VICTOR MAY

Professor
Anatomy and Neurobiology

Ph.D., Northwestern University, 1983
Postdoctoral training, Johns Hopkins University

Victor.May@uvm.edu

Sympathetic ganglia use both small molecule classical neurotransmitters and neuropeptides as chemical messengers. The coexpression of bioactive peptides and neurotransmitters permits functional diversity in the nervous system; however, the regulatory signals that modulate neurotransmitter and neuropeptide expression and neuroplasticity are poorly understood. The principal neurons of the superior cervical ganglion (SCG) are a unique model system used extensively to examine the regulation of neuronal transmitter and peptide expression. Most SCG neurons are catecholaminergic, and these cells produce high levels of norepinephrine and neuropeptide Y (NPY), and lower levels of several other bioactive peptides. SCG neurons also exhibit neurochemical plasticity, and under specific conditions, change from a noradrenergic to dopaminergic, adrenergic, or cholinergic phenotype with coordinate changes in neuropeptide expression. Our research uses primary cultured SCG neurons, to examine regulatory factors, including presynaptic signals, hormones, growth factors, cytokines, and target tissue factors, that modulate SCG neurotransmitter and neuropeptide expression. The questions we are addressing include: (1) What external signals or factors regulate sympathetic neuron transmitter and peptide expression? (2) What intracellular signaling pathways mediate these regulatory events? (3) What cellular processes, such as transcription, biosynthesis, and secretion, are modulated to alter neurotransmitter and neuropeptide expression? (4) What mechanisms are involved in altered gene expression? (5) How do these factors modulate sympathetic neuron survival, differentiation, and signaling? Our studies use a combination of disciplines, including biochemistry, cell biology, and molecular biology to examine these questions.

Recently, our work has focused on the roles of presynaptic signal modulation of SCG functions. We demonstrated that preganglionic neurons in the spinal cord projecting to the SCG express the bioactive peptide pituitary adenylate cyclase-activating polypeptide (PACAP). Further investigations have identified and localized the specific isoforms of the PACAP-selective PAC1 receptor, a putative seven transmembrane G-protein-coupled receptor, expressed by sympathetic neurons. In SCG neurons, these receptors are coupled to the activation of multiple intracellular signaling pathways; we are currently characterizing the mechanisms by which PACAP activation of these second messenger pathways regulates sympathetic neuron development, function, neurophenotypic plasticity.

Hansel, D. E., V. May, B. A. Eipper, G. V. Ronnett (2001). Pituitary adenylyl cyclase-activating peptides and alpha-amidation in olfactory neurogenesis and neuronal survival in vitro. J. Neurosci. 21:4625-36.

Beaudet, M. M., R. L. Parsons, K. M. Braas, and V. May (2000). Mechanisms mediating pituitary adenylate cyclase-activating polypeptide depolarization of rat sympathetic neurons. J. Neurosci. 20:7353-61.

Braas, K. M. and V. May (1999). Pituitary adenylate cyclase-activating polypeptides directly stimulate sympathetic neuron neuropeptide Y release through PAC1 receptor isoform activation of specific intracellular signaling pathways. J. Biol. Chem. 274:27702-27710.

May, V., M. M. Beaudet, R. L. Parsons, J. C. Hardwick, E. Gauthier, J. P. Durda, and K. M. Braas (1998). Mechanisms of pituitary adenylate cyclase activating polypeptide (PACAP)-induced depolarization of sympathetic superior cervical ganglion (SCG) neurons. Ann. N. Y. Acad. Sci. 865:164-175.

Beaudet, M. M., K. M. Braas, and V. May (1998). Pituitary adenylate cyclase-activating polypeptide (PACAP) expression in sympathetic preganglionic projection neurons to the superior cervical ganglion. J. Neurobiol. 36:325-36.

May, V. and K. M. Braas (1995). Pituitary adenylate cyclase activating polypeptide (PACAP) regulation of superior cervical ganglion neuropeptide Y and catecholamine expression. J. Neurochem. 65:978-987.