The DOI matches its Crossref record; 2 of the 2 references it cites were found in a registry or an index.
Transient and Progressive Electrophysiological Alterations in the Corticostriatal Pathway in a Mouse Model of Huntington's Disease
Abstract
Alterations in the corticostriatal pathway may precede symptomatology and striatal cell death in Huntington's disease (HD) patients. Here we examined spontaneous EPSCs in striatal medium-sized spiny neurons in slices from a mouse model of HD (R6/2). Spontaneous EPSC frequency was similar in young (3–4 weeks) transgenics and controls but decreased significantly in transgenics when overt behavioral symptoms began (5–7 weeks) and was most pronounced in severely impaired transgenics (11–15 weeks). These differences were maintained after bicuculline or tetrodotoxin, indicating they were specific to glutamatergic input and likely presynaptic in origin. Decreases in presynaptic and postsynaptic protein markers, synaptophysin and postsynaptic density-95, occurred in 11–15 week R6/2 mice, supporting the electrophysiological results. Furthermore, isolated, large-amplitude synaptic events (>100 pA) occurred more frequently in transgenic animals, particularly at 5–7 weeks, suggesting additional dysregulation of cortical inputs. Large events were blocked by tetrodotoxin, indicating a possible cortical origin. Addition of bicuculline and 4-aminopyridine facilitated the occurrence of large events. Riluzole, a compound that decreases glutamate release, reduced these events. Together, these observations indicate that both progressive and transient alterations occur along the corticostriatal pathway in experimental HD. These alterations are likely to contribute to the selective vulnerability of striatal medium-sized spiny neurons.
Overview
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
Our findings confirm the role of astrocytes as important regulatory cell types in brain function and behavior and in neurodegenerative disorders, including HD.
“In conclusion, our findings confirm the role of astrocytes as important regulatory cell types in brain function and behavior 40,57 and in neurodegenerative disorders, including HD 58,59 .”
From SREBP2 gene therapy targeting striatal astrocytes ameliorates Huntington’s disease phenotypes (2021) · cites this paper as [40]
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Citations
Cites
Regulation of F-Actin Stability in Dendritic Spines by Glutamate Receptors and Calcineurin
Halpain, S., Hipolito, A., & Saffer, L. (1998) · The Journal of Neuroscience · doi:10.1523/jneurosci.18-23-09835.1998 · Cited by 408 · cited 3×
“Whatever the mechanism of spine elimination in R6/2 transgenics, one consequence of spine loss is that neurons become more vulnerable to subsequent excitotoxic stimuli (Segal, 1995; Halpain et al., 1998).”
BackgroundMurphy, K. P. S. J., Carter, R. J., Lione, L. A., Mangiarini, L., Mahal, A., Bates, G. P., Dunnett, S. B., & Morton, A. J. (2000) · The Journal of Neuroscience · doi:10.1523/jneurosci.20-13-05115.2000 · Cited by 398
Flagged first, then by citations
Research works printed but not linked: 50
- 10.1002/jnr.10272 · DOI
- 10.1093/brain/awf180 · DOI
- 10.1002/jnr.490040507 · DOI
- 10.1161/01.STR.31.3.766 · DOI
- 10.1523/JNEUROSCI.21-14-05110.2001 · DOI
- 10.1523/JNEUROSCI.19-08-03248.1999 · DOI
- Cepeda, 1998, Dopaminergic modulation of NMDA-induced whole cell currents in neostriatal neurons in slices: contribution of calcium conductances., J Neurophysiol, 79, 82, 10.1152/jn.1998.79.1.82 · DOI
- 10.1002/jnr.1244 · DOI
- Cepeda, 2001, Facilitated glutamatergic transmission in the striatum of D2 dopamine receptor-deficient mice., J Neurophysiol, 85, 659, 10.1152/jn.2001.85.2.659 · DOI
- 10.1073/pnas.95.11.6480 · DOI · Paper page
- 10.1016/0304-3940(92)90597-Z · DOI
- Cherry, 2001, Voltage-gated calcium channels: a potential role in Huntington's disease (HD)., Soc Neurosci Abstr, 27, 99.6
- 10.1016/S0092-8674(00)80513-9 · DOI
- 10.1016/0166-2236(90)90111-M · DOI
- 10.1126/science.277.5334.1990 · DOI · Paper page
- Flores-Hernández, 1994, Patterns of excitatory and inhibitory synaptic transmission in the rat neostriatum as revealed by 4-AP., J Neurophysiol, 72, 2246, 10.1152/jn.1994.72.5.2246 · DOI
- 10.1073/pnas.96.15.8727 · DOI · Paper page
- 10.1073/pnas.82.12.4137 · DOI
- Klapstein, 2001, Electrophysiological and morphological changes in striatal spiny neurons in R6/2 Huntington's disease transgenic mice., J Neurophysiol, 86, 2667, 10.1152/jn.2001.86.6.2667 · DOI
- Köhler, 1978, Perforant path transections protect hippocampal granule cells from kainate lesion., Neurosci Lett, 10, 241, 10.1016/0304-3940(78)90233-1 · DOI
- Kremer, 1999, Influence of lamotrigine on progression of early Huntington disease: a randomized clinical trial., Neurology, 53, 1000, 10.1212/WNL.53.5.1000 · DOI
- Laforet, 2001, Changes in cortical and striatal neurons predict behavioral and electrophysiological abnormalities in a transgenic murine model of Huntington's disease., J Neurosci, 21, 9112, 10.1523/JNEUROSCI.21-23-09112.2001 · DOI
- 10.1002/(SICI)1097-4547(19991115)58:4<515::AID-JNR5>3.0.CO;2-F · DOI
- 10.1006/nbdi.2001.0430 · DOI
- 10.1006/mcne.2002.1152 · DOI
- 10.1523/JNEUROSCI.19-23-10428.1999 · DOI
- 10.1093/hmg/11.17.1911 · DOI
- 10.1016/S0092-8674(00)81369-0 · DOI · Paper page
- 10.1016/0006-8993(78)90941-1 · DOI
- 10.1046/j.1471-4159.2001.00059.x · DOI
- 10.1016/S0361-9230(00)00238-0 · DOI
- 10.1046/j.0953-816X.2000.01379.x · DOI
- 10.1006/exnr.2000.7542 · DOI
- 10.1006/exnr.2002.7885 · DOI
- 10.1016/0306-4522(95)00533-1 · DOI
- 10.1055/s-2000-7461 · DOI
- Rebec, 2002, Dysregulation of ascorbate release in the striatum of behaving mice expressing the Huntington's disease gene., J Neurosci, 22, RC202, 10.1523/JNEUROSCI.22-02-j0006.2002 · DOI
- 10.1002/1531-8257(199903)14:2<326::AID-MDS1019>3.0.CO;2-Q · DOI
- 10.1097/00005072-199902000-00006 · DOI
- 10.1002/mds.10229 · DOI
- 10.1016/0166-2236(95)92765-I · DOI
- 10.1073/pnas.031374698 · DOI
- 10.1002/(SICI)1096-9861(19980105)390:1<5::AID-CNE2>3.0.CO;2-6 · DOI
- 10.1073/pnas.110078997 · DOI · Paper page
- 10.1046/j.1460-9568.2000.00242.x · DOI
- 10.1002/cne.10086 · DOI
- 10.1016/0006-8993(94)91320-X · DOI
- 10.1016/S0896-6273(02)00615-3 · DOI
- 10.1016/S0896-6273(00)80409-2 · DOI
- 10.1126/science.1059581 · DOI · Paper page
Cited by
Sorted by citations
Huntington's disease: from pathology and genetics to potential therapies
Imarisio, S., Carmichael, J., Korolchuk, V., Chen, C.-W., Saiki, S., Rose, C., Krishna, G., Davies, J. E., Ttofi, E., Underwood, B. R., et al. (2008) · Biochemical Journal · doi:10.1042/bj20071619 · Cited by 409
Microglial CB2 cannabinoid receptors are neuroprotective in Huntington's disease excitotoxicity
Palazuelos, J., Aguado, T., Pazos, M. R., Julien, B., Carrasco, C., Resel, E., Sagredo, O., Benito, C., Romero, J., Azcoitia, I., et al. (2009) · Brain · doi:10.1093/brain/awp239 · Cited by 382
Miller, B. R., Dorner, J. L., Shou, M., Sari, Y., Barton, S. J., Sengelaub, D. R., Kennedy, R. T., & Rebec, G. V. (2008) · Neuroscience · doi:10.1016/j.neuroscience.2008.02.004 · Cited by 280
The Energetics of Huntington's Disease
Browne, S. E., & Beal, M. F. (2004) · Neurochemical Research · doi:10.1023/b:nere.0000014824.04728.dd · Cited by 240
Mielcarek, M., Landles, C., Weiss, A., Bradaia, A., Seredenina, T., Inuabasi, L., Osborne, G. F., Wadel, K., Touller, C., Butler, R., et al. (2013) · PLoS Biology · doi:10.1371/journal.pbio.1001717 · Cited by 172
Synaptic dysfunction in Huntington's disease: a new perspective
Smith, R., Brundin, P., & Li, J.-Y. (2005) · Cellular and Molecular Life Sciences · doi:10.1007/s00018-005-5084-5 · Cited by 166
Pan, W. X., Mao, T., & Dudman, J. T. (2010) · Frontiers in Neuroanatomy · doi:10.3389/fnana.2010.00147 · Cited by 150
“…and DeAmicis, 1977; Hersch and White, 1982; Porter and White, 1983; Bernardo and Woolsey, 1987; Mattiace et al., 1989; Hofstetter and Ehret, 1992; Cepeda et al., 2003; Miura et al., 2007; Brazhnik et al., 2008; Usunoff et al., 2009; Ibáñez-Sandoval et al., 2010; Tlamsa and Brumberg, 2010) and to…”
BackgroundMilnerwood, A. J., & Raymond, L. A. (2007) · The Journal of Physiology · doi:10.1113/jphysiol.2007.142448 · Cited by 126
Mehta, S. R., Tom, C. M., Wang, Y., Bresee, C., Rushton, D., Mathkar, P. P., Tang, J., & Mattis, V. B. (2018) · Cell Reports · doi:10.1016/j.celrep.2018.09.076 · Cited by 112
Mazarakis, N. K., Cybulska-Klosowicz, A., Grote, H., Pang, T., Van Dellen, A., Kossut, M., Blakemore, C., & Hannan, A. J. (2005) · The Journal of Neuroscience · doi:10.1523/jneurosci.4320-04.2005 · Cited by 115
Ochaba, J., Monteys, A. M., O’Rourke, J. G., Reidling, J. C., Steffan, J. S., Davidson, B. L., & Thompson, L. M. (2016) · Neuron · doi:10.1016/j.neuron.2016.03.016 · Cited by 94
Bone Marrow Transplantation Confers Modest Benefits in Mouse Models of Huntington's Disease
Kwan, W., Magnusson, A., Chou, A., Adame, A., Carson, M. J., Kohsaka, S., Masliah, E., Möller, T., Ransohoff, R., Tabrizi, S. J., et al. (2012) · The Journal of Neuroscience · doi:10.1523/jneurosci.4846-11.2012 · Cited by 75
Axonopathy in Huntington's disease
Li, J.-Y., & Conforti, L. (2013) · Experimental Neurology · doi:10.1016/j.expneurol.2012.08.010 · Cited by 55
SREBP2 gene therapy targeting striatal astrocytes ameliorates Huntington’s disease phenotypes
Birolini, G., Verlengia, G., Talpo, F., Maniezzi, C., Zentilin, L., Giacca, M., Conforti, P., Cordiglieri, C., Caccia, C., Leoni, V., et al. (2021) · Brain · doi:10.1093/brain/awab186 · Cited by 48
Metadata
- Authors
- Cepeda, C., Hurst, R. S., Calvert, C. R., Hernández-Echeagaray, E., Nguyen, O. K., Jocoy, E., Christian, L. J., Ariano, M. A., & Levine, M. S.
- Venue
- The Journal of Neuroscience
- Publisher
- Society for Neuroscience
- Published
- 2003-02-01
- Volume
- 23
- Issue
- 3
- Pages
- 961-969
- ISSN
- 0270-6474
- 1529-2401
- Cited by
- 321
- References
- 2
- Language
- en
About these checks
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.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
