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Role of Neurexin-1β and Neuroligin-1 in Cognitive Dysfunction After Subarachnoid Hemorrhage in Rats.

Shen H, Chen Z, Wang Y, Gao A, Li H, Cui Y, Zhang L, Xu X, Wang Z, Chen G - Stroke (2015)

Bottom Line: Both in vivo and in vitro experiments showed SAH-induced decrease in the expressions of neurexin-1β and neuroligin-1 and the interaction between neurexin-1β and neuroligin-1 in neurons.In addition, the interaction between neurexin-1β and neuroligin-1 was reduced by their knockdown and increased by their overexpression.The formation of excitatory synapses was inhibited by oxyhemoglobin treatment, which was significantly ameliorated by overexpression of neurexin-1β and neuroligin-1 and aggravated by the knockdown of neurexin-1β and neuroligin-1.

View Article: PubMed Central - PubMed

Affiliation: From the Department of Neurosurgery & Brain and Nerve Research Laboratory, The First Affiliated Hospital of Soochow University, Suzhou, China (H.S., Z.C., Y.W., A.G., H.L., Y.C., L.Z., X.X., Z.W., G.C.); and Department of Neurosurgery, Anhui Provincial Hospital Affiliated to Anhui Medical University, Anhui Province Key Laboratory of Brain Function and Brain Disease, Hefei, Anhui, China (Y.W.).

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Effects of neurexin-1β and neuroligin-1 knockdown and overexpression on behavioral and cognitive function in subarachnoid hemorrhage (SAH) rats. A, Neurological behavior scores in each group. Data are presented as mean±SEM. *P<0.05, **P<0.01; n=16. B, Representative tracing images from the Morris water maze test. C, Escape latency and (D) swim path length of 4 trials per day for 4 days, n=10.
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Figure 6: Effects of neurexin-1β and neuroligin-1 knockdown and overexpression on behavioral and cognitive function in subarachnoid hemorrhage (SAH) rats. A, Neurological behavior scores in each group. Data are presented as mean±SEM. *P<0.05, **P<0.01; n=16. B, Representative tracing images from the Morris water maze test. C, Escape latency and (D) swim path length of 4 trials per day for 4 days, n=10.

Mentions: SAH-induced neurological behavior impairment and whether knockdown or overexpression of neurexin-1β and neuroligin-1 affects impairment were tested (Figure 6A). Compared with the sham group, neurological score in the SAH group was significantly higher, suggesting a remarkable neurological defect induced by SAH. Scramble siRNA and empty vector treatment did not affect neurological outcome. Neurexin-1β and neuroligin-1 when silenced either individually or simultaneously could significantly aggravate SAH-induced neurological defect. Given the overexpression of neurexin-1β or neuroligin-1, the neurological behavior impairment was significantly reversed, whereas the overexpression of both neurexin-1β and neuroligin-1 simultaneously had a greater effect than the overexpression of neurexin-1β or neuroligin-1 individually.


Role of Neurexin-1β and Neuroligin-1 in Cognitive Dysfunction After Subarachnoid Hemorrhage in Rats.

Shen H, Chen Z, Wang Y, Gao A, Li H, Cui Y, Zhang L, Xu X, Wang Z, Chen G - Stroke (2015)

Effects of neurexin-1β and neuroligin-1 knockdown and overexpression on behavioral and cognitive function in subarachnoid hemorrhage (SAH) rats. A, Neurological behavior scores in each group. Data are presented as mean±SEM. *P<0.05, **P<0.01; n=16. B, Representative tracing images from the Morris water maze test. C, Escape latency and (D) swim path length of 4 trials per day for 4 days, n=10.
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4542569&req=5

Figure 6: Effects of neurexin-1β and neuroligin-1 knockdown and overexpression on behavioral and cognitive function in subarachnoid hemorrhage (SAH) rats. A, Neurological behavior scores in each group. Data are presented as mean±SEM. *P<0.05, **P<0.01; n=16. B, Representative tracing images from the Morris water maze test. C, Escape latency and (D) swim path length of 4 trials per day for 4 days, n=10.
Mentions: SAH-induced neurological behavior impairment and whether knockdown or overexpression of neurexin-1β and neuroligin-1 affects impairment were tested (Figure 6A). Compared with the sham group, neurological score in the SAH group was significantly higher, suggesting a remarkable neurological defect induced by SAH. Scramble siRNA and empty vector treatment did not affect neurological outcome. Neurexin-1β and neuroligin-1 when silenced either individually or simultaneously could significantly aggravate SAH-induced neurological defect. Given the overexpression of neurexin-1β or neuroligin-1, the neurological behavior impairment was significantly reversed, whereas the overexpression of both neurexin-1β and neuroligin-1 simultaneously had a greater effect than the overexpression of neurexin-1β or neuroligin-1 individually.

Bottom Line: Both in vivo and in vitro experiments showed SAH-induced decrease in the expressions of neurexin-1β and neuroligin-1 and the interaction between neurexin-1β and neuroligin-1 in neurons.In addition, the interaction between neurexin-1β and neuroligin-1 was reduced by their knockdown and increased by their overexpression.The formation of excitatory synapses was inhibited by oxyhemoglobin treatment, which was significantly ameliorated by overexpression of neurexin-1β and neuroligin-1 and aggravated by the knockdown of neurexin-1β and neuroligin-1.

View Article: PubMed Central - PubMed

Affiliation: From the Department of Neurosurgery & Brain and Nerve Research Laboratory, The First Affiliated Hospital of Soochow University, Suzhou, China (H.S., Z.C., Y.W., A.G., H.L., Y.C., L.Z., X.X., Z.W., G.C.); and Department of Neurosurgery, Anhui Provincial Hospital Affiliated to Anhui Medical University, Anhui Province Key Laboratory of Brain Function and Brain Disease, Hefei, Anhui, China (Y.W.).

Show MeSH
Related in: MedlinePlus