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Biological Research of Rhythms in the Nervous System

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Neurobiology".

Deadline for manuscript submissions: 20 August 2025 | Viewed by 1983

Special Issue Editors


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Guest Editor
Department of Psychiatry, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA
Interests: neuropharmacology; neurochemistry systems; integrative neuroscience

E-Mail Website
Guest Editor
Medizinischen Fakultät Heidelberg, Heidelberg, Germany
Interests: GABAergic synapses; epilepsy; rapid network oscillations in the hippocampus

Special Issue Information

Dear Colleagues,

Network oscillations are essential for cognitive functions, they are modified by psychoactive substances, and oscillopathies contribute to cognitive dysfunction in neurologic and psychiatric diseases. Biological research of rhythms in the nervous system involves a wide variety of approaches, and requires the collaboration of scientists in different fields, from mathematical modeling and signal analysis to neurophysiological experiments on membrane, cellular, and network levels, to human electroencephalography and clinical studies of cognitive deficits due to impairments of these mechanisms. The past decades saw major advances in understanding the origin of neural oscillations and in collecting essential observations on altered patterns of rhythmic activity serving as biomarkers in clinical practice.

This Special Issue will focus on recent research of rhythmic activity of the nervous system including basic research concerning cellular and network mechanisms, the effect of psychoactive compounds on oscillations, and its pathology in neuropsychiatric disorders with cognitive deficits.

Dr. Bernát Kocsis
Prof. Dr. Andreas Draguhn
Guest Editors

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Keywords

  • mechanisms of rhythmic synchronization
  • rhythmic firing
  • neural network oscillations
  • rhythmic components in EEG
  • oscillopathy
  • theta and gamma rhythm
  • sleep spindle
  • rhythmic activity and cognition
  • pathology of rhythmic synchronization in the nervous system
  • altered rhythmic activity in neuropsychiatric disorders

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Published Papers (2 papers)

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19 pages, 9288 KiB  
Article
Neural Mechanism of 5-HT4R-Mediated Memory Enhancement in Hippocampal–Prefrontal Circuits in a Mouse Model of Schizophrenia
by Thomas Gener, Sara Hidalgo-Nieves, Cristina López-Cabezón and Maria Victoria Puig
Int. J. Mol. Sci. 2025, 26(8), 3659; https://doi.org/10.3390/ijms26083659 - 12 Apr 2025
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Abstract
We investigated the cellular and neurophysiological mechanisms underlying the pro-cognitive effects of 5-HT4R activation in hippocampal–prefrontal pathways. Our findings show that, in addition to pyramidal neurons, 30–60% of parvalbumin+ interneurons in the CA1, CA3, and dentate gyrus (DG) of the hippocampus and the [...] Read more.
We investigated the cellular and neurophysiological mechanisms underlying the pro-cognitive effects of 5-HT4R activation in hippocampal–prefrontal pathways. Our findings show that, in addition to pyramidal neurons, 30–60% of parvalbumin+ interneurons in the CA1, CA3, and dentate gyrus (DG) of the hippocampus and the anterior cingulate (ACC), prelimbic (PL), and infralimbic (IL) regions of the prefrontal cortex co-express 5-HT4Rs. Additionally, 15% of somatostatin+ interneurons in CA1 and CA3 express 5-HT4Rs. Partial 5-HT4R agonist RS-67333 (1 mg/kg, i.p.) exerted anxiolytic effects and ameliorated short-term (3-min) and long-term (24-h) memory deficits in a mouse model of schizophrenia-like cognitive impairment induced by sub-chronic phencyclidine (sPCP) but did not enhance memory in healthy mice. At the neurophysiological level, RS-67333 normalized sPCP-induced disruptions in hippocampal–prefrontal neural dynamics while having no effect in healthy animals. Specifically, sPCP increased delta oscillations in CA1 and PL, leading to aberrant delta–high-frequency coupling in CA1 and delta–high-gamma coupling in PL. RS-67333 administration attenuated this abnormal delta synchronization without altering phase coherence or signal directionality within the circuit. Collectively, these results highlight the therapeutic potential of 5-HT4R activation in pyramidal, parvalbumin+, and somatostatin+ neurons of hippocampal–prefrontal pathways for mitigation of cognitive and negative symptoms associated with schizophrenia. Full article
(This article belongs to the Special Issue Biological Research of Rhythms in the Nervous System)
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15 pages, 1903 KiB  
Article
Wakefulness Induced by TAAR1 Partial Agonism in Mice Is Mediated Through Dopaminergic Neurotransmission
by Sunmee Park, Jasmine Heu, Marius C. Hoener and Thomas S. Kilduff
Int. J. Mol. Sci. 2024, 25(21), 11351; https://doi.org/10.3390/ijms252111351 - 22 Oct 2024
Cited by 1 | Viewed by 886
Abstract
Trace amine-associated receptor 1 (TAAR1) is a negative regulator of dopamine (DA) release. The partial TAAR1 agonist RO5263397 promotes wakefulness and suppresses NREM and REM sleep in rodents and non-human primates. We tested the hypothesis that the TAAR1-mediated effects on sleep/wake regulation were [...] Read more.
Trace amine-associated receptor 1 (TAAR1) is a negative regulator of dopamine (DA) release. The partial TAAR1 agonist RO5263397 promotes wakefulness and suppresses NREM and REM sleep in rodents and non-human primates. We tested the hypothesis that the TAAR1-mediated effects on sleep/wake regulation were due, in part, to DA release. Male C57BL6/J mice (n = 8) were intraperitoneally administered the D1R antagonist SCH23390, the D2R antagonist eticlopride, a combination of D1R + D2R antagonists, or saline at ZT5.5, followed 30 min later by RO5263397 or vehicle per os. EEG, EMG, subcutaneous temperature, and activity were recorded across the 8 treatments and sleep architecture was analyzed for 6 h post-dosing. As described previously, RO5263397 increased wakefulness and delayed NREM and REM sleep onset. D1, D2, and D1 + D2 pretreatment reduced RO5263397-induced wakefulness for 1–2 h after dosing but only the D1 antagonist significantly reduced the TAAR1-mediated increase in NREM latency. Neither the D1 nor the D2 antagonist affected the TAAR1-mediated suppression of REM sleep. These results suggest that, whereas the TAAR1 effects on wakefulness are mediated, in part, through the D2R, D1R activation plays a role in reversing the TAAR1-mediated increase in NREM sleep latency. In contrast, the TAAR1-mediated suppression of REM sleep appears not to involve D1R or D2R mechanisms. Full article
(This article belongs to the Special Issue Biological Research of Rhythms in the Nervous System)
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