Schizophrenia is a complex psychiatric disorder characterised by positive and negative symptoms, cognitive impairments, attentional problems, anxiety and depressive symptoms. The use of atypical antipsychotics has generally improved clinical outcome yet medical need remains in the treatment of this disease. The potential use of 5-HT(1A) receptor agonism is emerging as one potential area that could be exploited to improve clinical management of the disease. 5-HT(1A) receptor agonism will not reduce hyperprolactinaemia but does appear to enhance effects on positive, negative and cognitive symptoms and also treat attentional depressive and anxiety symptoms. However, these improvements are not at the expense extrapyramidal side effects and indeed may attenuate the effects of D(2) receptor antagonism. Agonism at the 5-HT(1A) receptor might therefore offer potential benefits to the pallet of existing strategies for the treatment of schizophrenia. We review existing data in support of this. However, further clinical data are needed to prove these hypotheses.
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http://dx.doi.org/10.2174/138161210790361470 | DOI Listing |
Eur J Neurosci
January 2025
Laboratory of Cortico-Visceral Physiology, Pavlov Institute of Physiology of the Russian Academy of Sciences, Saint Petersburg, Russia.
The serotonergic raphe magnus (RMg) and dorsal raphe (DR) nuclei are crucial pain-regulating structures, which nociceptive activity is shown to be altered in gut pathology, but the underlying neuroplastic changes remain unclear. Considering the importance of 5-HT1A receptors in modulating both pain and raphe neuronal activity, in this study, we aimed to determine whether 5-HT1A-dependent visceral and somatic nociceptive processing within the RMg and DR is modified in postcolitis conditions. In anaesthetised male Wistar rats, healthy control and recovered from TNBS-induced colitis, the microelectrode recordings of RMg and DR neuron responses to noxious colorectal distension (CRD) or tail squeezing (TS) were performed prior and after intravenous administration of 5-HT1A agonist, buspirone.
View Article and Find Full Text PDFJ Nat Prod
January 2025
Charlotte's Web, 700 Tech Court, Louisville, Colorado 80027, United States.
Cannabicyclol ((±)-CBL), a minor phytocannabinoid, is largely unexplored, with its biological activity previously undocumented. We studied its conversion from cannabichromene (CBC) using various acidic catalysts. Montmorillonite (K30) in chloroform at room temperature had the highest yield (60%) with minimal byproducts.
View Article and Find Full Text PDFInt J Mol Sci
December 2024
Department of Neurosciences, Lerner Research Institute, Cleveland Clinic, Cleveland, OH 44195, USA.
Spinal cord injury (SCI) results in functional deficits below the injured spinal level. The descending serotonergic system in the spinal cord is critically involved in the control of motor and autonomic functions. Specifically, SCI damages the projections of serotonergic fibers, which leads to reduced serotonin inputs and increased amounts of spinal serotonergic receptors.
View Article and Find Full Text PDFBiochem Pharmacol
January 2025
Department of Biomedical Sciences, Tilman J. Fertitta Family College of Medicine, University of Houton, Houston, TX, 77204, USA. Electronic address:
Cannabidiol (CBD), a phytocannabinoid, has emerged as a promising candidate for addressing a wide array of symptoms. It has the ability to bind to multiple proteins and receptors, including 5-HT1AR, transient receptor potential vanilloid 1 (TRPV1), and cannabinoid receptors. However, CBD's pharmacodynamic interaction with 5-HT1AR and its medicinal outcomes are still debated.
View Article and Find Full Text PDFJ Neurodev Disord
January 2025
Graduate Neuroscience Program, University of California, Riverside, CA, USA.
Background: Fragile X syndrome (FXS) is a leading known genetic cause of intellectual disability and autism spectrum disorders (ASD)-associated behaviors. A consistent and debilitating phenotype of FXS is auditory hypersensitivity that may lead to delayed language and high anxiety. Consistent with findings in FXS human studies, the mouse model of FXS, the Fmr1 knock out (KO) mouse, shows auditory hypersensitivity and temporal processing deficits.
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