The University of Texas at Dallas School of Behavioral and Brain Sciences

The Ploski Lab

LABORATORY OF JONATHAN E. PLOSKI, PHD

Jonathan Ploski

Associate Professor

School of Behavioral and Brain Sciences
Department of Molecular & Cell Biology
The University of Texas at Dallas

PhD in Biomedical Science from Mount Sinai School of Medicine – 6/2004

Mentor: Aurelian Radu, PhD

Postdoctoral training

Yale Medical School, Department of Psychiatry – 6/2004-9/2006
Mentor: Ronald S. Duman, PhD

Yale University, Department of Psychology – 9/2006-5/2010
Mentor: Glenn E. Schafe, PhD

Research Interests

My research interests are directed toward elucidating the molecular and cellular mechanisms of neuronal plasticity that govern emotional memory as well as identifying the causes and consequences of aberrant forms of plasticity that occur in psychiatric disorders, such as anxiety. Collectively my research utilizes a myriad of molecular, biochemical and behavioral approaches.

My laboratory is currently directing its research efforts toward the molecular basis of memory modification. Memory modification utilizing reconsolidation updating is being examined as one of the potential treatment approaches for attenuating maladaptive memories associated with emotional disorders. However, studies have shown that while weak memories can be modified using reconsolidation updating, strong memories can be resistant to this approach. This may be due to the fact that these memories are resistant to becoming destabilized following retrieval, rendering them impervious to agents that are intended to block the restabilization phase of reconsolidation. The mechanisms that control the initiation of reconsolidation updating (i.e., memory destabilization) are still poorly understood. This lack of knowledge has hampered the development of treatments which can modify/attenuate maladaptive memories via reconsolidation updating.

My laboratory has recently determined that an increase in the GluN2A/GluN2B ratio interferes with retrieval-dependent memory destabilization and inhibits the modification of an existing fear memory trace. We are currently investigating methods to enhance the initiation of reconsolidation updating so strong memories can be therapeutically modified utilizing a variety of pharmacological and molecular genetic approaches.

In the News

New Pre-Print Available: Increasing Synaptic GluN2B levels within the Basal and Lateral Amygdala Enables the Modification of Strong Reconsolidation Resistant Fear Memories

Ploski, Balsara Chosen for Research Mentoring Awards

Team Aims to Update Gene Editing for Brain Studies

Cellular Changes May Explain Why Strong Fearful Memories Last

Specialties

Pavlovian fear conditioning, memory consolidation and reconsolidation, AAV and Lenti virus production for in vivo delivery of recombinant transgenes, Gene expression analysis, Viral mediated genome editing and associated CRISPR/Cas9 approaches.

Amygdala Neurons

Amygdala neurons within the rat brain are infected with Adeno-Associated Virus expressing Green Fluorescence Protein (GFP) and a Silencing RNA (siRNA) to suppress the expression of a specific neuronal gene. (a-b). Localization of GFP-expressing cells from two different rostro-caudal levels. Note the significant amount of infection in lateral nucleus of the amygdala (LA) and the basal nucleus of the amygdala (B). The central nucleus of the amygdala (CE) and surrounding cortical regions are not transfected. The cannula track is depicted by arrows. (c) Higher level (20X) magnification of transfected cells from panel B. (d). Brightfield image of the same section depicted in panel B, showing the location of the cannula track (arrows).