Neuroscience
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Antisecretory Factor (AF) is an endogenous peptide known for its powerful antisecretory and anti-inflammatory properties. We have previously shown that AF also acts as a neuromodulator of GABAergic synaptic transmission in rat hippocampus in a way that results in disinhibition of CA1 pyramidal neurons. Disinhibition is expected to facilitate the induction of long-term potentiation (LTP), and LTP is known to play a crucial role in learning and memory acquisition. ⋯ In the presence of the GABAA-receptor antagonist picrotoxin (PTX) there was however no significant enhancement of LTP. Moreover, rats fed with SPC demonstrated enhanced spatial learning and short-term memory, compared with control animals. These results show that the disinhibition of GABAergic transmission in the hippocampus by the endogenous peptide AF enhances LTP as well as spatial learning and memory.
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Glaucoma is a neurodegenerative disease characterized by progressive retinal ganglion cell (RGC) death. Recently, many studies have reported that the N-methyl D-aspartate receptor 2B (NR2B) subunit is excitotoxic in the pathogenesis of glaucoma, but the molecular mechanism should be further explored. In our present study, we investigated the involvement of the NR2B-postsynaptic density protein-95 (PSD95) complex in RGC apoptosis in an experimental glaucoma animal model and determined whether inhibition of the NR2B-PSD95 interaction protected RGCs. ⋯ Levels of the apoptosis-related proteins Bax and cleaved caspase-3 decreased as the number of surviving RGCs increased. Together, our results suggest that the NR2B-PSD95 complex was involved in RGC death in the retinal I/R injury model. Tat-NR2B9c exerted a neuroprotective effect on RGC survival in the retinal I/R injury model by disrupting the NR2B-PSD95 interaction.
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Spinal cord injury (SCI) is a common disease of the nervous system, including primary and secondary injuries. Neuronal inflammation after SCI is the most important pathological process of SCI and a chemical barrier to nerve function recovery after injury. Ski, an evolutionarily conserved functional transcriptional regulator protein, is upregulated in reactive astrocytes after SCI and regulates the biological characteristics of astrocytes. ⋯ These findings suggest that Ski is a promising therapeutic target for inflammatory responses after SCI. In conclusion, Ski downregulation can effectively inhibit glial inflammation in SCI by inhibiting the activity of the NF-κB pathway. These findings suggest that Ski might serve as a promising target for the treatment of inflammatory responses after SCI.