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The Munmun Chattopadhyay Laboratory


Munmun Chattopadhyay, Ph.D.

Dr. Munmun Chattopadhyay is a Research Assistant Professor in the Department of Neurology. Her lab studies peripheral neuropathy and the pathogenesis and treatment of pain caused by neuropathy.

Dr. Chattopadhyay’s doctoral work was focused on nerve injury and aging. She established that flunarizine, a calcium channel antagonist, is effective in eliminating the age-pigment by dissolving its lipid content. She also demonstrated that flunarizine has a positive influence on neuron survival in the aging nervous system, restricts initial degenerative changes that follow axotomy, and influences the rate of regeneration of affected neurons 1.

Dr. Chattopadhyay’s work in the Mata-Fink laboratory at the University of Michigan has focused on the pathogenesis of peripheral neuropathy and the use of replication defective herpes simplex virus (HSV)-mediated gene transfer to the peripheral nervous system as a treatment for neuropathy. Her research focus is to understand the pathogenesis and development of novel treatments for painful neuropathies by gene therapy, using viral vectors and the mechanisms responsible in pain pathways involving the regulation of inhibitory neurotransmitter receptors and ion channel trafficking.

She established that replication defective herpes simplex virus-mediated gene transfer of nerve growth factor (NGF) 2, neurotrophin-3 (NT-3) 3-6, vascular endothelial growth factor (VEGF) 7 and erythropoietin (EPO) 8 can prevent diabetic, chemotherapy or drug-induced peripheral sensory neuropathy in animals. She also established that gene transfer mediated release of inhibitory neurotransmitters- enkephalin 9 and gamma amino butyric acid (GABA) 10 in diabetic animals reduces pain coincident with a reduction in sodium channel NaV1.7 levels in DRG, in vivo.

Her recent work established that altered levels of voltage gated sodium channel (NaV) plays a key role in the development of painful diabetic neuropathy parallel to the development of diabetic neuropathy, primary DRG neurons in culture shows similar increase in levels of sodium channels under hyperglycemia 9.  In order to explicitly test the role of increased levels of NaV in DRG in the pathogenesis of pain in diabetic neuropathy, she established that reduction in NaVα protein by knocking down Navα in DRG by HSV vector expression a microRNA (miRNA) against NaVα reduced pain-related behaviors in animals with pain diabetic neuropathy 11.

Dr. Chattopadhyay's current work is focused on understanding the role of neuroinflammation in the development of painful diabetic neuropathy in Type 1 and Type 2 animal model of diabetes, and how exercise could alleviate the development of neuropathy in these models.