Journal
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
Volume 101, Issue 36, Pages 13329-13334Publisher
NATL ACAD SCIENCES
DOI: 10.1073/pnas.0405084101
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Funding
- NIGMS NIH HHS [T32 GM007108, GM07108-29] Funding Source: Medline
- NIMH NIH HHS [R01 MH058755, F32 MH067399, MH67399, R56 MH058755, MH58755] Funding Source: Medline
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To examine the regulation of midbrain dopamine neurons, recordings were obtained from single neurons of freely moving, genetically engineered dopamine-deficient (DD) mice. DD mice were tested without dopamine signaling (basal state) and with endogenous dopamine signaling (after L-dopa administration). In the basal state, when dopamine concentration in DD mice is < 1 % of that in control animals, the firing properties of midbrain dopamine neurons were remarkably similar among genotypes. However, L-dopa treatment, which restores dopamine and feeding and locomotor behavior in DD mice, profoundly inhibited the firing rate and bursting of dopamine neurons in DD mice. In addition, dopamine neurons in DD mice were hypersensitive to the dopamine receptor agonists quinpirole and SKF 81297. Anesthesia markedly reduced the firing rate of dopamine neurons in DD mice but did not significantly decrease the firing rate in control dopamine neurons. These data suggest that restoration of endogenous dopamine signaling activates hypersensitive long-loop feedback pathways that serve to limit dopamine release and underscore the importance of recording from awake animals.
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