The DOI matches its Crossref record; 22 of the 22 references it cites were found in a registry or an index.
Prevention of 6-hydroxydopamine-induced rotational behavior by BDNF somatic gene transfer
Abstract
Brain-derived neurotrophic factor (BDNF) was expressed via injection of viral vector into the substantia nigra pars compacta (SNc) to investigate its influence on nigrostriatal dopaminergic activity and locomotor behavior. The recombinant adeno-associated virus (rAAV) vector, pTR-BDNFmyc, incorporated the neuron-specific enolase (NSE) promoter and the internal ribosome entry site (IRES) element driving expression of both epitope-tagged BDNF and green fluorescent protein (GFP) bicistronically. The control vector, pTR-UF4, incorporated NSE promoter-driven GFP expression only. Transgene expression persisted in both vector groups throughout the 9 month course of the study. Partial 6-hydroxydopamine (6-OHDA) lesions were conducted in the SNc ipsilateral to, and 6 months after, transduction with either the pTR-BDNFmyc or the pTR-UF4. Transgenic BDNFmyc had no effect on the number of tyrosine hydroxylase (TH)-labeled neurons in the SNc after 6-OHDA-lesions, but did block the amphetamine-induced, ipsiversive, turning-behavior caused by the lesion in the pTR-UF4 group. The BDNFmyc-transduced group also demonstrated more locomotor activity and rotational activity contralateral to the lesioned side than did the pTR-UF4-transduced group. Long-term, stable expression of BDNF can therefore modulate locomotor activity without significantly affecting nigrostriatal dopaminergic survival.
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“In the vast majority of studies with BDNF administration before induction of parkinsonism, the research results revealed at least partial prevention of neuronal cell loss [89,90,92,93,99,101].”
From BDNF as a Promising Therapeutic Agent in Parkinson’s Disease (2020) · cites this paper as [90]
In the citing paper
“However, the reports are not consistent; some have shown no increase in neuronal survival when BDNF was applied before intoxication with 6-hydroxydopamine (6-OHDA) in PD animal model [90,91].”
From BDNF as a Promising Therapeutic Agent in Parkinson’s Disease (2020) · cites this paper as [90]
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Functional Repression of cAMP Response Element in 6-Hydroxydopamine-treated Neuronal Cells
Chalovich, E. M., Zhu, J.-H., Caltagarone, J., Bowser, R., & Chu, C. T. (2006) · Journal of Biological Chemistry · doi:10.1074/jbc.m602632200 · Cited by 1,385
Murer, M. G., Yan, Q., & Raisman-Vozari, R. (2001) · Progress in Neurobiology · doi:10.1016/s0301-0082(00)00014-9 · Cited by 874
GDNF, NGF and BDNF as Therapeutic Options for Neurodegeneration
Allen, S. J., Watson, J. J., Shoemark, D. K., Barua, N. U., & Patel, N. K. (2013) · Pharmacology & Therapeutics · doi:10.1016/j.pharmthera.2013.01.004 · Cited by 820
BDNF as a Promising Therapeutic Agent in Parkinson’s Disease
Palasz, E., Wysocka, A., Gasiorowska, A., Chalimoniuk, M., Niewiadomski, W., & Niewiadomska, G. (2020) · International Journal of Molecular Sciences · doi:10.3390/ijms21031170 · Cited by 504
Martin, K. R. G., Quigley, H. A., Zack, D. J., Levkovitch-Verbin, H., Kielczewski, J., Valenta, D., Baumrind, L., Pease, M. E., Klein, R. L., & Hauswirth, W. W. (2003) · Investigative Opthalmology & Visual Science · doi:10.1167/iovs.02-1332 · Cited by 362
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Metadata
- Authors
- Klein, R. L., Lewis, M. H., Muzyczka, N., & Meyer, E. M.
- Affiliations
- University of Florida (US)
- Corresponding author
- Klein, Ronald L.
- ORCID
- Lewis, Mark H.
- Venue
- Brain Research
- Publisher
- Elsevier BV
- Published
- 1999-11
- Volume
- 847
- Issue
- 2
- Pages
- 314-320
- ISSN
- 0006-8993 (ISSN-L)
- OpenAlex
- W1987647111
- Cited by
- 128
- References
- 22
- Citations by year
- 2025: 1 · 2024: 1 · 2023: 2 · 2022: 7 · 2021: 4 · 2020: 5 · 2019: 3 · 2018: 5 · 2017: 3 · 2016: 3 · 2015: 4 · 2014: 4 · 2013: 4 · 2012: 6
- FWCI
- 4.02
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Brain Research (publishedVersion)
- PubMed (publishedVersion)
- Funders
- American Cancer Society
- National Institutes of Health (2r01gm035723-15)
- National Heart, Lung, and Blood Institute (HL 53665, HL/DK 50257, R01HL053665)
- National Institute of General Medical Sciences (GM35723)
- National Institute of Diabetes and Digestive and Kidney Diseases (R01DK050257)
- Topics
- Health Sciences › Medicine › Clinical Neurology › Parkinson's Disease Mechanisms and Treatments
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Nerve injury and regeneration
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
- Keywords
- brain-derived neurotrophic factor, 6-hydroxydopamine lesion, substantia nigra pars compacta, gene transfer, adeno-associated virus vectors, neuron-specific enolase promoter, internal ribosome entry site, amphetamine-induced rotation, locomotor activity, dopaminergic neuron survival, tyrosine hydroxylase, neuroprotection
- MeSH terms
- Amphetamine, Central Nervous System Stimulants, Animals, Genetic Vectors, Humans, Motor Activity, Parkinson Disease, Substantia Nigra, Oxidopamine, Rats, Sprague-Dawley, Gene Transfer Techniques, Adrenergic Agents, Brain-Derived Neurotrophic Factor, Rats
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