Abstract
Synapses, the junctions between nerve cells through which they communicate, are formed by the coordinated assembly and tight attachment of pre- and postsynaptic specializations. Synaptic cell adhesion molecule 1 (SynCAM 1) has been proved to be an important factor for synapse function and behavior cognition. The current research aimed to investigate the expression of the SynCAM 1 in the brain after experimental subarachnoid hemorrhage (SAH) in rats. A total of 42 rats were randomly divided into seven groups: control group, sham 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 days 1, 3, 5, 7, and 14, respectively. The rat SAH model was induced by injection of 0.3 ml fresh arterial, non-heparinized blood into the prechiasmatic cistern in 20 s. Immunostaining and immunoblotting experiments were performed to detect the expression of SynCAM 1 protein. The clinical behavior scale was measured on day 14 after SAH. The expression of SynCAM 1 protein was decreased remarkably in SAH groups compared with the sham group. The down-regulated expression of SynCAM 1 was detected after SAH and the low ebb was on days 1-3. The immunohistochemical staining demonstrated expression of SynCAM 1 was present mainly in the neurons in all of the three different regions such as cortex, hippocampus, and cerebellum. The clinical behavior scale was significantly decreased compared with sham rats. Our results indicate that SynCAM 1 expression is down-regulated in the brain after experimental SAH. These finding suggests that decreased SynCAM 1 expression may facilitate the development of cognitive dysfunction after SAH.
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