Kathryn Hamilton, PhD
Professor of Cellular Biology and Anatomy
Bachelor of Science - Florida State University
Master of Arts - University of California, Santa Barbara
PhD - University of California, Santa Barbara
Post-Doctoral Fellow - Whitney Laboratory, University of Florida
The mammalian olfactory system is unique in that new neurons can be added to it throughout life. In the nasal epithelium, endogenous progenitor cells give rise to new olfactory sensory neurons that mature and replace neurons that have died. The new neurons project axons to the olfactory bulbs in the brain, where they form functional synaptic connections with mitral and tufted output neurons and inhibitory interneurons. New inhibitory interneurons can also be added to the olfactory bulbs throughout life, via the rostral migratory stream. Thus, the olfactory system is a remarkably plastic portion of the mammalian nervous system.
Odors require complex synaptic interactions to decipher. In the nasal epithelium, odorant molecules having different chemical structures excite olfactory sensory neurons that express different odorant receptors. The sensory neurons synapse with and excite different subsets of mitral and tufted neurons in the olfactory bulbs. The excitation is shaped by a multitude of inhibitory interneuron subtypes before being projected by the mitral and tufted neuron axons to other brain regions, resulting in perception of the odors.
Our research aims to identify mechanisms that that endow the mammalian olfactory system with its remarkable ability to function continuously despite ongoing neuronal death and neurogenesis. We are quantifying characteristics of subsets of olfactory bulb interneurons by recording from single neurons in olfactory bulb brain slices using whole cell patch clamp recording methods. We then quantify characteristics of neuronal activity and correlate it with neuroanatomical characteristics quantified by 3D reconstruction, immunohistochemical staining, and confocal imaging of the brain slices.
Publications related to this work include:
Hamilton, KA, M Ennis, T Heinbockel, G Szabó, F Erdélyi, and A Hayar (2005) Functional properties of intrinsic inhibitory interneurons in the external plexiform layer of the mouse olfactory bulb. Neuroscience 133:819-829. http://dx.doi.org/10.1016/j.neuroscience.2005.03.008 PMID: 15896912
Heinbockel T, KA Hamilton, and M Ennis (2007) Group I metabotropic glutamate receptors are differentially expressed by two populations of olfactory bulb granule cells. J Neurophysiol 97:3136-3141. DOI: 10.1152/jn.01202.2006 PMID: 17215500
Hamilton, KA, S Parrish-Aungst, FL Margolis, F Erdélyi, G Szabó, and AC Puche (2008) Sensory deafferentation transsynaptically alters neuronal GluR1 expression in the external plexiform layer of the adult mouse main olfactory bulb. Chem Sens 33:201-210. DOI: 10.1093/chemse/bjm079 https://doi.org/10.1093/chemse/bjm079 PMID: 18184638
Dong, H-W, T Heinbockel, KA Hamilton, A Hayar, and M Ennis (2009) Metabotropic glutamate receptors and dendrodendritic synapses in the main olfactory bulb. Ann NY Acad Sci 1170:224-238. DOI: 10.1111/j.1749-6632.2009.03891.x PMID: 19686141
More recently, we have begun to identify markers for different developmental stages in a subset of olfactory sensory neurons, using immunohistochemical staining, confocal imaging and PCR methods. We have also worked with Dr. Ed Glasscock and his lab on characterizing Kv1.1 channels in cardiac myocytes. In another study, a former postdoctoral associate and I examined how synergistic interactions between astrocytes and GABAergic inhibition can ensure the firing of vasopressin neurons is transiently suppressed under hypoosmotic conditions.
Publications related to this work include:
Wang, Y-F, M-Y Sun, Q. Hou and K.A. Hamilton (2013) GABAergic inhibition through astrocytic neuronal interaction transiently decreases vasopressin neuronal activity during hypoosmotic challenge. Eur. J. Neuroscience 37:126−1269 doi:10.1111/ejn.12137. PMCID: PMC3627741
Trosclair, K, M Si, M Watts, P Dominic, K Hamilton and E Glasscock (2017) Kv1.1 potassium channel deficiency prolongs ventricular action potentials and decreases tachycardia susceptibility. FASEB J 31:S86.8.
Si, M, K Trosclair, KA Hamilton and E. Glasscock (2019) Genetic ablation or pharmacological inhibition of Kv1.1 potassium channel subunits impairs atrial repolarization in mice. Am. J Physiol., Cell Physiol. 316(2):C154-C161. doi: 10.1152/ajpcell.00335.2018. Epub 2018 Nov 14.
Research Positions Available
We welcome inquiries from undergraduate students through the Louisiana Biomedical Research Network, Centenary College of Louisiana and LSU-Shreveport, and from.recent graduates interested in pursuing a M.S. degree through the interdepartmental program in Biomedical Sciences at LSU Health-Shreveport.
LSU Health Shreveport
Department of Cellular Biology & Anatomy
1501 Kings Hwy
Shreveport, LA 71103