| First Author | Chen X | Year | 2017 |
| Journal | Am J Med Genet B Neuropsychiatr Genet | Volume | 174 |
| Issue | 8 | Pages | 828-838 |
| PubMed ID | 28981195 | Mgi Jnum | J:302075 |
| Mgi Id | MGI:6507642 | Doi | 10.1002/ajmg.b.32600 |
| Citation | Chen X, et al. (2017) Nhe5 deficiency enhances learning and memory via upregulating Bdnf/TrkB signaling in mice. Am J Med Genet B Neuropsychiatr Genet 174(8):828-838 |
| abstractText | Nhe5, a Na(+) /H(+) exchanger, is predominantly expressed in brain tissue and is proposed to act as a negative regulator of dendritic spine growth. Up to now, its physiological function in vivo remains unclear. Here we show that Nhe5-deficient mice exhibit markedly enhanced learning and memory in Morris water maze, novel object recognition, and passive avoidance task. Meanwhile, the pre- and post-synaptic components, synaptophysin (Syn) and post-synaptic density 95 (PSD95) expression levels were found increased in hippocampal regions lacking of Nhe5, suggesting a possible alterations in neuronal synaptic structure and function in Nhe5(-/-) mice. Further study reveals that Nhe5 deficiency leads to higher Bdnf expression levels, followed by increased phosphorylated TrkB and PLCgamma levels, indicating that Bdnf/TrkB signaling is activated due to Nhe5 deficiency. Moreover, the corresponding brain regions of Nhe5(-/-) mice display elevated ERK/CaMKII/CREB phosphorylation levels. Taken together, these findings uncover a novel physiological function of Nhe5 in regulating learning and memory, further implying Nhe5 as a potential therapeutic target for improving cognition. |
