ArticleBritish journal of pharmacology2018
5-HT
Article in British journal of pharmacology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
30 citing papers in PubMed, 46 citations in OpenAlex.
- Targeting GPCR Signaling in Parkinson's Disease: From Molecular Pathology to Exercise-Based Therapeutics.Molecular neurobiology · 2026Review
- Antecedent enhancer activity predicts future susceptibility to seizures in mice.Nature communications · 2026Article
- Exploring Mitochondrial DNA Copy Number in Italian Children with ADHD: Implications for Neurobiological Mechanisms.Diseases (Basel, Switzerland) · 2025Article
- Associations between dietary intake of mitochondria-related nutrients with the risk of migraine: a prospective study of 202,656 participants.The journal of headache and pain · 2025Article
- GPCRs identified on mitochondrial membranes: New therapeutic targets for diseases.Journal of pharmaceutical analysis · 2025Review
- The Mitochondrial Foundations of Parkinson's Disease: Therapeutic Implications.Aging and disease · 2025Review
- Evidence-based review and frontiers of migraine therapy.Neurogastroenterology and motility · 2025Review
- Targeting 5-HT Is a Potential Therapeutic Strategy for Neurodegenerative Diseases.International journal of molecular sciences · 2024Review
- 5-Hydroxytryptamine 1F Receptor Agonist Lasmiditan Differentially Regulates Successful Repair and Failed Repair Genes in a Mouse Model of Acute Kidney Injury.ACS pharmacology & translational science · 2024Article
- Serotonin effects on human iPSC-derived neural cell functions: from mitochondria to depression.Molecular psychiatry · 2024Article
- Activation of the 5-HT1A Receptor by Eltoprazine Restores Mitochondrial and Motor Deficits in aInternational journal of molecular sciences · 2024Article
- Serotonin regulation of mitochondria in kidney diseases.Pharmacological research · 2024Review
- Activation of G-protein-coupled receptor 39 reduces neuropathic pain in a rat model.Neural regeneration research · 2024Article
- Mitophagy regulates mitochondrial number following pharmacological induction of mitochondrial biogenesis in renal proximal tubule cells.Frontiers in pharmacology · 2024Article
- 5-HTFrontiers in cellular neuroscience · 2024Article
- Mitochondrial Dysfunction as a Signaling Target for Therapeutic Intervention in Major Neurodegenerative Disease.Neurotoxicity research · 2023Review
- The 5-HTNature reviews. Neurology · 2023Review
- 5-HTFrontiers in pharmacology · 2022Article
- A molecular framework for autistic experiences: Mitochondrial allostatic load as a mediator between autism and psychopathology.Frontiers in psychiatry · 2022Article
- FDA-approved 5-HTExperimental neurology · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
background and purposeParkinson's disease is characterized by progressive decline in motor function due to degeneration of nigrostriatal dopaminergic neurons, as well as other deficits including cognitive impairment and behavioural abnormalities. Mitochondrial dysfunction, leading to loss of ATP-dependent cellular functions, calcium overload, excitotoxicity and oxidative stress, is implicated in the pathophysiology of Parkinson's disease. Using the 5-HT EXPERIMENTAL APPROACH: Male C57BL/6 mice underwent bilateral intrastriatal 6-hydroxydopamine or saline injections and daily treatment with 2 mg·kg KEY
resultsIncreased mitochondrial DNA content and nuclear- and mitochondrial-encoded mRNA and protein expression was observed in specific brain regions of LY344864-treated naïve and lesioned mice, indicating augmented MB. LY344864 attenuated TH-ir loss in the striatum and substantia nigra compared to vehicle-treated lesioned animals. LY344864 treatment also increased locomotor activity in 6-hydroxydopamine lesioned mice, while vehicle treatment had no effect. CONCLUSIONS AND IMPLICATIONS: These data revealed that LY344864-induced MB attenuates dopaminergic neuron loss and improves behavioural endpoints in this model. We suggest that stimulating MB may be beneficial for the treatment of Parkinson's disease and that the 5-HT
Indexed as
Identifiers
What OpenQuestion holds
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.