The DOI matches its Crossref record; 65 of the 65 references it cites were found in a registry or an index.
Mice Homozygous for the L250T Mutation in the α7 Nicotinic Acetylcholine Receptor Show Increased Neuronal Apoptosis and Die Within 1 Day of Birth
Open accessAbstract
Abstract: The α7 nicotinic acetylcholine receptor (nAChR) has been implicated in modulating neurotransmitter release and may play a role in the regulation of neuronal growth and differentiation. A threonine for leucine 247 substitution in the channel domain of the chick α7 nAChR increases agonist affinity and decreases the rate of desensitization, creating a “gain of function” model for this receptor. We have generated mice that express the analogous mutation (L250T) in the α7 nAChR using the techniques of homologous recombination and here report their characteristics. Mice heterozygous (+/T) for the L250T mutation are viable, fertile, and anatomically normal compared with wild‐type littermates. In contrast, homozygous (T/T) L250T mice die within 2‐24 h of birth. Brains of T/T mouse pups exhibit a marked reduction in α7 nAChR protein levels and show extensive apoptotic cell death throughout the somatosensory cortex. Furthermore, α7 L250T nAChRs are functionally expressed on neurons within the brains of T/T neonatal mice and have properties that are consistent with those observed for the rat α7 L250T and the chick α7 L247T mutant nAChRs expressed in oocytes. These findings indicate that neurons in the developing brain expressing only α7 L250T mutant nAChRs are susceptible to abnormal apoptosis, possibly due to increased Ca 2+ influx.
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“We also conclude that lynx1 plays a critical role in maintaining a balance between the beneficial effects of short-term nAChR activation (117) and the potentially devastating degenerative excitotoxic effects of chronic over-activation of nAChRs (118,119).”
From Nicotine is a selective pharmacological chaperone of acetylcholine receptor number and stoichiometry. Implications for drug discovery (2009) · cites this paper as [118]
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Metadata
- Authors
- Orr‐Urtreger, A., Broide, R. S., Kasten, M. R., Dang, H., Dani, J. A., Beaudet, A. L., & Patrick, J. W.
- Affiliations
- Baylor College of Medicine (US)
- Venue
- Journal of Neurochemistry
- Publisher
- Wiley
- Published
- 2000-05
- Volume
- 74
- Issue
- 5
- Pages
- 2154-2166
- ISSN
- 0022-3042 (ISSN-L)
- 1471-4159
- OpenAlex
- W2030551857
- Cited by
- 129
- References
- 65
- Citations by year
- 2024: 2 · 2023: 2 · 2021: 1 · 2020: 6 · 2019: 2 · 2018: 5 · 2015: 3 · 2014: 5 · 2013: 5 · 2012: 3
- FWCI
- 5.43
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Neurochemistry (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institute on Drug Abuse (DA 04077, DA09411, R01DA009411)
- National Institute of Neurological Disorders and Stroke (NS 21229)
- 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 › Cell death mechanisms and regulation
- Keywords
- alpha7 nicotinic acetylcholine receptor, gain-of-function mutations, neuronal apoptosis, neonatal lethality, somatosensory cortex, receptor desensitization, calcium influx, brain development, mouse model
- MeSH terms
- Animals, Animals, Newborn, Death, Electric Conductivity, Heterozygote, Homozygote, Mutation, Nervous System, Neurons, Oocytes, Receptors, Nicotinic, Somatosensory Cortex, Xenopus laevis, Apoptosis, Mice
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