Neurosciences
Magyar, Aletta
HUN-REN Institute of Experimental Medicine/ Institute of Biophysics and Radiation Biology, Semmelweis University
Aletta Horváth-Magyar1, Péter Berki2, Sándor Borbély2, Boglárka Barsy2, Anna Virág Bakacsi2, Judit Berczik2, Magor L Lőrincz3, Danqian Liu4, Ferenc Mátyás2
1: HUN-REN Institute of Experimental Medicine/ Institute of Biophysics and Radiation Biology, Semmelweis University
2: HUN-REN Institute of Experimental Medicine
3: Department of Physiology, University of Szeged
4: Center for Excellence in Brain Science and Intelligence Technology, Chinese Academy of Sciences, China-Hungary Belt-and-Road Joint laboratory on Brain Science
Rapid eye movement (REM) sleep is a well-characterized stage defining sleep quality and prefrontal cortical functions. It is well-established that it is controlled by brainstem circuits; yet, the network mechanism underlying regulation of REM sleep and the associated cortical theta oscillations remain unknown. Here, we reveal that a subpopulation of paraventricular thalamic neurons (PVTNAc) transfers the medullary REM signal to the PFC in an activity- and firing mode-dependent manner, while bidirectionally modulates cortical theta oscillations. These thalamic cells also participate in stress-induced disturbances of REM sleep. In these alterations, progressively increasing PVTNAc activity underlies the transition from REM sleep enhancement following acute stress to REM sleep suppression after repeated stress. Frequency-dependent thalamic stimulation that mimics elevated PVTNAc activity replicates the bidirectional alterations in REM-related theta oscillations and induces corresponding shifts in cortical excitatory/inhibitory balance.
Together, these findings reveal a brain-wide circuit that integrates theta rhythm-generating and stress-related signals into the PVTNAc activity, enabling it to dynamically regulate REM sleep under homeostatic and stressful conditions. Through this mechanism, PVTNAc neurons reshape prefrontal cortical network activity, reorganize sleep architecture, and influence cognitive function.
This work was supported by the following funding agencies: Ministry of Innovation and Technology of Hungary from the National Research, Development and Innovation Fund (NKFI-138836, NKFI-153312 and KKP126998 to FM; NKFI-135285, NKFI-144583 to SB; NKFI-124034 to BB; HU-RIZONT-2024-00003 to AM); Cooperative Doctoral Program (KDP-2020-1015461 to AM); Hungarian Brain Research Program (2017-1.2.1-NKP-2017-00002 to FM; NAP2022-I-7/2022 to MLL); New National Excellence Program of the Ministry for Innovation and Technology (ÚNKP-21-5-ÁTE-2 to FM; ÚNKP-22-2-III-ELTE-539 to AVB, ELKH SA-48/2021); New national excellence program of the ministry for culture and innovation from the source of the national research, development and innovation fund (EKÖP-2024-87 to PB, EKÖP-2024-276 to AVB, 2025-2.1.1-EKÖP-2025-00014 to AM); National Natural Science Foundation of China (8234101126 to DL). FM was a János Bolyai Research Fellow.