| First Author | Hong J | Year | 2016 |
| Journal | Mol Brain | Volume | 9 |
| Issue | 1 | Pages | 100 |
| PubMed ID | 27998287 | Mgi Jnum | J:260583 |
| Mgi Id | MGI:6142585 | Doi | 10.1186/s13041-016-0276-5 |
| Citation | Hong J, et al. (2016) The thalamic mGluR1-PLCbeta4 pathway is critical in sleep architecture. Mol Brain 9(1):100 |
| abstractText | The transition from wakefulness to a nonrapid eye movement (NREM) sleep state at the onset of sleep involves a transition from low-voltage, high-frequency irregular electroencephalography (EEG) waveforms to large-amplitude, low-frequency EEG waveforms accompanying synchronized oscillatory activity in the thalamocortical circuit. The thalamocortical circuit consists of reciprocal connections between the thalamus and cortex. The cortex sends strong excitatory feedback to the thalamus, however the function of which is unclear. In this study, we investigated the role of the thalamic metabotropic glutamate receptor 1 (mGluR1)-phospholipase C beta4 (PLCbeta4) pathway in sleep control in PLCbeta4-deficient (PLCbeta4(-/-)) mice. The thalamic mGluR1-PLCbeta4 pathway contains synapses that receive corticothalamic inputs. In PLCbeta4(-/-) mice, the transition from wakefulness to the NREM sleep state was stimulated, and the NREM sleep state was stabilized, which resulted in increased NREM sleep. The power density of delta (delta) waves increased in parallel with the increased NREM sleep. These sleep phenotypes in PLCbeta4(-/-) mice were consistent in TC-restricted PLCbeta4 knockdown mice. Moreover, in vitro intrathalamic oscillations were greatly enhanced in the PLCbeta4(-/-) slices. The results of our study showed that thalamic mGluR1-PLCbeta4 pathway was critical in controlling sleep architecture. |
