Behavior and Behavior Mechanisms; Mental Disorders; Central Nervous System Diseases; Parkinson Disease; Psychiatry and Psychology; Phenomena and Processes
Our laboratory takes a neurochemical approach towards examining neurotransmitter function and the mechanism of action of psychotropic drugs. The major research investigates the biochemical organization, regulatory control, pharmacology, and function of catecholamine-containing neurons in the CNS. We also investigate the post-translational mechanisms by which neuronal impulse flow regulates tyrosine hydroxylase and examine the function of dopamine autoreceptors. Our focus recently has been on central dopamine systems and, in particular, on the mesocortical system. These studies, carried out both in rodents and non-human primates, have revealed that the mesotelencephalic dopamine systems are quite heterogeneous, exhibiting distinct physiological and pharmacological properties. Neural grafting is another research interest of our lab. We are currently investigating the function of neural grafts and stem cells in the MPTP primate model of Parkinson’s disease.
- Asenapine effects on cognitive and monoamine dysfunction elicited by subchronic phencyclidine administration. Elsworth JD, Groman SM, Jentsch JD, Valles R, Shahid M, Wong E, Marston H, Roth RH. Neuropharmacology. 2011 Aug 23
- Loss of asymmetric spine synapses in dorsolateral prefrontal cortex of cognitively impaired phencyclidine-treated monkeys. Elsworth JD, Hajszan T, Leranth C, Roth RH. Int J Neuropsychopharmacol. 2011 Jun 27:1-5
- Reduced locomotor responses to cocaine in ghrelin-deficient mice. Abizaid A, Mineur YS, Roth RH, Elsworth JD, Sleeman MW, Picciotto MR, Horvath TL. Neuroscience. 2011 Sep 29;192:500-6
- Phencyclidine-induced Loss of Asymmetric Spine Synapses in Rodent Prefrontal Cortex is Reversed by Acute and Chronic Treatment with Olanzapine. Elsworth JD, Morrow BA, Hajszan T, Leranth C, Roth RH. Neuropsychopharmacology. 2011 Sep;36(10):2054-61. doi: 10.1038/npp.2011.96
- Impact of methamphetamine on dopamine neurons in primates is dependent on age: implications for development of Parkinson's disease. Morrow BA, Roth RH, Redmond DE, Elsworth JD. Neuroscience. 2011 Aug 25;189:277-85
- Aged monkeys as a partial model for Parkinson's disease. Hurley PJ, Elsworth JD, Whittaker MC, Roth RH, Redmond DE Jr. Pharmacol Biochem Behav. 2011 Sep;99(3):324-32
- GPA protects the nigrostriatal dopamine system by enhancing mitochondrial function. Horvath TL, Erion DM, Elsworth JD, Roth RH, Shulman GI, Andrews ZB. Neurobiol Dis. 2011 Jul;43(1):152-62
- Iversen, L.L., Iversen, S.D., Bloom, F.E. and Roth, R.H., Introduction to Neuropsychopharmacology , Oxford University Press, 2009.
- AAV2-mediated gene transfer of GDNF to the striatum of MPTP monkeys enhances the survival and outgrowth of co-implanted fetal dopamine neurons. Elsworth, J. D., Redmond, Jr., D.E., Leranth, C., Bjugstad, K.B., Sladek J.R. Jr. Collier, T.J., Foti, S.B., Samulski, R.J. Vives, K.P. and Roth, R.H. AAV2-mediated gene transfer of GDNF to the striatum of MPTP monkeys enhances the survival and outgrowth of co-implanted fetal dopamine neurons.
- Elsworth, J.D., Jentsch, J.D., Morrow, B.A., Redmond, Jr., D.E., & Roth,R.H., Clozapine selectively normalizes frontal cortex dopamine transmission in monkeys subchronically exposed to phencyclidine. Neuropsychopharmacology 33:491-496, 2008.
- Morrow, B.A., Hajszan, T., Leranth, C. Elsworth, J.D., Roth, R.H., Prenatal exposure to cocaine is associated with increased number of spine synapses in rat prelimbic cortex. Synapse, 61: 862-865, 2007
- Elsworth, J.D., & Roth, R.H., “Dopamine: Neurotransmission, Neuromodulation and Regulation,” In: New Encyclopedia of Neuroscience. ((Squires L, Albright T, Bloom F, Gage F, Spitzer N, eds) 2007.
- Hajszan, T., Leranth. C., Roth, R.H., Subchronic Phencyclidine Treatment Decreases the Number of Dendtritic Spine Synapses in the Rat Prefrontal Cortex, Biological Psychiatry 60(6): pp. 639-644, 2006.
- Jentsch, J.D., Taylor, J.R., & Roth, R.H., Phencyclidine Model of Frontal Cortical Dysfunction in Non-Human Primates. The Neuroscientist, 6(4); 263-270, 2000.