- Postdoctoral Training, Johns Hopkins University School of Medicine, Baltimore, MD
- Ph.D., Anatomy and Cell Biology, Northwestern University, Chicago, IL
- B.A., Biology, Johns Hopkins University, Baltimore, MD
Areas of expertise
Ours is a cellular and molecular neuroscience laboratory studying transmitters, peptides, G-protein-coupled receptors (GPCRs) and their downstream signaling effectors including the roles of internalized GPCR endosomal platforms in neuronal function and plasticity. Our work has emphasized the expression and function of the pituitary adenylate cyclase activating polypeptide (PACAP, ADCYAP1) signaling at its cognate GPCR PAC1 receptor (ADCYAP1R1) and more recently, we are attempting to map central PACAPergic neurocircuits to study their roles in maladaptive plasticity associated with psychopathologies including anxiety disorders, PTSD and depression. In collaborations with the Chemistry and Psychological Sciences departments, we are also attempting to develop biased PAC1 receptor antagonists for migraine and stress-induced anxiety-related disorder therapeutics.
BIO
Dr. Victor May is the Samuel W. Thayer Professor in the Department of Neurological Sciences at the University of Vermont Larner College of Medicine. After graduating from Stuyvesant High School in New York City, he received his BA in Biology from the Johns Hopkins University, his PhD in Anatomy and Cell Biology from Northwestern University Medical School and completed his postdoctoral training in the laboratories of Dick Mains and Betty Eipper in the Department of Neuroscience at the Johns Hopkins University School of Medicine.
Dr. May’s laboratory is focused on the study of bioactive peptides, G protein coupled receptors (GPCRs) and the intersection of their downstream signaling cascades with other cellular effectors to regulate neural development, function and plasticity. For many years, the laboratory’s work has emphasized the expression and regulation of pituitary adenylate cyclase activating polypeptide (PACAP, ADCYAP1) and its cognate PAC1 receptor (ADCYAP1R1) in the central and peripheral nervous systems. The laboratory was the first to show that PACAP is a potent preganglionic non-cholinergic regulator of sympathetic neuronal function, which led to related studies examining PAC1 receptor isoform coupling to different signaling cascades and the mechanisms of neuronal PACAP induction. From their signaling work, they found that PAC1 receptor internalization and resulting intracellular endosomal activities represent a principal long term signaling mechanism for neuronal excitability and function. These investigations yielded important mechanistic insights which advanced the current work on PACAP/PAC1 receptor signaling in nociception and stress-related behaviors, and the association of the PACAPergic system to stress-related psychopathologies including posttraumatic stress disorder (PTSD). The work demonstrated that PACAP expression and signaling in the bed nucleus of the stria terminalis (BNST) participate in maladaptations leading to stress-related anxiety-related psychopathologies. The more recent work showing the abilities for parabrachial PACAP neurons to relay nociceptive signals to the amygdala may provide mechanisms for the high comorbidity between pain and stress-related disorders. The extensions of these studies on PACAP behavioral circuits have led to the novel observation that BNST PACAP projections to the medial habenula (MHb) may have key roles in depression. Accordingly, the laboratory has developed and distributed many PACAP-related reagents including antibodies, plasmids/probes and stable cell lines to many researchers, collaborated with national and international investigators and contributed significantly to the current peptide and PACAP literature in journals and book chapters. The laboratory strives for innovation and the generation of new ideas and concepts. Using computational approaches, the group is currently simulating PAC1 receptor structure and microstate dynamics for rational drug design. From assay development and work on receptor antagonists, he has received 3 patents to date; several other potential compounds are currently in development.
In addition to research, Dr. May has taught human gross anatomy and neurochemistry to learners of all ranks at the University of Vermont College of Medicine. From his teaching experiences, he is currently completing his first book on the human architecture and form.
Courses
- ANNB 6000, Gross Anatomy
- NSCI 6030, Human Gross & Microanatomy
Bio
Dr. Victor May is the Samuel W. Thayer Professor in the Department of Neurological Sciences at the University of Vermont Larner College of Medicine. After graduating from Stuyvesant High School in New York City, he received his BA in Biology from the Johns Hopkins University, his PhD in Anatomy and Cell Biology from Northwestern University Medical School and completed his postdoctoral training in the laboratories of Dick Mains and Betty Eipper in the Department of Neuroscience at the Johns Hopkins University School of Medicine.
Dr. May’s laboratory is focused on the study of bioactive peptides, G protein coupled receptors (GPCRs) and the intersection of their downstream signaling cascades with other cellular effectors to regulate neural development, function and plasticity. For many years, the laboratory’s work has emphasized the expression and regulation of pituitary adenylate cyclase activating polypeptide (PACAP, ADCYAP1) and its cognate PAC1 receptor (ADCYAP1R1) in the central and peripheral nervous systems. The laboratory was the first to show that PACAP is a potent preganglionic non-cholinergic regulator of sympathetic neuronal function, which led to related studies examining PAC1 receptor isoform coupling to different signaling cascades and the mechanisms of neuronal PACAP induction. From their signaling work, they found that PAC1 receptor internalization and resulting intracellular endosomal activities represent a principal long term signaling mechanism for neuronal excitability and function. These investigations yielded important mechanistic insights which advanced the current work on PACAP/PAC1 receptor signaling in nociception and stress-related behaviors, and the association of the PACAPergic system to stress-related psychopathologies including posttraumatic stress disorder (PTSD). The work demonstrated that PACAP expression and signaling in the bed nucleus of the stria terminalis (BNST) participate in maladaptations leading to stress-related anxiety-related psychopathologies. The more recent work showing the abilities for parabrachial PACAP neurons to relay nociceptive signals to the amygdala may provide mechanisms for the high comorbidity between pain and stress-related disorders. The extensions of these studies on PACAP behavioral circuits have led to the novel observation that BNST PACAP projections to the medial habenula (MHb) may have key roles in depression. Accordingly, the laboratory has developed and distributed many PACAP-related reagents including antibodies, plasmids/probes and stable cell lines to many researchers, collaborated with national and international investigators and contributed significantly to the current peptide and PACAP literature in journals and book chapters. The laboratory strives for innovation and the generation of new ideas and concepts. Using computational approaches, the group is currently simulating PAC1 receptor structure and microstate dynamics for rational drug design. From assay development and work on receptor antagonists, he has received 3 patents to date; several other potential compounds are currently in development.
In addition to research, Dr. May has taught human gross anatomy and neurochemistry to learners of all ranks at the University of Vermont College of Medicine. From his teaching experiences, he is currently completing his first book on the human architecture and form.
Courses
- ANNB 6000, Gross Anatomy
- NSCI 6030, Human Gross & Microanatomy
Select Publications
Ressler, K. J., K. B. Mercer, B. Bradley, T. Jovanovic, A. Mahan, K. Kerley, S. D. Norrholm, V. Kilaru, A. K. Smith, A. J. Myers, M. Ramirez, A. Engel, S. E. Hammack, D. Toufexis, K. M. Braas, E. B. Binder and V. May (2011) Post-traumatic stress disorder is associated with PACAP and the PAC1 receptor. Nature 470:492-497. PMID: 21350482; PMCID: PMC3046811.
Hammack, S. E., J. Cheung, K. M. Rhodes, K. C. Schutz, W. A. Falls, K. M. Braas and V. May (2009) Chronic stress increases pituitary adenylate cyclase-activating peptide (PACAP) and brain-derived neurotrophic factor (BDNF) mRNA expression in the bed nucleus of the stria terminalis (BNST): roles for PACAP in anxiety-like behavior. Psychoneuroendocrinology 34:833-843. PMID: 19181454; PMCID: PMC2705919.
Roman, C. W., K. R. Lezak, M. J. Hartsock, W. A. Falls, K. M. Braas, A. B. Howard, S. E. Hammack, V. May. (2014) PAC1 receptor antagonism in the bed nucleus of the stria terminalis (BNST) attenuates the behavioral and endocrine consequences of chronic stress. Psychoneuroendocrinology 47:151-165. PMID: 25001965; PMCID: PMC4342758.
Missig, G., L. Mei, M. A. Vizzard, K. M. Braas, J. A. Waschek, K. J. Ressler, S. E. Hammack and V. May (2017) Parabrachial PACAP activation of amygdala endosomal ERK signaling regulates the emotional component of pain. Biol Psychiatry 81:671-682. PMID: 28057459; PMCID: PMC5332340.
Johnson G. C., R. L. Parsons, V. May V, S. E. Hammack (2020) Pituitary adenylate cyclase-activating polypeptide-induced PAC1 receptor internalization and recruitment of MEK/ERK signaling enhance excitability of dentate gyrus granule cells. Am J Physiol Cell Physiol. 318:C870-C878. PMID: 32186931; PMCID: PMC7294323.
Clancy KJ, Q. Devignes, P. Kumar, V May, S. E. Hammack, E. Akman, E. J. Casteen, C. D. Pernia, S. A. Jobson, M. W. Lewis, N. P. Daskalakis, W. A. Carlezon Jr, K. J. Ressler, S. L. Rauch, I. M. Rosso (2023) Circulating PACAP levels are associated with increased amygdala-default mode network resting-state connectivity in posttraumatic stress disorder. Neuropsychopharmacology, 48:1245-1254.. PMID: 37161077; PMCID: PMC10267202.
Fontaine NR, L. Lepeak, M. Aktar, A. Mahler, W. Black, J. Hannibal, M. A. Vizzard MA, V. May, S. E. Hammack (2025) Bed nucleus of the stria terminalis PACAP signaling in the dorsal medial habenula mediates depression-related behavioral responses after chronic stress. Biol Psychiatry. doi: 10.1016/j.biopsych.2025.11.013. Online ahead of print. PMID: 41297784; PMCID: PMC12746342.
May, V., E. Lutz, C. MacKenzie, K. C. Schutz, K. Dozark and K. M. Braas (2010) Pituitary adenylate cyclase activating polypeptide (PACAP)/PAC1Hop1 receptor activation coordinates multiple neurotrophic signaling pathways: Akt activation through PI3K and vesicle endocytosis for neuronal survival. J. Biol. Chem. 285:9749-9761. PMID: 20093365; PMCID: PMC2843224.
Merriam, L. A., C. N. Baran, B. M. Girard, J . C. Hardwick, V. May, R. L. Parsons (2013) Pituitary adenylate cyclase 1 receptor internalization and endosomal signaling mediate the pituitary adenylate cyclase activating polypeptide-induced increase in guinea pig cardiac neuron excitability. J Neurosci. 33:4614-4622. PMID: 23467377; PMCID: PMC3623015.