Dr. Melissa Cavallin
Assistant Professor
Human Physiology and Neuroscience
mcavalli@westga.edu
678-839-4043
Education:
Ph.D. in Physiology from Medical College of Georgia, Augusta, GA
B.A. in Biology (minor: Chemistry) from LaGrange College, LaGrange, GA
Research Interests:
My research interest is exploring the intercellular and intracellular signaling cascades involved in the chemical senses (taste and smell). I am interested in understanding how ion channels are regulated and how this affects downstream signaling molecules. A voltage-gated potassium channel (Kv1.3) is important for regulating the firing of action potentials in mitral cell neurons of the olfactory bulb. The mitral cell neuron is the primary output neuron of the olfactory bulb that transmits olfactory information to the brain. Altering the activity of Kv1.3 will ultimately change how the brain perceives olfactory sensory information, or in other words, how the brain determines what odors you smell in the air. Tyrosine kinases are enzymes that add a phosphate group to the amino acid tyrosine in proteins. Phosphorylating Kv1.3 closes the channel and decreases K+ current flowing out of the mitral cell. This means that the mitral cell is more excitable because the resting membrane potential is less negative. I am interested in exploring the modulation of Kv1.3 by the tyrosine phosphatase SHP-2, an enzyme that removes phosphate groups from tyrosines in proteins. This reverse reaction may also be important in regulating the firing of action potentials by mitral cell neurons because it would increase K+ current flowing out of the mitral cell making the mitral cell less excitable. Patch-clamp electrophysiology, protein biochemistry, and histology are just a few of the techniques that will be utilized to understand phosphatase regulation of Kv1.3.
Courses Taught:
BIOL 3513/6513 Human Physiology
BIOL 4981 Independent Study (Pathophysiology)
Selected Publications
:
1. Cavallin, M.A. and L.P. McCluskey. 2005. Lipopolysaccharide-induced up-regulation of activated macrophages in the degenerating taste system. J. Neurosci. Res. 80: 75-84. (Figure selected as cover illustration).
2. Cavallin, M.A. and L.P. McCluskey. 2007a. Upregulation of intracellular adhesion molecule (ICAM)-1 and vascular adhesion molecule (VCAM)-1 after unilateral nerve injury in the peripheral taste system. J. Neurosci. Res. 85: 364-372.
3. Cavallin, M.A. and L.P. McCluskey. 2007b. Upregulation of the chemokine monocyte chemoattractant protein-1 following unilateral nerve injury in the peripheral taste system. Neurosci. Lett. 413: 187-190.
4. Colley, B.S.*, M.A. Cavallin*, K.C. Biju, and D.A. Fadool. 2009. Brain-derived neurotrophic factor modulation of Kv1.3 channel is disregulated by adaptor proteins Grb10 and nShc. BMC Neurosci. 10: 8. (*These two authors contributed equally to this publication.)
5. Marks, D.R., K. Tucker, M.A. Cavallin, T.G. Mast, and D.A. Fadool. 2009. Awake intranasal insulin delivery modifies protein complexes and alters memory, anxiety, and olfactory behaviors. J. Neurosci. 29: 6734-6751.
6. Cavallin, M.A., K.C. Biju, and D.A. Fadool. 2009. Sensory enrichment, odor deprivation, aging – state dependent sculpting of olfactory sensory neurons. (In preparation.)
7. Cavallin, M.A., K.C. Biju, and D.A. Fadool. 2009. Sensory enrichment –state dependent sculpting of olfactory bulb mitral cells. (In preparation.)
