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Dr. Barbara Gisabella

PhD
Department of Psychiatry Harvard Medical School
115 Mill Street
 

Brief Biography:


My interest in neuroscience began at the University of Bologna, where I specialized in neuropharmacology, with a focus on neurotoxicity of kainic acid in the goldfish brain (carassius auratus). During this period I gained experience in spectrophotometric and enzymatic analysis of proteins, including the use of GAD, Chat, and AchE. I then pursued this interest from a different prospective, acquiring electrophysiological techniques such as patch–clamping in isolated neurons while working as a trainee on a project to detect ionic channel activity. During this training in the Membrane Physiology Section at Vrije University in Amsterdam, I also acquired experience in molecular biology techniques such as DNA cloning and RT-PCR. In 1999, I moved to the Department of Physiology at Trinity College in Dublin where I completed my PhD in electrophysiology specializing in the field of synaptic plasticity. In particular, I investigated the properties and mechanism of inhibition of long- term potentiation (LTP) by preconditioning stimulation and the role of NMDARs, mGluRs and second messengers involved in inhibitory LTP mechanisms in slices of the rat dentate gyrus. During my PhD. program I taught 1st year medical & dental physiology tutorials. This resulted in teaching experience, which provides a basis to pursue future teaching endeavors. I decided to pursue my primary interest in schizophrenia by joining the Program of Structural and Molecular Neuroscience under the direction of Dr. F. M. Benes, during which I set up and established electrophysiology techniques in this lab to examine a rodent model of schizophrenia. I received funding (Adam Corneel Young investigator Award, 2005) for this work. These studies resulted in a first author publication in PNAS, which led to the Alfred Pope award for Young Investigators in 2006. I investigated electrophysiological changes on the hippocampal GABA system induced by amygdalar activation, in slices (in developmental and adult rodents), in a ‘partial’ rodent model for schizophrenia. Using both field potential recordings and patch clamp approaches, I provided evidence of decreased hippocampal feed-forward and tonic GABA-mediated inhibition and changes in electrophysiological properties of interneurons in this SZ animal model, complementing increased hippocampal activity seen in neuro-imaging and post-mortem studies. In addition, I demonstrated that GABA dysfunction increases long-term potentiation through activation of the cholinergic system. This study also involved the use of cell filling followed by immunology to identify the recorded interneurons in old animals as well.
 

Academic positions:


Instructor in Psychiatry Harvard Medical School
 

Research interests:


Schizophrenia, bipolar disorder, electrophysiology, memory, limbic system, metabolism
 

What I think of the idea behind WebmedCentral:


open access and transparency in scientific communication