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Cited by 130Nicotinic Acetylcholine Receptors StudyNeuroscience and Neuropharmacology ResearchCell death mechanisms and regulation

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

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Orr‐Urtreger, Avi, Broide, Ron S., Kasten, Michael R., Dang, Hong, Dani, John A., Beaudet, Arthur L., Patrick, James W.·2000·Journal of Neurochemistry
DOI 10.1046/j.1471-4159.2000.0742154.x
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Abstract

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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Crossref · 10.1046/j.1471-4159.2000.0742154.x

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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)
ORCID
Venue
Journal of Neurochemistry
Publisher
Wiley
Published
2000-05
Volume
74
Issue
5
Pages
2154-2166
ISSN
  • 0022-3042 (ISSN-L)
  • 1471-4159
DOI
10.1046/j.1471-4159.2000.0742154.x
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
Licence
onlinelibrary.wiley.com/termsAndConditions#vor (vor, 3012 d)
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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