Assistant Professor of Physiology
Dr. Gulledge received his B.S. in Psychobiology from the University of California, Riverside in 1991, and his Ph.D. in Biology from the University of Texas, San Antonio in 2000. He then conducted postdoctoral research at the Australian National University (2000-2005) as an NSF International Research Fellow, and at the National Institute for Physiological Sciences in Okazaki, Japan (2005-2007) as a JSPS Postdoctoral Fellow. Dr. Gulledge joined the faculty of Dartmouth Medical School as an Assistant Professor of Physiology in 2007.
The neocortex serves as the biological substrate for the higher cognitive functions that define us as individuals. However, the way in which information is processed within the cortex in not well understood. Our research focus is neuronal signaling at the cellular and local circuit level, and our aim is to elucidate the mechanisms by which cortical neurons process and transmit information. To accomplish this we employ electrical and optical recording techniques that can measure the activity of neocortical neurons under a variety of experimental conditions. One focus of the laboratory has been the signal transduction events initiated following exposure of neurons to neuromodulators critical for cognitive function. These modulators, such as dopamine, serotonin, and acetylcholine, can activate a number of receptor subtypes to initiate a variety of biochemical signaling cascades within neurons. We are conducting experiments to identify which receptors and cellular processes are activated by neuromodulators, and how these signaling systems interact to influence ongoing neuronal activity. Because there are many different cell types within the cortex, each expressing a unique combination of receptors and intracellular biochemistry, neuromodulators tend to generate cell-type specific responses. By examining how individual neuromodulators differentially regulate the activity of many types of cortical neuron, we aim to elucidate the functional role of modulators within the cortical circuit, and to gain insight into their contribution to cognitive function.
Gulledge, A.T. and Jaffe, D.B. Dopamine decreases the excitability of layer V pyramidal cells in the rat prefrontal cortex. Journal of Neuroscience, 18:9139-9151 (1998).
Gulledge, A.T. and Jaffe, D.B. Multiple effects of Dopamine on layer V pyramidal cell excitability in rat prefrontal cortex. Journal of Neurophysiology, 86:586-595 (2001).
Gulledge, A.T. and Stuart, G.J. Excitatory actions of GABA in the cortex. Neuron, 37:299-309 (2003).
Gulledge, A.T. and Stuart, G.J. Action potential initiation and propagation in layer 5 pyramidal neurons of the rat prefrontal cortex: Absence of dopamine modulation. Journal of Neuroscience 23:11363-11372 (2003).
Gulledge, A.T., Kampa, B.M., and Stuart, G.J. Synaptic integration in dendritic trees. Journal of Neurobiology, 64:75-90 (2005).
Gulledge, A.T. and Stuart, G.J. Cholinergic inhibition of neocortical pyramidal neurons. Journal of Neuroscience, 25:10308-10320 (2005).
Gulledge, A.T., Park, S.B., Kawaguchi, Y., and Stuart, G.J. Heterogeneity of phasic cholinergic signalling in neocortical neurons. Journal of Neurophysiology, 97:2215-2229 (2007).
Gulledge, A.T. and Kawaguchi, Y. Phasic cholinergic signaling in the hippocampus: Functional homology with the neocortex? Hippocampus, 17:327-332 (2007).
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