Research Topics
Genomes and Genes | RICHARD PALMITERSummaryAffiliation: University of Washington Country: USA Publications
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Publications
Distinguishing whether dopamine regulates liking, wanting, and/or learning about rewardsSiobhan Robinson
Neurobiology and Behavior Program, University of Washington, Seattle, WA, USA
Behav Neurosci 119:5-15. 2005....
Parkin-deficient mice are not more sensitive to 6-hydroxydopamine or methamphetamine neurotoxicityFrancisco A Perez
Graduate Program in Neurobiology and Behavior, University of Washington, Seattle, WA 98195, USA
BMC Neurosci 6:71. 2005..Because Parkin function has been linked to many of the pathways involved in METH and 6-OHDA toxicity, we predicted that Parkin-deficient mice would be more sensitive to the neurotoxic effects of these agents...- ZnT-3, a putative transporter of zinc into synaptic vesiclesR D Palmiter
Howard Hughes Medical Institute, University of Washington, Seattle 98195, USA
Proc Natl Acad Sci U S A 93:14934-9. 1996..We propose that ZnT-3 facilitates the accumulation of zinc in synaptic vesicles... - Is dopamine a physiologically relevant mediator of feeding behavior?Richard D Palmiter
Howard Hughes Medical Institute, Department of Biochemistry, University of Washington, Seattle, WA 98195 7370, USA
Trends Neurosci 30:375-81. 2007..Here, I discuss the predictions and implications of these new findings as they relate to dopamine signaling and the physiology of appetite control... - Protection against zinc toxicity by metallothionein and zinc transporter 1Richard D Palmiter
Howard Hughes Medical Institute and Department of Biochemistry, Box 357370, University of Washington, Seattle, WA 98195 7370, USA
Proc Natl Acad Sci U S A 101:4918-23. 2004..However, if Mt genes can be expressed, then they are preferentially amplified. Thus, both ZnT1 and MT genes contribute to zinc resistance in BHK cells, whereas ZnT1 plays a larger role in regulating free zinc levels... - Dopamine signaling in the dorsal striatum is essential for motivated behaviors: lessons from dopamine-deficient miceRichard D Palmiter
Howard Hughes Medical Institute and Department of Biochemistry, Box 357370, University of Washington, Seattle, WA 98195, USA
Ann N Y Acad Sci 1129:35-46. 2008..The results suggest that dopamine facilitates the output from dorsal striatum, which provides a permissive signal allowing feeding and other goal-directed behaviors... - Reduced levels of neurotransmitter-degrading enzyme PRCP promote a lean phenotype. [corrected]Richard D Palmiter
Howard Hughes Medical Institute and Department of Biochemistry, University of Washington, Seattle, Washington 98195, USA
J Clin Invest 119:2130-3. 2009..Their studies indicate that PRCP expression promotes obesity, while inhibitors of the enzyme counteract obesity... - The elusive function of metallothioneinsR D Palmiter
Howard Hughes Medical Institute and Department of Biochemistry, University of Washington, Box 357370, Seattle, WA 98195, USA
Proc Natl Acad Sci U S A 95:8428-30. 1998.... - Efflux and compartmentalization of zinc by members of the SLC30 family of solute carriersRichard D Palmiter
Howard Hughes Medical Institute and Department of Biochemistry, University of Washington, Box 357370, Seattle, WA 98195, USA
Pflugers Arch 447:744-51. 2004..No mutations in human counterparts of any of the members of the SLC30 family have been described... - A role for dopamine in feeding responses produced by orexigenic agentsThomas S Hnasko
Neurobiology and Behavior Graduate Program, University of Washington, Seattle, WA 98195, USA
Brain Res 1023:309-18. 2004..Since dopamine signaling in the CPu is not sufficient for glucoprivation-induced feeding, we propose that this feeding behavior may be mediated by dopamine in an anatomically distinct brain region... - Dysregulation of dopamine signaling in the dorsal striatum inhibits feedingBethany N Sotak
Howard Hughes Medical Institute and Department of Biochemistry, University of Washington, Health Sciences Building, Room J661D, 1959 NE Pacific Street, Box 357370, Seattle, WA 98195 7370, USA
Brain Res 1061:88-96. 2005.... 
Restricting dopaminergic signaling to either dorsolateral or medial striatum facilitates cognitionMartin Darvas
Howard Hughes Medical Institute and Department of Biochemistry, University of Washington, Seattle, Washington 98195, USA
J Neurosci 30:1158-65. 2010....- Viral restoration of dopamine signaling to the dorsal striatum restores instrumental conditioning to dopamine-deficient miceSiobhan Robinson
Graduate Program in Neurobiology and Behavior, Howard Hughes Medical Institute, University of Washington, Seattle, WA, 98195, USA
Psychopharmacology (Berl) 191:567-78. 2007..Instrumental responding was evaluated to determine whether mice lacking dopamine [dopamine-deficient mice (DD mice)] could learn to preferentially press a visually cued, active lever for food reward over an inactive lever... - The role of dopamine in learning, memory, and performance of a water escape taskVictor H Denenberg
Department of Biochemistry, University of Washington, Box 357370, Seattle, WA 98195 7370, USA
Behav Brain Res 148:73-8. 2004.... - Expression of mutant NMDA receptors in dopamine D1 receptor-containing cells prevents cocaine sensitization and decreases cocaine preferenceCarrie L Heusner
Department of Biochemistry, University of Washington, Seattle, Washington 98195, USA
J Neurosci 25:6651-7. 2005..These data suggest that intact NMDA receptor signaling in D1R-containing cells is required for the manifestation of behaviors associated with repeated drug exposure... - Absence of NMDA receptors in dopamine neurons attenuates dopamine release but not conditioned approach during Pavlovian conditioningJones G Parker
Howard Hughes Medical Institute and Department of Biochemistry, University of Washington, Seattle WA 98195, USA
Proc Natl Acad Sci U S A 107:13491-6. 2010.... - Cocaine-conditioned place preference by dopamine-deficient mice is mediated by serotoninThomas S Hnasko
Graduate Program in Neurobiology and Behavior, University of Washington, Seattle, Washington 98195, USA
J Neurosci 27:12484-8. 2007..These findings are consistent with the hypothesis that, in the absence of dopamine, cocaine-mediated SERT blockade activates dopamine neurons, which then release some other neurotransmitter that contributes to cocaine reward in DD mice... - Role of noradrenergic signaling by the nucleus tractus solitarius in mediating opiate rewardValerie G Olson
Howard Hughes Medical Institute and Department of Biochemistry, University of Washington, Seattle, WA 98195, USA
Science 311:1017-20. 2006..Morphine-induced locomotion was partially restored by DBH expression in either brain region. These data suggest that NE signaling by the nucleus tractus solitarius is necessary for morphine reward... - Mice with chronic norepinephrine deficiency resemble amphetamine-sensitized animalsDavid Weinshenker
Howard Hughes Medical Institute and Department of Biochemistry, University of Washington, Seattle, WA 98195, USA
Proc Natl Acad Sci U S A 99:13873-7. 2002..We conclude that in contrast to acute alpha1AR blockade, chronic NE deficiency induces changes similar to sensitization, perhaps by altering DA-signaling pathways... - Dopamine-dependent desensitization of dopaminergic signaling in the developing mouse striatumDouglas S Kim
Molecular and Cellular Biology Program, University of Washington, Seattle, Washington 98195-7370, USA
J Neurosci 22:9841-9. 2002..Dopaminoceptive neurons appear to reduce their sensitivity to dopamine as dopaminergic terminals innervate the striatum and functional neurotransmission begins... - Restriction of dopamine signaling to the dorsolateral striatum is sufficient for many cognitive behaviorsMartin Darvas
Department of Biochemistry, University of Washington, Howard Hughes Medical Institute, Seattle, WA 98195, USA
Proc Natl Acad Sci U S A 106:14664-9. 2009..These results indicate that dopaminergic signaling in the ventromedial striatum is not absolutely necessary for mastery of these behaviors, but may facilitate them... - Altered sleep latency and arousal regulation in mice lacking norepinephrineMelissa S Hunsley
Howard Hughes Medical Institute and Department of Biochemistry, Box 357370, University of Washington, Seattle, WA 98195 7370, USA
Pharmacol Biochem Behav 78:765-73. 2004..The results presented here suggest that NE promotes wakefulness during transitions between sleep and wake under conditions involving mild stress and SD, but not under baseline circumstances... - Parkin-deficient mice are not a robust model of parkinsonismFrancisco A Perez
Graduate Program in Neurobiology and Behavior, University of Washington, Seattle, WA 98195, USA
Proc Natl Acad Sci U S A 102:2174-9. 2005..Understanding why Parkin-deficient mice do not exhibit robust signs of parkinsonism could advance knowledge and treatment of PD... - Dopamine modulates release from corticostriatal terminalsNigel S Bamford
Department of Neurology, University of Washington, USA
J Neurosci 24:9541-52. 2004..Microdialysis revealed that basal extracellular striatal glutamate was normal in DD mice. These data indicate that dopamine deficiency results in morphologically normal corticostriatal terminals with hypersensitive D2 receptors... - Cre recombinase-mediated restoration of nigrostriatal dopamine in dopamine-deficient mice reverses hypophagia and bradykinesiaThomas S Hnasko
Graduate Program in Neurobiology and Behavior, Department of Biochemistry, and Howard Hughes Medical Institute, University of Washington, Seattle, WA 98195, USA
Proc Natl Acad Sci U S A 103:8858-63. 2006..This approach offers numerous advantages compared with previous models aimed at examining dopamine signaling in discrete dopaminergic circuits... - Disruption of NMDAR-dependent burst firing by dopamine neurons provides selective assessment of phasic dopamine-dependent behaviorLarry S Zweifel
Department of Psychology, University of Washington, Seattle, WA 98195, USA
Proc Natl Acad Sci U S A 106:7281-8. 2009.... - Morphine reward in dopamine-deficient miceThomas S Hnasko
Graduate Program in Neurobiology and Behavior, University of Washington, Seattle, Washington 98195, USA
Nature 438:854-7. 2005.... - Dopamine is necessary for cue-dependent fear conditioningJonathan P Fadok
Graduate Program in Neurobiology and Behavior, University of Washington, Seattle, Washington 98195, USA
J Neurosci 29:11089-97. 2009..These findings indicate that DA acting on multiple receptor subtypes within multiple target regions facilitates the stabilization of fear memory... - Attenuation of diabetic hyperphagia in neuropeptide Y--deficient miceDana K Sindelar
Department of Medicine, University of Washington, Seattle, Washington, USA
Diabetes 51:778-83. 2002.... - Adenosine receptor blockade reverses hypophagia and enhances locomotor activity of dopamine-deficient miceDouglas S Kim
Molecular and Cellular Biology Program, University of Washington, Seattle, WA 98195 7275, USA
Proc Natl Acad Sci U S A 100:1346-51. 2003..This study of a genetic model of dopamine depletion provides evidence that A(2A) receptor antagonists could ameliorate the hypokinetic symptoms of advanced Parkinson's disease patients without inducing excessive motor activity... - Interaction of dopamine and adenosine receptor function in behavior: studies with dopamine-deficient miceDouglas S Kim
Molecular and Cellular Biology Program, University of Washington, Seattle, Washington 98195, USA
Front Biosci 13:2311-8. 2008.... - Neonatal 6-hydroxydopamine administration to mice is fatalMichelle D Brot
Department of Orthodontics, University of Washington, Seattle, Wash 98195-7370, USA
Dev Neurosci 24:531-8. 2002..Some treated mice were raised in a heated chamber to help them conserve energy. The results demonstrate that regardless of genotype or environmental temperature, bilateral neonatal 6-OHDA lesions are lethal to mice... - Viral restoration of dopamine to the nucleus accumbens is sufficient to induce a locomotor response to amphetamineCarrie L Heusner
Department of Biochemistry, University of Washington, Seattle, WA 98195, USA
Brain Res 980:266-74. 2003..These data support previous studies in which accumbal dopamine is required for producing a normal locomotor response to amphetamine and further show that release of dopamine restricted to the NAc is sufficient for this response.. - A robust and high-throughput Cre reporting and characterization system for the whole mouse brainLinda Madisen
Allen Institute for Brain Science, Seattle, Washington, USA
Nat Neurosci 13:133-40. 2010..Our expression data are displayed in a public online database to help researchers assess the utility of various Cre-driver lines for cell-type-specific genetic manipulation... - Activation of the kappa opioid receptor in the dorsal raphe nucleus mediates the aversive effects of stress and reinstates drug seekingBenjamin B Land
Department of Pharmacology, University of Washington, Seattle, WA 98195, USA
Proc Natl Acad Sci U S A 106:19168-73. 2009..These results suggest that the adverse effects of stress may converge on the serotonergic system and offers an approach to controlling stress-induced dysphoria and relapse... - Norepinephrine-deficient mice exhibit normal sleep-wake states but have shorter sleep latency after mild stress and low doses of amphetamineMelissa S Hunsley
Howard Hughes Medical Institute, University of Washington, Seattle 98195 7370, USA
Sleep 26:521-6. 2003..Mice lacking the ability to make norepinephrine (NE) were used to investigate how NE may be involved in regulating sleep and sleep latency under normal conditions and as a response to mild stress or varying doses of amphetamine... - Lack of neuropeptide Y attenuates the somatic signs of opiate withdrawalValerie G Olson
Department of Biochemistry, University of Washington, Seattle, Washington 98195, USA
Synapse 60:553-6. 2006..Here we report that mice lacking the NPY gene show normal conditioned place aversion to opiate withdrawal, but show attenuated opiate withdrawal somatic signs... - Regulation of norepinephrine transporter abundance by catecholamines and desipramine in vivoDavid Weinshenker
Howard Hughes Medical Institute, Box 357370, University of Washington, Seattle 98195, USA
Brain Res 946:239-46. 2002..There are some qualitative and quantitative differences in the down-regulation of the NET by catecholamine depletion and DMI treatment, suggesting that different mechanisms may be involved... - Role of NMDA receptors in dopamine neurons for plasticity and addictive behaviorsLarry S Zweifel
Howard Hughes Medical Institute and Department of Biochemistry, University of Washington, Seattle, WA 98195, USA
Neuron 59:486-96. 2008..These findings provide evidence for a role of NMDAR signaling in DA neurons for specific behavioral modifications associated with drug seeking behaviors... - Modulation of neuropeptide Y expression in adult mice does not affect feedingLinda Ste Marie
Howard Hughes Medical Institute and Department of Biochemistry, University of Washington, Seattle, WA 98195, USA
Proc Natl Acad Sci U S A 102:18632-7. 2005..These observations suggest that pharmacological inhibition of NPY signaling is unlikely to have long-lasting effects on body weight... - Local dopamine production in the dorsal striatum restores goal-directed behavior in dopamine-deficient miceSiobhan Robinson
Neurobiology and Behavior Program, University of Washington, Seattle, WA 98195, USA
Behav Neurosci 120:196-200. 2006..The authors conclude that finely tuned dopaminergic signaling within the dorsal striatum is sufficient for performance of goal-directed behavior... - Mice lacking dopamine D1 receptors express normal lithium chloride-induced conditioned taste aversion for salt but not sucroseClaire Matson Cannon
Department of Biochemistry and Howard Hughes Medical Institute, University of Washington, Seattle, WA 98195 7370, USA
Eur J Neurosci 21:2600-4. 2005..2 m NaCl). Our results suggest that activation of D1 receptors might contribute to the strength of an aversive gustatory association, but might not be required for the formation of a CTA in general... - Reward without dopamineClaire Matson Cannon
Department of Biochemistry and Howard Hughes Medical Institute, University of Washington, Seattle, Washington 98195 7370, USA
J Neurosci 23:10827-31. 2003..Thus, DA is not required for mice to learn to consume sweet solutions preferentially. We conclude that DA is not required to find the sweet tastes of sucrose or saccharin rewarding... - Deletion of GAD67 in dopamine receptor-1 expressing cells causes specific motor deficitsCarrie L Heusner
Department of Biochemistry, University of Washington, Seattle, Washington 98195, USA
Genesis 46:357-67. 2008..We show that these mice are deficient in some types of motor skills, but normal for others, suggesting a differential role for GABA release from D1 receptor-containing neurons... - Firing properties of dopamine neurons in freely moving dopamine-deficient mice: effects of dopamine receptor activation and anesthesiaSiobhan Robinson
Neurobiology and Behavior Program, University of Washington, Seattle, WA 98195, USA
Proc Natl Acad Sci U S A 101:13329-34. 2004..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... - Complex I deficiency due to loss of Ndufs4 in the brain results in progressive encephalopathy resembling Leigh syndromeAlbert Quintana
Department of Biochemistry, Howard Hughes Medical Institute, University of Washington, Seattle, WA 98195, USA
Proc Natl Acad Sci U S A 107:10996-1001. 2010..These data suggest that dysfunctional complex I in specific brain regions results in progressive glial activation that promotes neuronal death that ultimately results in mortality... - Dysregulation of striatal dopamine signaling by amphetamine inhibits feeding by hungry miceClaire Matson Cannon
Department of Biochemistry and Howard Hughes Medical Institute, University of Washington, Seattle, WA 98195, USA
Neuron 44:509-20. 2004..We suggest that, at this moderate dose of AMPH, dysregulation of striatal DA is the primary cause of AMPH-induced hypophagia and that regulated striatal dopaminergic signaling may be necessary for normal feeding behaviors... - NPY/AgRP neurons are essential for feeding in adult mice but can be ablated in neonatesSerge Luquet
Howard Hughes Medical Institute and Department of Biochemistry, University of Washington, Box 357370, Seattle, WA 98195, USA
Science 310:683-5. 2005..These results suggest that network-based compensatory mechanisms can develop after the ablation of NPY/AgRP neurons in neonates but do not readily occur when these neurons become essential in adults... - Neuropeptide Y is required for hyperphagic feeding in response to neuroglucopeniaDana K Sindelar
Department of Medicine, Harborview Medical Centr, Howard Hughes Medical Institute, University of Washington, Seattle 98195, USA
Endocrinology 145:3363-8. 2004..We conclude that NPY signaling is required for hyperphagic feeding, but not neuroendocrine responses to moderate hypoglycemia... - Norepinephrine and epinephrine-deficient mice are hyperinsulinemic and have lower blood glucoseLinda Ste Marie
Department of Biochemistry, University of Washington, Seattle, Washington 98195, USA
Endocrinology 144:4427-32. 2003..We suggest 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... - Attenuated feeding responses to circadian and palatability cues in mice lacking neuropeptide YDana K Sindelar
Department of Medicine, University of Washington, Harborview Hospital, Division of Endocrinology, Box 359757, 325 9th Avenue, Seattle, WA 98104, USA
Peptides 26:2597-602. 2005.... - Ablation of neurons expressing agouti-related protein activates fos and gliosis in postsynaptic target regionsQi Wu
Howard Hughes Medical Institute, University of Washington, Seattle, Washington 98195, USA
J Neurosci 28:9218-26. 2008..Furthermore, glial cell activation in target areas of AgRP neurons appears to be a result of excitotoxicity... - Norepinephrine- and epinephrine-deficient mice gain weight normally on a high-fat dietLinda Ste Marie
Department of Biochemistry, Howard Hughes Medical Institute, Box 357370, University of Washington, Seattle, WA 98195, USA
Obes Res 13:1518-22. 2005..We characterized the response of Dbh-null and control mice to a HFD... - NPY/AgRP neurons are not essential for feeding responses to glucoprivationSerge Luquet
Howard Hughes Medical Institute and Department of Biochemistry, University of Washington, Box 357370, Seattle, WA 98195, United States
Peptides 28:214-25. 2007..We conclude that NPY/AgRP neurons are not necessary for generating or mediating the orexigenic response to glucose deficiency, but they are essential for the feeding response to ghrelin and refeeding on standard chow after a fast... - Genetic disruption of dopamine production results in pituitary adenomas and severe prolactinemiaThomas S Hnasko
Graduate Program in Neurobiology and Behavior, Children s Hospital and Regional Medical Center, University of Washington, Seattle, WA 98195, USA
Neuroendocrinology 86:48-57. 2007..Dopamine release from tuberoinfundibular dopamine neurons into the median eminence activates dopamine-D2 receptors in the pituitary gland where it inhibits lactotroph function... - Role of agouti-related protein-expressing neurons in lactationColin T Phillips
Howard Hughes Medical Institute and Department of Biochemistry, University of Washington, Seattle, WA 98195, USA
Endocrinology 149:544-50. 2008..We also show that constitutive inactivation of Npy and Agrp genes does not prevent pregnancy or lactation, nor does it protect lactating dams from diphtheria toxin-induced starvation... - Mitochondrial complex I inhibition is not required for dopaminergic neuron death induced by rotenone, MPP+, or paraquatWon Seok Choi
Toxicology Program, Department of Environmental and Occupational Health Sciences, Graduate Program in Neurobiology and Behavior, Institute for Stem Cell and Regenerative Medicine, University of Washington, Seattle, WA 98195 7234, USA
Proc Natl Acad Sci U S A 105:15136-41. 2008..In fact, the dopaminergic neurons were more sensitive to rotenone. These data suggest that dopaminergic neuron death induced by treatment with rotenone, MPP(+), or paraquat is independent of complex I inhibition... - Starvation after AgRP neuron ablation is independent of melanocortin signalingQi Wu
Howard Hughes Medical Institute and Department of Biochemistry, University of Washington, Box 357370, Seattle, WA 98195, USA
Proc Natl Acad Sci U S A 105:2687-92. 2008..These results indicate that both the appetitive and consummatory aspects of feeding become impaired in a melanocortin-independent manner after AgRP neuron ablation... - Mice with mitochondrial complex I deficiency develop a fatal encephalomyopathyShane E Kruse
Howard Hughes Medical Institute and Department of Biochemistry, University of Washington, Seattle, WA 98195, USA
Cell Metab 7:312-20. 2008..Nonetheless, total oxygen consumption and muscle ATP and phosphocreatine concentrations measured in vivo were within normal parameters... - Loss of GABAergic signaling by AgRP neurons to the parabrachial nucleus leads to starvationQi Wu
Howard Hughes Medical Institute and Department of Biochemistry, University of Washington, Seattle, WA 98195, USA
Cell 137:1225-34. 2009..Chronic delivery of bretazenil during loss of AgRP neurons provides time to establish compensatory mechanisms that eventually allow mice to eat... - Dopamine is necessary to endogenous morphine formation in mammalian brain in vivoCarla Neri
Institute of Medicine and Public Health, University of Verona, Verona, Italy
J Neurochem 106:2337-44. 2008..Thus, dopamine and endogenous opiates/opioid peptides may be interconnected in the physiological processes; yet, endogenous morphine may represent a basic link of this chain... - The NK1 receptor mediates both the hyperalgesia and the resistance to morphine in mice lacking noradrenalineLuc Jasmin
Department of Neurological Surgery, University of California, San Francisco, CA 94143 0112, USA
Proc Natl Acad Sci U S A 99:1029-34. 2002..We conclude that when unopposed by NA, substance P acting at the NK1 receptor causes chronic thermal hyperalgesia, and that the reduced opioid efficacy associated with a lack of NA is due to increased NK1-receptor stimulation... - Dbh(-/-) mice are hypotensive, have altered circadian rhythms, and have abnormal responses to dieting and stressSteven J Swoap
Department of Biology, Williams College, Williamstown, MA 01267, USA
Am J Physiol Regul Integr Comp Physiol 286:R108-13. 2004..In contrast, Epi and NE are required for the tachycardia in an open field but are not required for the increase in blood pressure... - Dopamine controls the firing pattern of dopamine neurons via a network feedback mechanismCarlos A Paladini
Vollum Institute, Oregon Health and Science University, Portland, OR 97201, USA
Proc Natl Acad Sci U S A 100:2866-71. 2003..These data suggest that endogenously released dopamine plays a critical role in the afferent control of dopamine neuron bursting activity and that this control is exerted via a network feedback mechanism... - Contribution by synaptic zinc to the gender-disparate plaque formation in human Swedish mutant APP transgenic miceJoo Yong Lee
National Creative Research Initiative Center for the Study of Central Nervous System Zinc and Department of Neurology, University of Ulsan College of Medicine, Seoul 138 736, Korea
Proc Natl Acad Sci U S A 99:7705-10. 2002..Hence, of endogenous metals, synaptic zinc contributes predominantly to amyloid deposition in hAPP(+) mice... - Zinc released from metallothionein-iii may contribute to hippocampal CA1 and thalamic neuronal death following acute brain injuryJoo Yong Lee
National Creative Research Initiative Center for the Study of CNS Zinc and Department of Neurology, University of Ulsan College of Medicine, 138 736, Seoul, Korea
Exp Neurol 184:337-47. 2003..These results suggest that intracellular zinc release from MT-III may contribute substantially to zinc-mediated neuronal death in certain brain areas, including the hippocampal CA1 region and the thalamus... - Estrogen decreases zinc transporter 3 expression and synaptic vesicle zinc levels in mouse brainJoo-Yong Lee
National Creative Research Initiative Center for the Study of Central Nervous System Zinc, and Department of Neurology, University of Ulsan College of Medicine, Seoul 138-736, Korea
J Biol Chem 279:8602-7. 2004.... - Induction of metallothionein I by phenolic antioxidants requires metal-activated transcription factor 1 (MTF-1) and zincYongyi Bi
Receptor Biology Laboratory, Toxicology and Molecular Biology Branch, Health Effects Laboratory Division, National Institute for Occupational Safety and Health, Centers for Disease Control and Prevention, Morgantown, WV 26505, USA
Biochem J 380:695-703. 2004..These findings establish that phenolic antioxidants activate Mt1 transcription by a zinc-dependent mechanism, which involves MTF-1 binding to metal regulator elements in the Mt1 gene promoter... - Neuronal zinc exchange with the blood vessel wall promotes cerebral amyloid angiopathy in an animal model of Alzheimer's diseaseAvi L Friedlich
Laboratory for Oxidation Biology, Genetics and Aging Research Unit, Massachusetts General Hospital, and Department of Psychiatry, Harvard Medical School, Charlestown, Massachusetts 02129 4404, USA
J Neurosci 24:3453-9. 2004..ZnT3 was not detected in the cerebral vessel walls or in blood components of wild-type mice. Thus, synaptic ZnT3 activity may promote CAA by indirectly raising exchangeable Zn2+ concentrations in the perivascular spaces of the brain... - Endogenous neurotensin attenuates dopamine-dependent locomotion and stereotypyElena H Chartoff
Department of Psychiatry, McLean Hospital, Harvard Medical School, 115 Mill Street, Belmont, MA 02478, USA
Brain Res 1022:71-80. 2004.... - Mouse zinc transporter 1 gene provides an essential function during early embryonic developmentGlen K Andrews
Department of Biochemistry and Molecular Biology, University of Kansas Medical Center, 3901 Rainbow Boulevard, Kansas City, KS 66160 7421, USA
Genesis 40:74-81. 2004.... - Dopamine is not required for the hyperlocomotor response to NMDA receptor antagonistsElena H Chartoff
Department of Psychiatry, Harvard Medical School, McLean Hospital Belmont, MA, USA
Neuropsychopharmacology 30:1324-33. 2005..These results suggest that glutamate, rather than dopamine, is required for the locomotor and molecular effects of NMDA receptor antagonists, but that glutamate and dopamine can act cooperatively... - Dopamine supersensitivity correlates with D2High states, implying many paths to psychosisPhilip Seeman
Pharmacology Department, Medical Science Building, Room 4344, University of Toronto, 1 King s College Circle, Toronto, ON, Canada M5S 1A8
Proc Natl Acad Sci U S A 102:3513-8. 2005..If many types of brain impairment cause dopamine behavioral supersensitivity and a common increase in D2High states, it suggests that there are many pathways to psychosis, any one of which can be disrupted... - Role of metallothionein-III following central nervous system damageJavier Carrasco
Institute of Neurosciences and Department of Cellular Biology, Physiology and Immunology, Animal Physiology Unit, Faculty of Sciences, Autonomous University of Barcelona, Bellaterra, Barcelona, Spain 08193
Neurobiol Dis 13:22-36. 2003.... - Dopamine depletion does not protect against acute 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine toxicity in vivoDaphne M Hasbani
Department of Anatomy and Neurobiology, Washington University School of Medicine, St Louis, Missouri 63110, USA
J Neurosci 25:9428-33. 2005..These results suggest that DA does not contribute to acute MPTP toxicity in vivo... - The d subunit of the vacuolar ATPase (Atp6d) is essential for embryonic developmentGrant I Miura
Transgenic Res 12:131-3. 2003 - Neuropeptide Y protects against methamphetamine-induced neuronal apoptosis in the mouse striatumNathalie Thiriet
Centre National de la Recherche Scientifique 6187, University of Poitiers, 86000 Poitiers, France
J Neurosci 25:5273-9. 2005..Given the similarity between the cell death patterns induced by METH and by disorders such as Huntington's disease, our results suggest that NPY analogs might be useful therapeutic agents against some neurodegenerative processes... - GAD67-mediated GABA synthesis and signaling regulate inhibitory synaptic innervation in the visual cortexBidisha Chattopadhyaya
Cold Spring Harbor Laboratory, Cold Spring Harbor, NY 11724, USA
Neuron 54:889-903. 2007..Since intracellular GABA levels are modulated by neuronal activity, our results implicate GAD67-mediated GABA synthesis in activity-dependent regulation of inhibitory innervation patterns... - Chronic neuropeptide Y infusion into the lateral ventricle induces sustained feeding and obesity in mice lacking either Npy1r or Npy5r expressionPaula D Raposinho
Division of Pediatric Endocrinology and Diabetology, University of Geneva School of Medicine, 1211 Geneva 14, Switzerland
Endocrinology 145:304-10. 2004..Taken together, these data strongly suggest biological redundancies between Y1 and Y5 receptor signaling in the NPY-mediated control of food intake...
Research Grants
- GENETICS OF NEUROPEPTIDE Y FUNCTIONRICHARD PALMITER; Fiscal Year: 2001..These genetic experiments should help rationalize the current disparate results obtained by permanent NPY gene silencing and by acute intervention of NPY signaling. ..
- Effect of Killing or Removing GABA from NPY/AgRP NeuronsRICHARD PALMITER; Fiscal Year: 2007..These experiments should provide insight into the neural circuits and signaling molecules that are critical for feeding. ..
- Effect of Killing or Removing GABA from NPY/AgRP NeuronsRICHARD PALMITER; Fiscal Year: 2009..These experiments should provide insight into the neural circuits and signaling molecules that are critical for feeding. ..
- Effect of Killing or Removing GABA from NPY/AgRP NeuronsRichard D Palmiter; Fiscal Year: 2010..These experiments should provide insight into the neural circuits and signaling molecules that are critical for feeding. ..