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In vivo dopamine release and uptake impairments in rats treated with 3-nitropropionic acid.
Neuroscience. 2009 Jul 07; 161(3):940-9.N

Abstract

Recent evidence has suggested that mitochondrial dysfunction may lead to impaired neurotransmitter exocytosis in transgenic Huntington's disease (HD) model mice. To gain insight into the impact of mitochondrial impairment on striatal dopamine release in vivo, we used fast-scan cyclic voltammetry (FSCV) at carbon fiber microelectrodes to measure dopamine release and uptake kinetics in anesthetized Lewis rats continuously treated for 5 days with 3-nitropropionic acid (3NP). Our results indicate that, even though striatal dopamine content was unchanged, remotely stimulated dopamine release evoked per electrical stimulus pulse ([DA](p)) is decreased in 3NP-treated rats (33% of that observed in sham control rats) and that this decrease is uniform throughout all stereotaxic depths tested. Nevertheless, unlike data collected previously from transgenic HD model rodents, the maximum rate of dopamine uptake (V(max)) in 3NP-treated rats is diminished (30% of controls) while K(m) is unchanged. Treatment with 3NP also resulted in a corresponding decrease in locomotor activity, presumably due in part to the impaired dopamine release. These results indicate that dopamine release is degraded in this HD model, as is observed in transgenic HD model rodents; however, the results also imply that there are fundamental differences in dopamine uptake between 3NP-treated animals and transgenic animals.

Authors+Show Affiliations

Department of Chemistry, The University of Kansas, Lawrence, KS 66045-7582, USA.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

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

Language

eng

PubMed ID

19362126

Citation

Kraft, J C., et al. "In Vivo Dopamine Release and Uptake Impairments in Rats Treated With 3-nitropropionic Acid." Neuroscience, vol. 161, no. 3, 2009, pp. 940-9.
Kraft JC, Osterhaus GL, Ortiz AN, et al. In vivo dopamine release and uptake impairments in rats treated with 3-nitropropionic acid. Neuroscience. 2009;161(3):940-9.
Kraft, J. C., Osterhaus, G. L., Ortiz, A. N., Garris, P. A., & Johnson, M. A. (2009). In vivo dopamine release and uptake impairments in rats treated with 3-nitropropionic acid. Neuroscience, 161(3), 940-9. https://doi.org/10.1016/j.neuroscience.2009.03.083
Kraft JC, et al. In Vivo Dopamine Release and Uptake Impairments in Rats Treated With 3-nitropropionic Acid. Neuroscience. 2009 Jul 7;161(3):940-9. PubMed PMID: 19362126.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - In vivo dopamine release and uptake impairments in rats treated with 3-nitropropionic acid. AU - Kraft,J C, AU - Osterhaus,G L, AU - Ortiz,A N, AU - Garris,P A, AU - Johnson,M A, Y1 - 2009/04/09/ PY - 2009/01/20/received PY - 2009/03/14/revised PY - 2009/03/30/accepted PY - 2009/4/14/entrez PY - 2009/4/14/pubmed PY - 2009/8/25/medline SP - 940 EP - 9 JF - Neuroscience JO - Neuroscience VL - 161 IS - 3 N2 - Recent evidence has suggested that mitochondrial dysfunction may lead to impaired neurotransmitter exocytosis in transgenic Huntington's disease (HD) model mice. To gain insight into the impact of mitochondrial impairment on striatal dopamine release in vivo, we used fast-scan cyclic voltammetry (FSCV) at carbon fiber microelectrodes to measure dopamine release and uptake kinetics in anesthetized Lewis rats continuously treated for 5 days with 3-nitropropionic acid (3NP). Our results indicate that, even though striatal dopamine content was unchanged, remotely stimulated dopamine release evoked per electrical stimulus pulse ([DA](p)) is decreased in 3NP-treated rats (33% of that observed in sham control rats) and that this decrease is uniform throughout all stereotaxic depths tested. Nevertheless, unlike data collected previously from transgenic HD model rodents, the maximum rate of dopamine uptake (V(max)) in 3NP-treated rats is diminished (30% of controls) while K(m) is unchanged. Treatment with 3NP also resulted in a corresponding decrease in locomotor activity, presumably due in part to the impaired dopamine release. These results indicate that dopamine release is degraded in this HD model, as is observed in transgenic HD model rodents; however, the results also imply that there are fundamental differences in dopamine uptake between 3NP-treated animals and transgenic animals. SN - 1873-7544 UR - https://www.unboundmedicine.com/medline/citation/19362126/In_vivo_dopamine_release_and_uptake_impairments_in_rats_treated_with_3_nitropropionic_acid_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0306-4522(09)00541-7 DB - PRIME DP - Unbound Medicine ER -