Julio J. Ramirez, Ph.D.

Administrative Accomplishments  

I am honored to be a candidate for President-Elect of the Society for Neuroscience.  Throughout my career I have had the distinct pleasure of serving in a number of leadership and administrative positions to promote the growth and well-being of the organizations with which I have been involved.  Across these positions, I particularly focused on helping young people achieve their professional aspirations and mid-career scientists to continue flourishing.  My principal goal as a leader has been to ensure that a diversity of voices and perspectives are shared and heard to facilitate the pursuit of an organization’s mission.  The positions include: Founding President of the Faculty for Undergraduate Neuroscience, Founding Senior Editor of the Journal of Undergraduate Neuroscience Education, Founding Director of the Davidson College Neuroscience Program, Secretary of the Board of Trustees for the Discovery Place Science Museum (Charlotte, North Carolina), Founding Chair of the Board’s Learning Experiences Committee of Discovery Place, Chair of the Mental Health Small Business Research Review Committee at the NIMH, Chair of the Biomedical Sciences Panel of the NSF Graduate Research Fellowship Program, Chair of the SfN Subcommittee on Mentoring, Founding Director of the Support of Mentors and their Students in the Neurosciences (SOMAS) Program, Co-Director of the SfN Neuroscience Scholars Program, Councilor of the SfN, Treasurer of the SfN, Director of the Neuroscience Program at Davidson College, and Chair of the Department of Psychology at Davidson College.

Degree, Institute, Year Earned

Research Areas

My research interests lie in the area of behavioral neuroscience with emphases on the recovery of function after central nervous system injury, on the neurobiology of learning and memory, and most specifically on the functional significance of lesion-induced hippocampal plasticity.

Current Position(s) at Your Current Institution

• R. Stuart Dickson Professor of Psychology
• Director, Neuroscience Program, Davidson College

Memberships

Service Positions

Editorial Boards:

Other Service Positions:

Science Biography

Since I first began my research as a graduate student of Donald Stein at Clark University in 1977, I have been captivated by the brain’s capacity to reorganize itself in response to injury.  I was fortunate to have entered neuroscience shortly after Carl Cotman, Gary Lynch, and their students discovered that a lesion of the entorhinal cortex in rat induces rapid and enduring changes in the connectivity in many of the surviving afferents to the dentate gyrus of the hippocampus.  Because of that discovery, the model system that I have been studying throughout my career is the hippocampal formation of rats. This system has provided a veritable feast for experimental exploration of neuroplasticity because it is a laminated structure wherein alterations in its known connectivity are readily discernible, its neurophysiological profile in response to activation of a number of its afferents is well established, and its contributions to behavior have been thoroughly investigated.  One of the hippocampal afferents that my students and I have been particularly interested in is the crossed temporodentate input (CTD) to the dentate gyrus.  The CTD has been of special interest to us because it emerges contralaterally from the same cell layer in the entorhinal cortex that gives rise to the perforant path, which projects ipsilaterally to the dentate gyrus.   Oswald Steward and his colleagues previously demonstrated that a unilateral entorhinal lesion induces significant axonal sprouting of the crossed pathway, whose electrophysiological profile after sprouting resembles that of the normal perforant path projection to the dentate gyrus.   Over a series of experiments throughout the last three decades, my students and I have explored the ability of the CTD to restore function in the denervated and subsequently reinnervated hippocampus.  In one set of experiments using quantitative autoradiographic techniques and behavioral assays, we have shown that unilateral, two-stage (progressive) lesions of entorhinal cortex accelerate the rate of CTD sprouting and that this accelerated sprouting response may contribute to sparing of spatial memory function in rats.  We also assessed neurophysiological correlates of this accelerated axonal sprouting response in other experiments and we observed that the rate of increase in the synaptic efficacy of the CTD following progressive lesions was significantly elevated and matched the rate of CTD sprouting as well as behavioral sparing after progressive entorhinal injury.  We have proposed that sprouting by a homotypic cortical pathway has the capacity to restore cognitive function following injury to its contralateral homologue.  In another series of experiments, we explored the possibility that surviving hippocampal afferents, heterologous to the original perforant path, following a bilateral entorhinal injury may contribute to postlesion behavioral change. We demonstrated that bilateral entorhinal lesions produce persistent deficits of working memory function on the acquisition of a spatial alternation task despite heterotypic sprouting; although rats may recover behavioral performance in a retention paradigm wherein memory demands are easier.  Our behavioral and neuroanatomical explorations following bilateral entorhinal cortex lesions suggest that organismic and contextual factors may significantly limit the role of heterotypic contribution to behavioral recovery after cortical injury.

The full CV for this candidate can be found within the ballot.