ArticleeLife2024
Serotonergic and dopaminergic neurons in the dorsal raphe are differentially altered in a mouse model for parkinsonism.
Article in eLife, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- BBX maintains mammalian brain development by repressing p53-mediated p21 expression.EMBO reports · 2026Article
- Diosgenin activates ERα-dependent PI3K/AKT/GSK3β signaling to enhance brain-derived serotonin and alleviate postmenopausal bone loss.Journal of advanced research · 2026Article
- From Synaptic Plasticity to Neurodegeneration: BDNF as a Transformative Target in Medicine.International journal of molecular sciences · 2025Review
- The brainstem reticular formation pivots abnormal neural transmission in the course of Anorexia Nervosa.Journal of neural transmission (Vienna, Austria : 1996) · 2025Review
- Brainstem serotonin amplifies nociceptive transmission in a mouse model of Parkinson's disease.NPJ Parkinson's disease · 2025Article
- Intranasal delivery of dodecyl creatine ester alleviates motor deficits and increases dopamine levels in a 6-OHDA rat model of parkinsonism.Frontiers in aging neuroscience · 2025Article
- Bidirectional crosstalk between microglia and serotonin signaling in neuroinflammation and CNS disorders.Frontiers in immunology · 2025Review
- GABALAGEN Alleviates Stress-Induced Sleep Disorders in Rats.Biomedicines · 2024Article
- Article
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Authors and funding
6 authors.
Funding
Abstract
Parkinson's disease (PD) is characterized by motor impairments caused by degeneration of dopamine neurons in the substantia nigra pars compacta. In addition to these symptoms, PD patients often suffer from non-motor comorbidities including sleep and psychiatric disturbances, which are thought to depend on concomitant alterations of serotonergic and noradrenergic transmission. A primary locus of serotonergic neurons is the dorsal raphe nucleus (DRN), providing brain-wide serotonergic input. Here, we identified electrophysiological and morphological parameters to classify serotonergic and dopaminergic neurons in the murine DRN under control conditions and in a PD model, following striatal injection of the catecholamine toxin, 6-hydroxydopamine (6-OHDA). Electrical and morphological properties of both neuronal populations were altered by 6-OHDA. In serotonergic neurons, most changes were reversed when 6-OHDA was injected in combination with desipramine, a noradrenaline (NA) reuptake inhibitor, protecting the noradrenergic terminals. Our results show that the depletion of both NA and dopamine in the 6-OHDA mouse model causes changes in the DRN neural circuitry.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.