Neurobiology and Anatomy - The University of Texas Medical School at Houston Dept of Neurobiology and Anatomy - The University of Texas Medical School at Houston
Dept of Neurobiology and Anatomy - The University of Texas Medical School at Houston
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Dept Home Page > Department Faculty > Pramod Dash, Ph.D.

Pramod Dash, Ph.D., Associate ProfessorPramod Dash, Ph.D.

Professor
Director of Research, The Vivian L. Smith Center for Neurologic Research

Telephone: 713.500.5625
E-mail: p.dash@uth.tmc.edu

 

 

 

Mechanisms Of Memory Formation And Memory Dysfunction

Learning And Cognition
The research objective of my laboratory is to explore the molecular mechanisms contributing to working memory (lasting seconds), short-term memory (lasting minutes-to-hours) and long-term memory (lasting days to a lifetime), and the relationships between these types of memories. To accomplish this, we disrupt or augment specific biochemical events in discrete brain regions such as the prefrontal cortex and the hippocampus, to determine the aspect of memory altered as a result of the manipulation. Human and animal studies have shown that the prefrontal cortex is required for holding information “online” for a period of seconds (referred to as working memory) which is used to guide goal-directed behavior. Working memory is critical for decision making and coherent thought processes, and is often impaired as a result of normal aging, and diseases such as Parkinson’s, Alzheimer’s and schizophrenia. Short-and long-term explicit memories are dependent on the function the hippocampus, a structure within the medial temporal lobe. We utilize a multi-disciplinary approach involving molecular, biochemical, genetic and behavioral techniques to manipulate molecular processes within the prefrontal cortex and hippocampus to determine their contribution to various memory processes.

Both the prefrontal cortex and hippocampus are highly vulnerable to insults such as traumatic brain injury. Injury to these structures often results in memory loss and a lack of coherent thought processes. Biochemical and molecular cascades initiated as a result of trauma are thought to alter inter- and intracellular signaling, causing changes in the brain ranging from survival and growth to neuronal dysfunction and death. We use an experimental brain injury model in rodents to explore some of the molecular mechanisms contributing to injury-related memory deficits. The long-term goal of this research is to identify potential targets for therapeutic interventions to alleviate the memory disorders associated with brain injuries and degenerative diseases.

Selected Reading

Runyan, J, Moore, AN, Dash, PK (2004) A role for prefrontal cortex in memory storage for trace fear conditioning. J. Neuroscience , 24:1288-1295.

Dash P.K., Hebert AE, Runyan JM. (2004) A unified theory for cellular and systems memory consolidation. Brain Res. Review 45:30-37.

Dash, PK, Mach, SA, Moody, MR, Moore, AN (2004) Performance in long-term memory tasks is augmented by a phosphorylated growth factor receptor fragment. J. Neuroscience Research 15:205-216.

Dash, PK, Kobori, N, Moore, AN. (2004) A molecular description of brain trauma pathophysiology using microarray technology: an overview. Neurochem. Res. 29:1275-1286.

Dash PK, Moore AN. (In press) Cellular and molecular mechanisms of simple and complex forms of learning and memory. Handbook of Neurochem.

Search PubMed for additional articles.

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