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Regulation of GAP-43 protein and mRNA in nigrostriatal dopaminergic neurons after the partial destruction of dopaminergic terminals with intrastriatal 6-hydroxydopamine.
Synapse. 2001 Jan; 39(1):16-22.S

Abstract

Changes in the level of GAP-43 and its mRNA in nigrostriatal dopaminergic neurons in an animal model of the presymptomatic period of Parkinson's disease were measured to find the characteristic features of GAP-43 in nigrostriatal dopaminergic neurons. Since the dopaminergic neurons possess a relatively large amount of GAP-43 protein and mRNA, the dopaminergic neurons must be endowed with specific functions related to those of GAP-43. In this study, dopaminergic axon terminals were partially destroyed by intrastriatal 6-hydroxydopamine (6-OHDA). Rats were decapitated 3, 14, and 56 days following treatment. Levels of GAP-43 and tyrosine hydroxylase (TH) in the striatum were detected by immunoblotting and quantified. The number of GAP-43 mRNA-positive neurons and that of TH mRNA-positive neurons in the substantia nigra pars compacta (SNc) were detected by in situ hybridization using alkaline phosphatase (ALP)-labeled probes. Levels of GAP-43 in the striatum showed no significant alteration during the period of the experiment, although levels of TH were gradually restored. The number of GAP-43 mRNA-positive neurons as well as that of TH mRNA-positive neurons in the SNc decreased. These results suggests that dopaminergic neurons restore their axon terminals with little change in GAP-43, and that transcription and/or stability of GAP-43 mRNA in the dopaminergic neurons are susceptible to the toxin, although the dopaminergic neurons can maintain the translational product in the terminals. This feature may be related with a degeneration of dopaminergic neurons in Parkinson's disease.

Authors+Show Affiliations

Department of Pharmacology, Faculty of Medicine, Kagoshima University, Kagoshima, Japan. shinichi@m.kufma-u.ac.jpNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

11071705

Citation

Iwata, S I., et al. "Regulation of GAP-43 Protein and mRNA in Nigrostriatal Dopaminergic Neurons After the Partial Destruction of Dopaminergic Terminals With Intrastriatal 6-hydroxydopamine." Synapse (New York, N.Y.), vol. 39, no. 1, 2001, pp. 16-22.
Iwata SI, Nomoto M, Fukuda T. Regulation of GAP-43 protein and mRNA in nigrostriatal dopaminergic neurons after the partial destruction of dopaminergic terminals with intrastriatal 6-hydroxydopamine. Synapse. 2001;39(1):16-22.
Iwata, S. I., Nomoto, M., & Fukuda, T. (2001). Regulation of GAP-43 protein and mRNA in nigrostriatal dopaminergic neurons after the partial destruction of dopaminergic terminals with intrastriatal 6-hydroxydopamine. Synapse (New York, N.Y.), 39(1), 16-22.
Iwata SI, Nomoto M, Fukuda T. Regulation of GAP-43 Protein and mRNA in Nigrostriatal Dopaminergic Neurons After the Partial Destruction of Dopaminergic Terminals With Intrastriatal 6-hydroxydopamine. Synapse. 2001;39(1):16-22. PubMed PMID: 11071705.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Regulation of GAP-43 protein and mRNA in nigrostriatal dopaminergic neurons after the partial destruction of dopaminergic terminals with intrastriatal 6-hydroxydopamine. AU - Iwata,S I, AU - Nomoto,M, AU - Fukuda,T, PY - 2000/11/9/pubmed PY - 2001/2/28/medline PY - 2000/11/9/entrez SP - 16 EP - 22 JF - Synapse (New York, N.Y.) JO - Synapse VL - 39 IS - 1 N2 - Changes in the level of GAP-43 and its mRNA in nigrostriatal dopaminergic neurons in an animal model of the presymptomatic period of Parkinson's disease were measured to find the characteristic features of GAP-43 in nigrostriatal dopaminergic neurons. Since the dopaminergic neurons possess a relatively large amount of GAP-43 protein and mRNA, the dopaminergic neurons must be endowed with specific functions related to those of GAP-43. In this study, dopaminergic axon terminals were partially destroyed by intrastriatal 6-hydroxydopamine (6-OHDA). Rats were decapitated 3, 14, and 56 days following treatment. Levels of GAP-43 and tyrosine hydroxylase (TH) in the striatum were detected by immunoblotting and quantified. The number of GAP-43 mRNA-positive neurons and that of TH mRNA-positive neurons in the substantia nigra pars compacta (SNc) were detected by in situ hybridization using alkaline phosphatase (ALP)-labeled probes. Levels of GAP-43 in the striatum showed no significant alteration during the period of the experiment, although levels of TH were gradually restored. The number of GAP-43 mRNA-positive neurons as well as that of TH mRNA-positive neurons in the SNc decreased. These results suggests that dopaminergic neurons restore their axon terminals with little change in GAP-43, and that transcription and/or stability of GAP-43 mRNA in the dopaminergic neurons are susceptible to the toxin, although the dopaminergic neurons can maintain the translational product in the terminals. This feature may be related with a degeneration of dopaminergic neurons in Parkinson's disease. SN - 0887-4476 UR - https://www.unboundmedicine.com/medline/citation/11071705/Regulation_of_GAP_43_protein_and_mRNA_in_nigrostriatal_dopaminergic_neurons_after_the_partial_destruction_of_dopaminergic_terminals_with_intrastriatal_6_hydroxydopamine_ L2 - https://doi.org/10.1002/1098-2396(20010101)39:1<16::AID-SYN3>3.0.CO;2-# DB - PRIME DP - Unbound Medicine ER -