The Prototoxin lynx1 Acts on Nicotinic Acetylcholine Receptors to Balance Neuronal Activity and Survival In Vivo
Open accessAbstract
Nicotinic acetylcholine receptors (nAChRs) affect a wide array of biological processes, including learning and memory, attention, and addiction. lynx1, the founding member of a family of mammalian prototoxins, modulates nAChR function in vitro by altering agonist sensitivity and desensitization kinetics. Here we demonstrate, through the generation of lynx1 null mutant mice, that lynx1 modulates nAChR signaling in vivo. Its loss decreases the EC(50) for nicotine by approximately 10-fold, decreases receptor desensitization, elevates intracellular calcium levels in response to nicotine, and enhances synaptic efficacy. lynx1 null mutant mice exhibit enhanced performance in specific tests of learning and memory. Consistent with reports that mutations resulting in hyperactivation of nAChRs can lead to neurodegeneration, aging lynx1 null mutant mice exhibit a vacuolating degeneration that is exacerbated by nicotine and ameliorated by null mutations in nAChRs. We conclude that lynx1 functions as an allosteric modulator of nAChR function in vivo, balancing neuronal activity and survival in the CNS.
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Lynx1KO mice demonstrate cognitive enhancements and neurological changes.
“Lynx1KO mice demonstrate cognitive enhancements and neurological changes (116), features associated with hyperactive nAChRs, including improved learning, increased intracellular Ca2+ in response to nicotine treatment, less receptor desensitization, and heightened nicotine sensitivity.”
From Nicotine is a selective pharmacological chaperone of acetylcholine receptor number and stoichiometry. Implications for drug discovery (2009) · cites this paper as [116]
Aging lynx1 KO mice undergo a striatal degeneration that is exacerbated by nicotine and ameliorated by crossing lynx1KO mice with those lacking α7 nAChRs, indicating that both α7 and α4β2-type nAChRs may be important targets of lynx1 genes.
“Aging lynx1 KO mice undergo a striatal degeneration which is exacerbated by nicotine and ameliorated by crossing lynx1KO mice with those lacking α7 nAChRs, indicating that both α7 and α4β2-type nAChRs may be important targets of lynx1 genes (116).”
From Nicotine is a selective pharmacological chaperone of acetylcholine receptor number and stoichiometry. Implications for drug discovery (2009) · cites this paper as [116]
Lynx1 KO mice display decreased ACh EC50 values, closer to EC50 values of the receptor expressed in oocytes alone.
“Indeed, lynx1 KO mice display decreased ACh EC50 values, closer to EC50 values of the receptor expressed in oocytes alone (116).”
From Nicotine is a selective pharmacological chaperone of acetylcholine receptor number and stoichiometry. Implications for drug discovery (2009) · cites this paper as [116]
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- Authors
- Miwa, J. M., Stevens, T. R., King, S. L., Caldarone, B. J., Ibanez-Tallon, I., Xiao, C., Fitzsimonds, R. M., Pavlides, C., Lester, H. A., Picciotto, M. R., & Heintz, N.
- Affiliations
- Howard Hughes Medical Institute (US)
- Yale University (US)
- California Institute of Technology (US)
- Rockefeller University (US)
- Corresponding author
- Heintz, Nathaniel
- ORCID
- Venue
- Neuron
- Publisher
- Elsevier BV
- Published
- 2006-09
- Volume
- 51
- Issue
- 5
- Pages
- 587-600
- ISSN
- 0896-6273 (ISSN-L)
- OpenAlex
- W2103841407
- Cited by
- 154
- References
- 70
- Citations by year
- 2026: 1 · 2025: 2 · 2024: 6 · 2023: 4 · 2022: 4 · 2021: 10 · 2020: 10 · 2019: 6 · 2018: 4 · 2017: 8 · 2016: 9 · 2015: 12 · 2014: 13 · 2013: 7 · 2012: 8
- FWCI
- 3.26
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- www.elsevier.com/tdm/userlicense/1.0/ (tdm)
- www.elsevier.com/legal/tdmrep-license (tdm)
- www.elsevier.com/open-access/userlicense/1.0/ (vor, 2511 d)
- doi.org/10.15223/policy-017 (stm-asf)
- doi.org/10.15223/policy-037 (stm-asf)
- doi.org/10.15223/policy-012 (stm-asf)
- doi.org/10.15223/policy-029 (stm-asf)
- doi.org/10.15223/policy-004 (stm-asf)
- Locations
- Neuron (publishedVersion)
- PubMed (publishedVersion)
- CaltechAUTHORS (California Institute of Technology) (submittedVersion)
- Figshare (submittedVersion, cc-by)
- Funders
- National Institute on Alcohol Abuse and Alcoholism (P50AA015632, AA15632)
- National Institute on Drug Abuse (DA 15241, DA17279, R01DA017279, DA 00436)
- National Cancer Institute (CA 09673, T32CA009673)
- National Institute of Neurological Disorders and Stroke (R21NS047751)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Nicotinic Acetylcholine Receptors Study
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Receptor Mechanisms and Signaling
- Keywords
- Lynx1, nicotinic acetylcholine receptors, allosteric modulation, nicotine sensitivity, receptor desensitization, intracellular calcium, synaptic efficacy, learning and memory, neurodegeneration, neuronal activity, neuronal survival, null mice
- MeSH terms
- Age Factors, Animals, Association Learning, Brain, Cell Survival, Membrane Glycoproteins, Membrane Potentials, Mice, Mutant Strains, Mutation, Nerve Degeneration, Neurons, Neuropeptides, Nicotine, Receptors, Nicotinic, Patch-Clamp Techniques, Excitatory Amino Acid Agonists, Nicotinic Agonists, Adaptor Proteins, Signal Transducing, Mice
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