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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 the formation of excitatory synapses in cultured hippocampal neurons under oxyhemoglobin (OxyHb) treatment. A, Cultured primary hippocampal neurons were transfected with small interfering RNAs (siRNAs) or plasmids as indicated and stained for postsynaptic density protein 95 (PSD-95;an excitatory postsynaptic marker) and synapsin (a presynaptic marker). Scale bar=32 μm. B, Quantification of the number of excitatory synapses per 100 μm of neurite, as defined by synapsin-positive PSD-95 clusters and indicated by arrows. Data are presented as mean±SEM. *P<0.05, **P<0.01; n=3.
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Figure 5: Effects of neurexin-1β and neuroligin-1 knockdown and overexpression on the formation of excitatory synapses in cultured hippocampal neurons under oxyhemoglobin (OxyHb) treatment. A, Cultured primary hippocampal neurons were transfected with small interfering RNAs (siRNAs) or plasmids as indicated and stained for postsynaptic density protein 95 (PSD-95;an excitatory postsynaptic marker) and synapsin (a presynaptic marker). Scale bar=32 μm. B, Quantification of the number of excitatory synapses per 100 μm of neurite, as defined by synapsin-positive PSD-95 clusters and indicated by arrows. Data are presented as mean±SEM. *P<0.05, **P<0.01; n=3.

Mentions: We next observed the effects of neurexin-1β and neuroligin-1 knockdown or overexpression on the number of excitatory synapses in cultured hippocampal neurons under oxyhemoglobin treatment (Figure 5). The results showed oxyhemoglobin-induced decrease in the number of excitatory synapses, as defined by synapsin (a presynaptic marker)-positive postsynaptic density protein 95 clusters, which was aggravated by the knockdown of neurexin-1β and neuroligin-1 and ameliorated by the overexpression of neurexin-1β and neuroligin-1. The results also showed that there were no significant differences between neurexin-1β siRNA+neuroligin-1 siRNA group and neurexin-1β siRNA group or neuroligin-1 siRNA group, whereas there were significant differences between neurexin-1β plasmid+neuroligin-1 plasmid group and neurexin-1β plasmid group or neuroligin-1 plasmid group.


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 the formation of excitatory synapses in cultured hippocampal neurons under oxyhemoglobin (OxyHb) treatment. A, Cultured primary hippocampal neurons were transfected with small interfering RNAs (siRNAs) or plasmids as indicated and stained for postsynaptic density protein 95 (PSD-95;an excitatory postsynaptic marker) and synapsin (a presynaptic marker). Scale bar=32 μm. B, Quantification of the number of excitatory synapses per 100 μm of neurite, as defined by synapsin-positive PSD-95 clusters and indicated by arrows. Data are presented as mean±SEM. *P<0.05, **P<0.01; n=3.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

Figure 5: Effects of neurexin-1β and neuroligin-1 knockdown and overexpression on the formation of excitatory synapses in cultured hippocampal neurons under oxyhemoglobin (OxyHb) treatment. A, Cultured primary hippocampal neurons were transfected with small interfering RNAs (siRNAs) or plasmids as indicated and stained for postsynaptic density protein 95 (PSD-95;an excitatory postsynaptic marker) and synapsin (a presynaptic marker). Scale bar=32 μm. B, Quantification of the number of excitatory synapses per 100 μm of neurite, as defined by synapsin-positive PSD-95 clusters and indicated by arrows. Data are presented as mean±SEM. *P<0.05, **P<0.01; n=3.
Mentions: We next observed the effects of neurexin-1β and neuroligin-1 knockdown or overexpression on the number of excitatory synapses in cultured hippocampal neurons under oxyhemoglobin treatment (Figure 5). The results showed oxyhemoglobin-induced decrease in the number of excitatory synapses, as defined by synapsin (a presynaptic marker)-positive postsynaptic density protein 95 clusters, which was aggravated by the knockdown of neurexin-1β and neuroligin-1 and ameliorated by the overexpression of neurexin-1β and neuroligin-1. The results also showed that there were no significant differences between neurexin-1β siRNA+neuroligin-1 siRNA group and neurexin-1β siRNA group or neuroligin-1 siRNA group, whereas there were significant differences between neurexin-1β plasmid+neuroligin-1 plasmid group and neurexin-1β plasmid group or neuroligin-1 plasmid group.

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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Related in: MedlinePlus