James I. Nagy, Ph.D.
Professor, Physiology & Pathophysiology
University of Manitoba
- 418 BMSB
- Summary of Research
- Identification of gap junction proteins, connexins, expressed by astrocytes, oligodendrocytes and neurons in the central nervous system.
- Analysis of the regulation of glial gap junctional communication and the contribution of glial gap junctions to neural injury and to neuroprotection in animal models of stroke.
- Elucidation of the role of neuronal gap junctions and connexins in electrical synaptic transmission and inter-neuronal communication in the adult central nervous system in normal and disease conditions.
- Studies on the developmental regulation of neuronal connexins and the contribution of inter-neuronal gap junctions to neuronal development in mammalian CNS.
- Identification of proteins associated with gap junctions and analysis of their regulatory and structural roles in connexin trafficking, phosphorylation, assembly and junctional communication.
- Development of antibodies against connexins and gap junction-associated proteins.
- Research Interests
- We are conducting studies of interneuronal communication that occurs via electrical neurotransmission or electrical coupling. Over the years, numerous chemical neurotransmitters have been identified, however, electronic coupling is accomplished without the aid of chemical substances and is instead mediated via gap junctions composed of gap junctional proteins called connexins. We and co-workers are identifying neurons where this form of transmission occurs in developing and adult mammalian CNS. We expect that the research will indicate the importance of neuronal gap junctional communication at dendritic as well as at synaptic connections in mammalian brain. Using animal models, we also aim to determine how neuronal gap junctions contributes to various disease states and neurological disorders.
- In a related project, we together with collaborators have made considerable advances in understanding gap junctional communication between glial cells and how glial coupling responds to brain and spinal cord injury. Our aim is to understand how neurons as well as glial signaling pathways exert regulatory control on this form of glial communication via processes involving connexin phosphorylation, trafficing and degredation. We use culture and brain slice as well as in vivo models combined with immunohistochemical, dye-coupling and biochemical methods. Ultimately, we wish to understand how glial gap junctional coupling either promotes or compromises neuronal survival after injury.
- At a more cellular level, we use biochemical, molecular and proteomic approaches to identify and study the functional roles of proteins that directly interact with connexins or are otherwise associated with gap junctions. Our focus is mainly on connexins expressed in the CNS, including those expressed in astrocytes (Cx26, Cx30, Cx43), oligodendrocytes (Cx29, Cx32, Cx47) and neurons (Cx36, Cx45, Cx57).
- Areas of Expertise
- Neurochemistry, neuroanatomy, biochemistry, cell biology, immunohistochemistry, models of spinal cord and brain injury, gap junction structure and function, CNS inflammatory mechanisms.
- Hossein Tavakoli, M.Sc. Student