A5087609987- Neuroscience and Neuropharmacology Research
- Memory and Neural Mechanisms
- Neurobiology and Insect Physiology Research
- Developmental Biology and Gene Regulation
- Photoreceptor and optogenetics research
- Alzheimer's disease research and treatments
- Receptor Mechanisms and Signaling
- Retinal Development and Disorders
- Neuroinflammation and Neurodegeneration Mechanisms
- Neurogenesis and neuroplasticity mechanisms
- Immunotherapy and Immune Responses
- Cholesterol and Lipid Metabolism
- Immune Cell Function and Interaction
- Marine Invertebrate Physiology and Ecology
- Zebrafish Biomedical Research Applications
- Genetics, Aging, and Longevity in Model Organisms
- T-cell and B-cell Immunology
- Protein Kinase Regulation and GTPase Signaling
- Nuclear Receptors and Signaling
- Nicotinic Acetylcholine Receptors Study
- Connexins and lens biology
New York University
2013-2016
The University of Texas Southwestern Medical Center
2014
University of California, Irvine
2006-2011
The Ohio State University Wexner Medical Center
2006
The Ohio State University
2006
University of Nevada, Reno
2005
Alzheimer's disease (AD) is a currently incurable neurodegenerative disorder and the most common form of dementia in people over age 65 years. The predominant genetic risk factor for AD ε4 allele encoding apolipoprotein E (ApoE4). secreted glycoprotein Reelin enhances synaptic plasticity by binding to multifunctional ApoE receptors receptor 2 (Apoer2) very low density lipoprotein (Vldlr). We have previously shown that presence ApoE4 renders neurons unresponsive impairing recycling receptors,...
Although the importance of spaced training trials in formation long-term memory (LTM) is widely appreciated, surprisingly little known about molecular mechanisms that support interactions between individual trials. The intertrial dynamics ERK/MAPK activation have recently been correlated with effective patterns for LTM. However, whether and how MAPK required to mediate remains unknown. Using a novel two-trial pattern which induces LTM Aplysia, we show first two recruits delayed protein...
Although it is commonly appreciated that spaced training superior to massed in memory formation, the molecular mechanisms underlying this feature of are largely unknown. We previously described selective benefit multiple (vs massed) trials induction long-term (LTM) for sensitization Aplysia californica. now report LTM can be induced with only two [tail shocks (TSs)] when second TS administered 45 min after first. In contrast, spacing intervals 15 and 60 ineffective. This surprisingly narrow...
In the analysis of memory it is commonly observed that, even after a apparently forgotten, its latent presence can still be revealed in subsequent learning task. Although well established on behavioral level, mechanisms underlying are not understood. To begin to explore these mechanisms, we have used Aplysia, model system that permits simultaneous study at behavioral, cellular, and molecular levels. We first demonstrate robust induced by long-term sensitization training tail-elicited siphon...
The defensive withdrawal reflexes of Aplysia californica have provided powerful behavioral systems for studying the cellular and molecular basis memory formation. Among these tail-elicited tail reflex (T-TWR) has been especially useful. In vitro studies examining monosynaptic circuit T-TWR, sensory-motor (SN-MN) synapses, identified induction requirements different temporal phases synaptic facilitation that underlie sensitization in this system. They also permitted more recent elucidating...
In this study, we explore the mechanistic relationship between growth factor signaling and kinase activity that supports protein synthesis-dependent phase of long-term memory (LTM) consolidation for sensitization Aplysia . Specifically, examine LTM tail shock-induced tail-elicited siphon withdrawal (T-SW) reflex, a form requires both (i) extracellular signal-regulated (ERK1/2; MAPK) within identified sensory neurons (SNs) mediate T-SW (ii) activation transforming β (TGFβ) signaling. We now...