5HT3A Assays
Background of 5HT3A Receptors
5HT3A receptors belong to the ligand-gated ion channel (LGIC) superfamily. Serotonin receptor subtype 5HT3A is an ion channel that is involved in the etiological pathways of several neurological diseases. The 5HT3 receptor is well-known to mediate nausea and vomiting associated with anesthesia, surgery, and anticancer chemotherapy.
Fig.1 Hypothetical schematic representation of the 5 -HT3AR induction of neurovascular coupling within the somatosensory cortex. (Perrenoud, 2012)
Structure of 5HT3A Receptors
The α7-5HT3A receptor is a chimera that is made of two different receptors: (a) the extracellular N-terminal region of the rat α7 nicotinic acetylcholine receptor (nAChR) until Val201, and (b) the C-terminal region of the mouse 5-HT3A receptor (5-HT3AR), which includes the ion channel forming transmembrane segments and the large cytoplasmic loop.
5HT3A for Disease
Serotonin (5-HT) is a biogenic monoamine with different functions in many physiological and pathophysiological processes such as neuropsychiatric disorders such as depression, schizophrenia, anxiety, diet, sexual behavior, asthma, etc. A study indicates that one kind of the serotonin receptors, named 5HT3A, on PBMCs, causes secretion of a series of pro-inflammatory cytokines which play important roles in allergic asthma disease.
Assay List of 5HT3A Channel
Creative Biolabs can provide a range of assays of the 5HT3A channel. You can choose the assay in the list or contact us for more information:
Published Data
Paper Title | Serotonergic projections govern postnatal neuroblast migration |
Journal | Neuron |
Published | 2017 |
Abstract | Some migration principles are evolutionarily conserved, while others are species and cell-type-specific. Here, the investigators identified a serotonergic mechanism that controls the migration of postnatal-generated neurons in the mouse brain. Serotonergic axons originating from the raphe nucleus were aligned with neuroblasts derived from the subventricular zone. Optogenetic axonal activation provides functional evidence for serotonergic regulation of neuroblast migration. In addition, they found that the underlying mechanism was related to serotonin receptor 3A (5HT3A) -mediated calcium influx. Thus, loss of the 5HT3A receptor in neuroblasts impaired the speed and directionality of migration and abolished calcium spikes. They speculated that serotonergic regulation of postnatal neuroblastic migration is evolutionarily conserved, suggesting the presence of serotonergic axons in migratory pathways in other vertebrates. |
Result |
The present work provides evidence that serotonergic axons located along the migratory route control postnatal neuroblast migration via the ionized serotonin receptor 5HT3A. They found that neuroblast migration was affected upon Htr3a ablation, resulting in decreased velocity and impaired directionality. Furthermore, Htr3a knockdown abolished large calcium spikes in migrating neuroblasts, suggesting that the presence of a calcium-threshold 5HT3A receptor is a prerequisite for calcium activity. It is important to note that tangential migration of neuroblasts occurs not only in the RMS but also in the SVZ itself, which is often overlooked. Serotonergic modulation appears to be restricted to CGE-derived interneurons. Thus, loss of the serotonin transporter did not affect the laminar distribution of cortical interneurons derived from medial ganglion projections but changed the location of CGE-derived interneurons.
Fig.2 Htr3a knockout alters RMS-OB morphology and interneuron distribution in the OB. (García, 2017) |
References
- Perrenoud, Q.; et al. Activation of cortical 5-HT3 receptor-expressing interneurons induces NO mediated vasodilatations and NPY mediated vasoconstrictions. Frontiers in neural circuits. 2012, 6: 50.
- García, G.D.; et al. Serotonergic projections govern postnatal neuroblast migration. Neuron. 2017, 94(3): 534-549. e9.