Heterozygosity for the mood disorder-associated variant Gln460Arg alters P2X7 receptor function and sleep quality
Open accessAbstract
A single nucleotide polymorphism substitution from glutamine (Gln, Q) to arginine (Arg, R) at codon 460 of the purinergic P2X7 receptor (P2X7R) has repeatedly been associated with mood disorders. The P2X7R-Gln460Arg variant per se is not compromised in its function. However, heterologous expression of P2X7R-Gln460Arg together with wild-type P2X7R has recently been demonstrated to impair receptor function. Here we show that this also applies to humanized mice coexpressing both human P2X7R variants. Primary hippocampal cells derived from heterozygous mice showed an attenuated calcium uptake upon agonist stimulation. While humanized mice were unaffected in their behavioral repertoire under basal housing conditions, mice that harbor both P2X7R variants showed alterations in their sleep quality resembling signs of a prodromal disease stage. Also healthy heterozygous human subjects showed mild changes in sleep parameters. These results indicate that heterozygosity for the wild-type P2X7R and its mood disorder-associated variant P2X7R-Gln460Arg represents a genetic risk factor, which is potentially able to convey susceptibility to mood disorders. SIGNIFICANCE STATEMENTDepression and bipolar disorder are the most common mood disorders. The P2X7 receptor (P2X7R) regulates many cellular functions. Its polymorphic variant Gln460Arg has repeatedly been associated with mood disorders. Genetically engineered mice, with human P2X7R, revealed that heterozygous mice (i.e., they coexpress the disease-associated Gln460Arg variant together with its normal version) have impaired receptor function and showed sleep disturbances. Human participants with the heterozygote genotype also had subtle alterations in their sleep profile. Our findings suggest that altered P2X7R function in heterozygote individuals disturbs sleep and might increase the risk for developing mood disorders.
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hP2X7R-Gln460Arg mice show increased vulnerability to chronic social defeat stress.
“Finally, hP2X7R-Gln460Arg mice show increased vulnerability to chronic social defeat stress.”
From P2X7 Receptor Signaling in Stress and Depression (2019) · cites this paper as [77]
Mice expressing human P2X7R with either normal or altered gene present with no behavioral changes or alterations in P2X7R activity.
“Specifically, regarding the controversy on the association of Gln460Arg polymorphism in the P2X7R gene with MDD as discussed above, recent data show that mice expressing human P2X7R, with either normal (hP2X7R-wild type) or altered gene (hP2X7R-Gln460Arg), present with no behavioral changes or alterations in P2X7R activity [77].”
From P2X7 Receptor Signaling in Stress and Depression (2019) · cites this paper as [77]
Heterozygotic individuals may be more susceptible to development of depression through interaction between genetic predisposition and stress exposure.
“These results indicate that heterozygotic individuals may be more susceptible to development of depression through interaction between genetic predisposition and stress exposure [77].”
From P2X7 Receptor Signaling in Stress and Depression (2019) · cites this paper as [77]
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Self-citationFarooq, R. K., Tanti, A., Ainouche, S., Roger, S., Belzung, C., & Camus, V. (2018) · Psychoneuroendocrinology · doi:10.1016/j.psyneuen.2018.07.016 · Cited by 83 · see citing works
- Authors
- Metzger, M. W., Walser, S. M., Dedic, N., Aprile-Garcia, F., Jakubcakova, V., Adamczyk, M., Webb, K. J., Uhr, M., Refojo, D., Schmidt, M. V., Friess, E., Steiger, A., Kimura, M., Chen, A., Holsboer, F., Arzt, E., Wurst, W., & Deussing, J. M.
- Affiliations
- Max Planck Institute of Psychiatry (DE)
- Max Planck Society (DE)
- German Center for Neurodegenerative Diseases (DE)
- ORCID
- Venue
- The Journal of Neuroscience
- Publisher
- Society for Neuroscience
- Published
- 2017-10-27
- Volume
- 37
- Issue
- 48
- Pages
- 11688-11700
- ISSN
- 0270-6474 (ISSN-L)
- 1529-2401
- PMC
- PMC6705750
- OpenAlex
- W2766237804
- Cited by
- 59
- References
- 72
- Citations by year
- 2026: 4 · 2025: 3 · 2024: 7 · 2023: 9 · 2022: 10 · 2021: 7 · 2020: 4 · 2019: 6 · 2018: 8
- FWCI
- 3.77
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Journal of Neuroscience (publishedVersion, cc-by-nc-sa)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- LA Referencia (Red Federada de Repositorios Institucionales de Publicaciones Científicas) (publishedVersion, other-oa)
- Americanae (AECID Library) (submittedVersion, cc-by-nc-sa)
- Max Planck Digital Library (submittedVersion)
- Site cant be reached (submittedVersion)
- MPG.PuRe (Max Planck Society) (submittedVersion)
- PuSH - Publication Server of Helmholtz Zentrum München (submittedVersion)
- Funders
- Bundesministerium für Bildung und Forschung (FKZ 01ZX1314H, 01DN16028, FKZ 01DN16028)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Physiology › Adenosine and Purinergic Signaling
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Keywords
- P2X7 receptor, heterozygosity, mood disorders, sleep quality, depression, bipolar disorder, genetic risk factors, purinergic signaling, calcium uptake, humanized mice, hippocampal cells, sleep disorders
- MeSH terms
- Animals, Arginine, Cells, Cultured, Glutamine, Heterozygote, Hippocampus, Humans, Male, Mice, Inbred C57BL, Mice, Transgenic, Sleep, Genetic Variation, Mood Disorders, Mice, Mice, 129 Strain, Receptors, Purinergic P2X7
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Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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