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Thomas M. Engber

Researcher at National Institutes of Health

Publications -  29
Citations -  4514

Thomas M. Engber is an academic researcher from National Institutes of Health. The author has contributed to research in topics: Levodopa & Agonist. The author has an hindex of 21, co-authored 29 publications receiving 4346 citations.

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D1 and D2 dopamine receptor-regulated gene expression of striatonigral and striatopallidal neurons

TL;DR: The differential effects of dopamine on striatonigral and striatopallidal neurons are mediated by their specific expression of D1 and D2 dopamine receptor subtypes, respectively.
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Levodopa replacement therapy alters enzyme activities in striatum and neuropeptide content in striatal output regions of 6-hydroxydopamine lesioned rats.

TL;DR: Results indicate that striatal neuronal populations are differentially affected by chronic levodopa therapy and by the continuous or intermittent nature of the treatment regimen, which exacerbated the lesion-induced changes or altered neurochemical markers which had been unaffected by the lesions.
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Continuous and intermittent levodopa differentially affect basal ganglia function.

TL;DR: Findings suggest a relation between the schedule of chronic levodopa administration and the development of behavioral sensitization, possibly as a consequence of alterations in neuronal systems located downstream from striatal dopamine receptors.
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Continuous and intermittent levodopa differentially affect rotation induced by D-1 and D-2 dopamine agonists.

TL;DR: The effects of continuous and intermittent levodopa treatment on rotational behavior induced by dopamine agonists were examined in rats with a unilateral 6-hydroxydopamine lesion of the nigrostriatal dopamine pathway and suggest that the intermittence of central dopamine receptor stimulation may be an important factor in determining the subsequent responses of the dopamine system.
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Nmda receptor blockade reverses motor response alterations induced by levodopa

TL;DR: It is suggested thatNMDA receptor-mediated mechanisms contribute to the behavioral plasticity associated with chronic levodopa treatment and that NMDA antagonists might be effective in reversing the motor response complications of the long-term levodOPA therapy.