The DOI matches its Crossref record; 5 of the 5 references it cites were found in a registry or an index.
Mice Lacking Ataxin-1 Display Learning Deficits and Decreased Hippocampal Paired-Pulse Facilitation
Open accessAbstract
Spinocerebellar ataxia type 1 (SCA1) is a neurodegenerative disorder characterized by ataxia, progressive motor deterioration, and loss of cerebellar Purkinje cells. To investigate SCA1 pathogenesis and to gain insight into the function of the SCA1 gene product ataxin-1, a novel protein without homology to previously described proteins, we generated mice with a targeted deletion in the murine Sca1 gene. Mice lacking ataxin-1 are viable, fertile, and do not show any evidence of ataxia or neurodegeneration. However,Sca1 null mice demonstrate decreased exploratory behavior, pronounced deficits in the spatial version of the Morris water maze test, and impaired performance on the rotating rod apparatus. Furthermore, neurophysiological studies performed in area CA1 of the hippocampus reveal decreased paired-pulse facilitation in Sca1 null mice, whereas long-term and post-tetanic potentiations are normal. These findings demonstrate that SCA1 is not caused by loss of function of ataxin-1 and point to the possible role of ataxin-1 in learning and memory.
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Cites
Place navigation impaired in rats with hippocampal lesions
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Expansion of an unstable trinucleotide CAG repeat in spinocerebellar ataxia type 1
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“The genetic basis of SCA1 involves an expansion of an unstable CAG trinucleotide repeat located within the coding region of the SCA1 gene (Orr et al., 1993; Banfi et al., 1994).”
BackgroundSelf-citationControl of memory formation through regulated expression of a CaMKII transgene
Mayford, M., Bach, M. E., Huang, Y.-Y., Wang, L., Hawkins, R. D., & Kandel, E. R. (1996) · Science · doi:10.1126/science.274.5293.1678 · Cited by 1,550
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Short-Term Synaptic Plasticity
Zucker, R. S., & Regehr, W. G. (2002) · Annual Review of Physiology · doi:10.1146/annurev.physiol.64.092501.114547 · Cited by 5,068
Calcium- and activity-dependent synaptic plasticity
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Polyglutamine expansion down-regulates specific neuronal genes before pathologic changes in SCA1
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Metadata
- Authors
- Matilla, A., Roberson, E. D., Banfi, S., Morales, J., Armstrong, D. L., Burright, E. N., Orr, H. T., Sweatt, J. D., Zoghbi, H. Y., & Matzuk, M. M.
- Venue
- The Journal of Neuroscience
- Publisher
- Society for Neuroscience
- Published
- 1998-07-15
- Volume
- 18
- Issue
- 14
- Pages
- 5508-5516
- ISSN
- 0270-6474 (ISSN-L)
- 1529-2401
- OpenAlex
- W2131768571
- Cited by
- 218
- References
- 5
- FWCI
- 3.78
- Type
- journal article
- Language
- en
- Open access
- hybrid
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- CoChat. (2026). Citation check: Mice Lacking Ataxin-1 Display Learning Deficits and Decreased Hippocampal Paired-Pulse Facilitation. https://app.cochat.ai/papers/10.1523/jneurosci.18-14-05508.1998
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- Matilla, A., Roberson, E. D., Banfi, S., Morales, J., Armstrong, D. L., Burright, E. N., Orr, H. T., Sweatt, J. D., Zoghbi, H. Y., & Matzuk, M. M. (1998). Mice Lacking Ataxin-1 Display Learning Deficits and Decreased Hippocampal Paired-Pulse Facilitation. The Journal of Neuroscience. https://doi.org/10.1523/jneurosci.18-14-05508.1998
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Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.