Primary Research Areas
Brain dopamine systems; alcohol craving; fetal alcohol syndrome.
Addiction Propensity After Prenatal Ethanol Exposure (funded by NIAAA). This study is taking a multidisciplinary approach to investigating the effects of prenatal ethanol exposure on brain mechanisms that lead to increased risk of addiction later in life. The animal model utilized is anticipated to provide important insights into the risk factors of human addiction as well as better therapeutic strategies for behavioral problems associated with fetal alcohol spectrum disorders. Principal Investigator Shen’s research team includes Co-Investigators Samir Haj-Dahmane, PhD and Cynthia Dlugos, PhD of UB’s Department of Pathology and Anatomical Sciences in the School of Medicine and Biomedical Sciences. Consultants on the study include Jerry Richards, PhD and Paul Vezina, PhD of the University of Chicago.
Dopamine Function After Prenatal Ethanol Exposure (funded by NIAAA). Dr. Shen investigated how prenatal ethanol exposure influences the postnatal development of dopamine neurotransmission, how dopamine neurotransmission can be normalized by amphetamine-like stimulants, and more about the cellular mechanisms leading to these changes.
Chronic Ethanol, Dopamine Electrophysiology and Craving (funded by NIAAA). Dr. Shen investigated the neurological basis of alcohol craving with electrophysiological and neurochemical methods. The results obtained will improve our understanding for the neural mechanisms of alcohol craving and may lead to more effective pharmacological therapy for alcoholism.
Representative and Recent Publications
Haj-Dahmane, S., & Shen, R. Y. (in press). Modulation of the serotonin system by endocannabinoid signaling. Neuropharmacology, xxx, 1-7.
Haj-Dahmane, S., & Shen, R. Y. (2010). Regulation of plasticity of glutamate synapses by endocannabinoids and the cyclic-AMP/protein kinase A pathway in midbrain dopamine neurons. Journal of Physiology, 588,14, 2589-2604.
Haj-Dahmane, S., & Shen, R. Y. (2009). Endocannabinoids suppress excitatory synaptic transmission to dorsal raphe serotonin neurons through the activation of presynaptic CB1 receptors, Journal of Pharmacology and Experimental Therapeutics Fast Forward, 2009 July 10; [Epub ahead of print]. Retrieved July 23, 2009 from http://jpet.aspetjournals.org/
Aman, R. K., Shen, R., & Haj-Dahmane, S. (2007). D2-like dopamine receptors depolarize dorsal raphe serotonin neurons through the activation of nonselective cationic conductance. Journal of Pharmacology and Experimental Therapeutics, 320, 376-385.
Shen, R., Choong, K. C., & Thompson, A. C. (2007). Long-term reduction in ventral tegmental area dopamine neuron population activity following repeated stimulant or ethanol treatment. Biological Psychiatry, 61, 93-100.
Shen, R., & Choong, K.C. (2006). Different adaptations in ventral tegmental area dopamine neurons in control and ethanol exposed rats after methylphenidate treatment. Biological Psychiatry, 59, 635-642.
Wang, J., Haj-Dahmane, S., Shen, R. (2006). Effects of prenatal ethanol exposure on the excitability of ventral tegmental area dopamine neurons in vitro. Journal of Pharmacology and Experimental Therapeutics, 319, 857-863.
Haj-Dahmane, S., & Shen, R. (2005). The wake-promoting peptide orexin-B inhibits glutamatergic transmission to dorsal raphe nucleus serontonin neurons through retrograde endocannabinoid signaling. Journal of Neuroscience, 25, 896-905.
Choong, K. C., & Shen, R. (2004). Methylphenidate restores VTA dopamine neuron activity in prenatal ethanol exposed rats by augmenting dopamine neurotransmission. Journal of Pharmacology and Experimental Therapeutics, 309, 444-451.
Choong, K. C., & Shen, R. (2004). Prenatal ethanol exposure alters the postnatal development of the spontaneous electrical activity of dopamine neurons in the ventral tegmental area. Neuroscience, 126, 1083-1091.
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