ArticleNeuropharmacology2012
Impact of human D398N single nucleotide polymorphism on intracellular calcium response mediated by α3β4α5 nicotinic acetylcholine receptors.
Article in Neuropharmacology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 55 citations in OpenAlex.
- The many enigmas of nicotine.Advances in pharmacology (San Diego, Calif.) · 2024Review
- Article
- A common SNP in Chrna5 enhances morphine reward in female mice.Neuropharmacology · 2022Article
- Functional studies of lung cancer GWAS beyond association.Human molecular genetics · 2022Review
- Article
- The Intergenerational Transmission of Developmental Nicotine Exposure-Induced Neurodevelopmental Disorder-Like Phenotypes is Modulated by the Chrna5 D397N Polymorphism in Adolescent Mice.Behavior genetics · 2021Article
- Chr15q25 Genetic Variant rs16969968 Alters Cell Differentiation in Respiratory Epithelia.International journal of molecular sciences · 2021Article
- Linking the CHRNA5 SNP to drug abuse liability: From circuitry to cellular mechanisms.Neuropharmacology · 2021Review
- Concatemers to re-investigate the role of α5 in α4β2 nicotinic receptors.Cellular and molecular life sciences : CMLS · 2021Article
- Genetic Modifiers of Oral Nicotine Consumption inFrontiers in psychiatry · 2021Article
- 2018 Langley Award for Basic Research on Nicotine and Tobacco: Bringing Precision Medicine to Smoking Cessation.Nicotine & tobacco research : official journal of the Society for Research on Nicotine and Tobacco · 2020Review
- The α5 Nicotinic Acetylcholine Receptor Subunit Differentially Modulates α4β2Frontiers in synaptic neuroscience · 2020Review
- The role of the nAChR subunits α5, β2, and β4 on synaptic transmission in the mouse superior cervical ganglion.Physiological reports · 2019Article
- Clarifying the Role of the Rostral Interpeduncular Nucleus in Aversion to Nicotine.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019Article
- Compartmentalized Devices as Tools for Investigation of Human Brain Network Dynamics.Developmental dynamics : an official publication of the American Association of Anatomists · 2019Review
- The interaction of the Chrna5 D398N variant with developmental nicotine exposure.Genes, brain, and behavior · 2018Article
- Chrna5-Expressing Neurons in the Interpeduncular Nucleus Mediate Aversion Primed by Prior Stimulation or Nicotine Exposure.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018Article
- Human nicotinic receptors in chromaffin cells: characterization and pharmacology.Pflugers Archiv : European journal of physiology · 2018Review
- Insights Into Nicotinic Receptor Signaling in Nicotine Addiction: Implications for Prevention and Treatment.Current neuropharmacology · 2018Review
- Deletion of α5 nicotine receptor subunits abolishes nicotinic aversive motivational effects in a manner that phenocopies dopamine receptor antagonism.The European journal of neuroscience · 2017Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
The human CHRNA5 D398N polymorphism (rs16969968) causes an aspartic acid to asparagine change in the nicotinic acetylcholine receptor (nAChR) α5 subunit gene. The N398 variant of CHRNA5 is linked to increased risk for nicotine dependence. In this study, we explored the effect of the CHRNA5 D398N polymorphism on the properties of human α3β4* nicotinic acetylcholine receptors in human embryonic kidney (HEK) cells. Addition of either D398 or N398 variant of α5 subunit in the α3β4* receptor did not affect total [(125)I]-epibatidine binding or surface expression of the receptor. However, addition of α5(D398) into α3β4* receptor decreased the maximal response to agonist without significantly affecting EC(50) in aequorin intracellular calcium assay. α3β4α5(N398) nAChRs showed further decreased maximal response. The differences in agonist efficacy between the receptor subtypes were found to be dependent upon the concentration of external calcium but independent of external sodium. Moreover, activation of α3β4α5 nAChRs led to significantly greater intracellular calcium release from IP(3) stores relative to α3β4 nAChRs although no effect of the α5 polymorphism was observed. Finally, inclusion of the α5 variant caused a small shift to the left in IC(50) for some of the antagonists tested, depending upon α5 variant but did not affect sensitivity of α3β4* receptors to desensitization in response to incubation with nicotine. In conclusion, addition of either variant of α5 into an α3β4α5 receptor similarly effects receptor pharmacology and function. However, the N398 variant exhibits a reduced response to agonists when extracellular calcium is high and it may lead to distinct downstream cellular signaling.
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