Department of Physiology and Membrane Biology

Department of Physiology and Membrane Biology

Michael Ferns, Ph.D.

Michael Ferns, Ph.D.

Professor
4218 Tupper Hall
Davis Campus
(530) 754-4973
e-mail


Recent/Current
Research Funding

Muscular Dystrophy
Foundation


National Institute
of Health

Graduate Group Affiliations

Cell and Developmental
Biology


Molecular Cellular and
Integrative Physiology


Neuroscience

Research Interests

My interest is in understanding the cellular and molecular basis of synapse formation in the mammalian nervous system. Synapse formation is critical for the formation, maintenance and plasticity of the nervous system and perturbations in synaptic structure and function have been implicated in a range of neurological disorders. My research focuses on cholinergic synapses that play critical roles in the functioning of both the peripheral and central nervous systems. Our main aims are (1) to define the extracellular synaptogenic factors that regulate the formation and maintenance of neuromuscular and neuronal autonomic synapses in the PNS, and (2) to define the intracellular mechanisms that regulate the trafficking and localization of nicotinic acetylcholine receptors at these synapses. This includes collaborative studies with clinician-scientists at UCD to establish how defects in synapse formation or receptor localization contribute to neurological diseases such as myasthenia gravis and congenital myasthenic syndromes.

 

Representative Publications

Gingras, J., Rassadi, S., Cooper, E., & Ferns, M.  (2002) Agrin plays an organizing role in the formation of sympathetic synapses. J. Cell Biol. 158(6): 1109-1118.

Gingras, J., Rassadi, S., Cooper, E., and Ferns, M.  (2007) Synaptic transmission is impaired at neuronal autonomic synapses in agrin null mice.  Dev. Neurobiol. 67(5): 521-534.

Borges LS, Yechikhov S, Lee YI, Rudell JB, Friese MB, Burden SJ, Ferns MJ (2008) Identification of a motif in the acetylcholine receptor beta subunit whose phosphorylation regulates rapsyn association and postsynaptic receptor localization. J Neurosci. 28:11468-11476.

Lee Y, Rudell J, and Ferns M (2009) Rapsyn interacts with the muscle AChR via a-helical domains in the a, b, and e subunit intracellular loops. Neuroscience, 163: 222-232.  

Richman DP, Nishi K, Morell SW, Chang JM, Ferns MJ, Wollmann RL, Maselli RA, Schnier J, Agius MA. (2012) Acute Severe Animal Model of Anti-Muscle-Specific Kinase Myasthenia: Combined Postsynaptic and Presynaptic Changes. Arch Neurol. 69(4): 453-60

Maselli, RA., Fernandez, JM., Arredondo, J., Navarro, C., Ngo, M., Beeson, D., Cagney, O., Williams, DC., Wollmann, RL., and Yarov-Yarovoy, V., and Ferns, M. (2012) LG2 agrin mutation causing severe congenital myasthenic syndrome mimics functional characteristics of non-neural (z-) agrin. Human Genetics 131(7): 1123-35.               

Maselli, RA., Arredondo, J., Ferns, MJ., and Wollmann, RL. (2012) Synaptic basal lamina-associated congenital myasthenic syndromes. Annals of NY Acad. Sci. 1275:36-48.

Rudell, JB., and Ferns, MJ. (2013) Regulation of muscle acetylcholine receptor turnover by b subunit tyrosine phosphorylation. Dev. Neurobiol. In press.

 

Recent/Current Teaching

HPH400, Human Physiology
MCP210A, Advanced Physiology, Co-Instructor of Record