| First Author | Koga K | Year | 2015 |
| Journal | J Neurosci | Volume | 35 |
| Issue | 5 | Pages | 2033-43 |
| PubMed ID | 25653361 | Mgi Jnum | J:219898 |
| Mgi Id | MGI:5629917 | Doi | 10.1523/JNEUROSCI.2644-14.2015 |
| Citation | Koga K, et al. (2015) Impaired presynaptic long-term potentiation in the anterior cingulate cortex of Fmr1 knock-out mice. J Neurosci 35(5):2033-43 |
| abstractText | Fragile X syndrome is a common inherited form of mental impairment. Fragile X mental retardation protein (FMRP) plays important roles in the regulation of synaptic protein synthesis, and loss of FMRP leads to deficits in learning-related synaptic plasticity and behavioral disability. Previous studies mostly focus on postsynaptic long-term potentiation (LTP) in Fmr1 knock-out (KO) mice. Here, we investigate the role of FMRP in presynaptic LTP (pre-LTP) in the adult mouse anterior cingulate cortex (ACC). Low-frequency stimulation induced LTP in layer II/III pyramidal neurons under the voltage-clamp mode. Paired-pulse ratio, which is a parameter for presynaptic changes, was decreased after the low-frequency stimulation in Fmr1 wild-type (WT) mice. Cingulate pre-LTP was abolished in Fmr1 KO mice. We also used a 64-electrode array system for field EPSP recording and found that the combination of low-frequency stimulation paired with a GluK1-containing kainate receptor agonist induced NMDA receptor-independent and metabotropic glutamate receptor-dependent pre-LTP in the WT mice. This potentiation was blocked in Fmr1 KO mice. Biochemical experiments showed that Fmr1 KO mice displayed altered translocation of protein kinase A subunits in the ACC. Our results demonstrate that FMRP plays an important role in pre-LTP in the adult mouse ACC, and loss of this pre-LTP may explain some of the behavioral deficits in Fmr1 KO mice. |
