By a News Reporter-Staff News Editor at Gene Therapy Weekly -- Investigators publish new report on Selective Serotonin Reuptake Inhibitor. According to news reporting out of Paris, France, by NewsRx editors, research stated, "Selective serotonin reuptake inhibitors (SSRI) are aimed at increasing brain 5-HT tone; however, this expected effect has a slow onset after starting SSRI treatment because of initial activation of 5-HT1A autoreceptor-mediated negative feedback of 5-HT release. After chronic SSRI treatment, 5-HT1A autoreceptors desensitize, which allows 5-HT tone elevation."
Our news journalists obtained a quote from the research from National Center for Scientific Research (CNRS), "Because 5-HT1A receptor (5-HT1AR) internalization has been proposed as a possible mechanism underlying 5-HT1A autoreceptor desensitization, we examined whether this receptor could internalize under well controlled in vitro conditions in the LLC-CPK1 cell line and in raphe or hippocampal neurons from rat embryos. To this goal, cells were transfected with recombinant lentiviral vectors encoding N-terminal tagged 5-HT1AR, and exposed to various pharmacological conditions. Constitutive endocytosis and plasma membrane recycling of tagged-5-HT1AR was observed in LLC-PK1 cells as well as in neurons. Acute exposure (for 1 h) to the full 5-HT1AR agonists, 5-HT and 5-carboxamido-tryptamine, but not the partial agonist 8-OH-DPAT, triggered internalization of tagged 5-HT1AR in serotonergic neurons only. In contrast, sustained exposure (for 24 h) to all agonists induced tagged-5-HT1AR endocytosis in raphe serotonergic neurons and a portion of hippocampal neurons, but not LLC-PK1 cells and partial agonist displayed an effect only in serotonergic neurons. In all cases, agonist-induced tagged 5-HT1AR endocytosis was prevented by the 5-HT1AR antagonist, WAY-100635, which was inactive on its own. These data showed that agonist-induced 5-HT1AR internalization does exist in neurons and depends on agonist efficacy and neuronal phenotype."
According to the news editors, the research concluded: "Its differential occurrence in serotonergic neurons supports the idea that 5-HT1AR internalization might underlie 5-HT1A autoreceptor desensitization under SSRI antidepressant therapy."
For more information on this research see: Neuronal Phenotype Dependency of Agonist-Induced Internalization of the 5-HT1A Serotonin Receptor. Journal of Neuroscience, 2014;34(1):282-294. Journal of Neuroscience can be contacted at: Soc Neuroscience, 11 Dupont Circle, NW, Ste 500, Washington, DC 20036, USA. (Society for Neuroscience - www.sfn.org/; Journal of Neuroscience - www.sfn.org/index.aspx?pagename=JournalOfNeuroscience)
Our news journalists report that additional information may be obtained by contacting E. Bouaziz, Inst Cerveau & Moelle Epiniere, Center Rech, CNRS UMR 7225, INSERM UMR 975, F-75013 Paris, France. Additional authors for this research include M.B. Emerit, G. Vodjdani, V. Gautheron, M. Hamon, M. Darmon and J. Masson (see also Selective Serotonin Reuptake Inhibitor).
Keywords for this news article include: Biotechnology, Paris, France, Europe, Neurons, Autacoids, Treatment, Endocytosis, Tryptamines, Gene Therapy, Autoreceptors, Bioengineering, Membrane Proteins, Organic Chemicals, Serotonin Receptors, Presynaptic Receptors, Cell Surface Receptors, Biogenic Amine Receptors, G-Protein-Coupled Receptors
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