The Laboratory of Cellular Biology of the Basal Ganglia
Lab Director: Jean-Jacques Soghomonian, Ph.D.
Research is focused on the functional organization and the cellular biology of the basal ganglia with a specific interest in the pathophysiology of Parkinson¹s disease and l-DOPA-induced dyskinesias.
Dopamine and the basal ganglia
Parkinson’s disease is a neurodegenerative disease characterized by a loss of dopamine neurons in the brain. Movement abnormalities observed in Parkinson¹s disease are secondary to the loss of dopamine neurons and involve abnormal cell signaling in brain regions such as the basal ganglia. The most common therapeutic intervention in Parkinson¹s disease consists in administering the precursor of dopamine, l-dopa. However, long-term exposure to l-DOPA results in severe secondary effects and abnormal movements such as dyskinesias. One major research objective in the laboratory is to understand the mechanisms involved in dyskinesias in experimental models of Parkinson¹s disease.
Post-mortem studies in Parkinson’s disease and Autism
Dr. Soghomonian’s laboratory also investigates the neuropathology of Parkinson’s disease and Autism on post-mortem human tissue.
GABA is a major inhibitory neurotransmitter in the mammalian brain. Another focus of the laboratory is to study the mechanisms involved in the regulation of GABA-mediated signaling by dopamine receptors in the normal brain and in models of Parkinson’s disease.
Dr. Soghomonian’s laboratory uses a number of behavioral, pharmacological, anatomical and molecular approaches to the study of Parkinson’s disease and motor disorders in Parkinson’s disease. The major approaches and techniques used in the laboratory are behavioral assessments of motor activity, in situ hybridization histochemistry, immunohistochemistry, light and fluorescent microscopy, quantitative image analysis, western blotting and RT-PCR.
Jean-Jacques Soghomonian, Ph.D.
Dr. Soghomonian is the director of the laboratory. His research is focused on the functional and cellular organization of the basal ganglia and associated motor disorders
Kunzhong Zang is a post-doctoral fellow who investigates the mechanisms involved in l-DOPA-induced dyskinesia.
Amelie Lanoue graduated with a Ph.D. in 2013. She was working on the pathophysiology of the prefrontal cortex in Parkinson’s disease.
Current laboratory members:
Kunzhong Zhang (Post-doctoral fellow)
Amelie Lanoue (Ph.D. Student)
Sarah Chisholm (undergraduate student)
Christina Medeiros (undergraduate student)
Kelley Anderson (undergraduate student)
Andrew Acciardo (undergraduate student)
Zhang C. Chammas, Soghomonian JJ. Loss of glutamic acid decarboxylase (Gad67) in striatal neurons expressing the Drdr1a dopamine receptor prevents l-DOPA-induced dyskinesia in 6-hydroxydopamine-lesioned mice. Neuroscience. 2015 Sep 10;303:586-94.
Zhang K, Hill K, Labak S, Blatt GJ, Soghomonian JJ. Loss of glutamic acid decarboxylase (Gad67) in Gpr88-expressing neurons induces learning and social behavior deficits in mice. Neuroscience. 2014 Sep 5;275:238-47.
Lanoue AC, Blatt GJ, Soghomonian JJ. (2013) Decreased parvalbumin mRNA expression in dorsolateral prefrontal cortex in Parkinson’s disease. Brain Res. 2013 Sep 19;1531:37-47.
Lanoue AC, Dumitriu A, Myers RH, Soghomonian JJ. (2010) Decreased glutamic acid decarboxylase mRNA expression in prefrontal cortex in Parkinson’s disease. Exp Neurol. 226(1):207-17.
Soghomonian, JJ, Sethares, C, Peters A. (2010) Effects of age on axon terminals forming axodendritic and axosomatic inhibitory synapses in prefrontal cortex. In press. Neuroscience. 168(1):74-81
For more publications, please see Dr. Soghomonian’s Faculty Page