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Richard D. Palmiter
Researcher at University of Washington
Publications - 455
Citations - 74646
Richard D. Palmiter is an academic researcher from University of Washington. The author has contributed to research in topics: Dopamine & Gene. The author has an hindex of 141, co-authored 444 publications receiving 69977 citations. Previous affiliations of Richard D. Palmiter include University of Pennsylvania & Howard Hughes Medical Institute.
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Journal ArticleDOI
Viral restoration of dopamine to the nucleus accumbens is sufficient to induce a locomotor response to amphetamine.
Carrie L. Heusner,Thomas S. Hnasko,Mark S. Szczypka,Yuhong Liu,Matthew J. During,Richard D. Palmiter +5 more
TL;DR: Restoration of dopamine specifically to the nucleus accumbens (NAc) of DD mice completely restores the ability of these mice to respond to amphetamine, and shows that release of dopamine restricted to the NAc is sufficient for this response.
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Regulation of norepinephrine transporter abundance by catecholamines and desipramine in vivo.
TL;DR: NET levels are normal in dopamine beta-hydroxylase knockout mice that lack NE, demonstrating that the NET does not require endogenous NE for appropriate regulation under physiological conditions, and chronic treatment with the NET inhibitor, desipramine, reduced NET levels.
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Attenuating GABA(A) receptor signaling in dopamine neurons selectively enhances reward learning and alters risk preference in mice.
Jones Griffith Parker,Matthew J. Wanat,Marta E. Soden,Kinza Ahmad,Larry S. Zweifel,Nigel S. Bamford,Nigel S. Bamford,Richard D. Palmiter +7 more
TL;DR: A selective role for GABAA signaling in DA neurons in appetitive learning and decision-making is identified and β3-KO mice had enhanced risk preference in a probabilistic selection task that required mice to choose between a small certain reward and a larger uncertain reward.
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Norepinephrine and epinephrine-deficient mice are hyperinsulinemic and have lower blood glucose.
TL;DR: It is suggested that the primary difference in Dbh-/- mice is chronic hyperinsulinemia associated with an altered glucose set point, however, these animals compensate for NE/Epi-mediated glycogenolysis and feeding.
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Interaction of estrogen, progesterone, and testosterone in the regulation of protein synthesis in chick oviduct.
TL;DR: Testosterone given with estrogen increased weight of oviduct and acted synergistically on differentiation initiated by estrogen and if given with progesterone promotes function of differentiated tubular gland cells.