Jean-Jacques R. Soghomonian, Ph.D.
Location: R – 1014, BUSM
Dr. Soghomonian received a doctorate in Neuroscience from the University of Aix-Marseille and a Ph.D. in Neurological Sciences from the University of Montreal. He completed postdoctoral training at the Medical College of Pennsylvania and the University of Pennsylvania and then worked as an Assistant Professor in the Department of Physiology and Anatomy at Laval University. He joined the Department of Anatomy and Neurobiology at Boston University School of Medicine in 1998. Dr. Soghomonian maintains an active research program on the anatomical and functional organization of the basal ganglia in the normal brain and in experimental models of Parkinson’s disease.
Dr. Soghomonian’s research focuses on the pathophysiology of Parkinson’s disease and l-DOPA-induced dyskinesia. His laboratory, The Laboratory for the Cellular Biology of the Basal Ganglia and Motor Disorders, is also studying the mechanisms involved in the regulation of GABA-mediated signaling in the basal ganglia and the role of the basal ganglia in sensori-motor learning. The laboratory uses a combination of anatomical, neurochemical and molecular biology techniques.
Dr. Soghomonian teaches Medical Histology and Medical Neuroscience to Medical School and Graduate Medical Sciences students. He is also involved in the teaching of Departmental graduate courses and is director of the graduate course “Methods in Neuroscience”.
Dr. Soghomonian has served as the Graduate Director in the Department. He currently serves on the MD-PhD Admission Committee at Boston University School of Medicine and on the Qualifying Committee in the Department of Anatomy and Neurobiology.
Lanoue AC, Dumitriu A, Myers RH, Soghomonian JJ. Decreased glutamic acid decarboxylase mRNA expression in prefrontal cortex in Parkinson’s disease. Exp Neurol. 2010 Nov;226(1):207-17. Epub 2010 Sep 9. PubMed PMID: 20832408; PubMed Central PMCID: PMC3108022.
Soghomonian JJ, Sethares C, Peters A. Effects of age on axon terminals forming axosomatic and axodendritic inhibitory synapses in prefrontal cortex. Neuroscience. 2010 Jun 16;168(1):74-81. Epub 2010 Mar 16. PubMed PMID: 20302918; PubMed Central PMCID: PMC2873101.
Yamamoto N, Soghomonian JJ. Metabotropic glutamate mGluR5 receptor blockade opposes abnormal involuntary movements and the increases in glutamic acid decarboxylase mRNA levels induced by l-DOPA in striatal neurons of 6-hydroxydopamine-lesioned rats. Neuroscience. 2009 Nov 10;163(4):1171-80. Epub 2009 Aug 4. PubMed PMID: 19660528; PubMed Central PMCID: PMC2760628.
Yip J, Soghomonian JJ, Blatt GJ. Decreased GAD65 mRNA levels in select subpopulations of neurons in the cerebellar dentate nuclei in autism: an in situ hybridization study. Autism Res. 2009 Feb;2(1):50-9. PubMed PMID: 19358307; PubMed Central PMCID: PMC2724747.
Yamamoto N, Soghomonian JJ.Time-course of SKF-81297-induced increase in glutamic acid decarboxylase 65 and 67 mRNA levels in striatonigral neurons and decrease in GABA(A) receptor alpha1 subunit mRNA levels in the substantia nigra, pars reticulata, in adult rats with a unilateral 6-hydroxydopamine lesion. Neuroscience. 2008 Jun 26;154(3):1088-99. Epub 2008 Apr 16. PMID: 18495353 [PubMed – indexed for MEDLINE]
Yip J, Soghomonian JJ, Blatt GJ. Increased GAD67 mRNA expression in cerebellar interneurons in autism: implications for Purkinje cell dysfunction. J Neurosci Res. 2008 Feb 15;86(3):525-30. PMID: 17918742 [PubMed – indexed for MEDLINE]
Hatzipetros T, Raudensky JG, Soghomonian JJ, Yamamoto BK. Haloperidol treatment after high-dose methamphetamine administration is excitotoxic to GABA cells in the substantia nigra pars reticulata. J Neurosci. 2007 May 30;27(22):5895-902.
PMID: 17537960 [PubMed – indexed for MEDLINE]
Yip J, Soghomonian JJ, Blatt GJ. Decreased GAD67 mRNA levels in cerebellar Purkinje cells in autism: pathophysiological implications. Acta Neuropathol. 2007 May;113(5):559-68. Epub 2007 Jan 18. PMID: 17235515 [PubMed – indexed for MEDLINE]
Wang H, Katz J, Dagostino P, Soghomonian JJ. Unilateral 6-hydroxydopamine lesion of dopamine neurons and subchronic L-DOPA administration in the adult rat alters the expression of the vesicular GABA transporter in different subsets of striatal neurons and in the substantia nigra, pars reticulata. Neuroscience. 2007 Mar 16;145(2):727-37. Epub 2007 Jan 9. PMID: 17218060 [PubMed – indexed for MEDLINE]
Yamamoto N, Pierce RC, Soghomonian JJ. Subchronic administration of L-DOPA to adult rats with a unilateral 6-hydroxydopamine lesion of dopamine neurons results in a sensitization of enhanced GABA release in the substantia nigra, pars reticulata. Brain Res. 2006 Dec 6;1123(1):196-200. Epub 2006 Oct 9. PMID: 17027936 [PubMed – indexed for MEDLINE]
Soghomonian JJ. L-DOPA-induced dyskinesia in adult rats with a unilateral 6-OHDA lesion of dopamine neurons is paralleled by increased c-fos gene expression in the subthalamic nucleus. Eur J Neurosci. 2006 May;23(9):2395-403. Erratum in: Eur J Neurosci. 2006 Sep;24(5):1505. PMID: 16706847 [PubMed – indexed for MEDLINE]
Katz J, Nielsen KM, Soghomonian JJ. Comparative effects of acute or chronic administration of levodopa to 6-hydroxydopamine-lesioned rats on the expression of glutamic acid decarboxylase in the neostriatum and GABAA receptors subunits in the substantia nigra, pars reticulata. Neuroscience. 2005;132(3):833-42. PMID: 15837143 [PubMed – indexed for MEDLINE]
Nielsen KM, Soghomonian JJ. Normalization of glutamate decarboxylase gene expression in the entopeduncular nucleus of rats with a unilateral 6-hydroxydopamine lesion correlates with increased GABAergic input following intermittent but not continuous levodopa. Neuroscience. 2004;123(1):31-42.
Nielsen KM, Soghomonian JJ. Dual effects of intermittent or continuous L-DOPA administration on gene expression in the globus pallidus and subthalamic nucleus of adult rats with a unilateral 6-OHDA lesion. Synapse. 2003 Sep 15;49(4):246-60.