MAR 18, 2015 12:00 PM PDT

Keynote - Psychosis as a Learning and Memory Disorder

Presented At Neuroscience
  • McKenzie Foundation Chair in Psychiatry; Distinguished Chair in Psychiatric Research, Chair in Brain Science, Professor, UT Southwestern Medical Center
      Dr. Tamminga holds the Lou and Ellen McGinley Distinguished Chair and the McKenzie Chair in Psychiatry at the University of Texas Southwestern Medical School and is the Chairman of the Department of Psychiatry and the Chief of the Translational Neuroscience Division in Schizophrenia at UTSW.   She received her M.D. degree from Vanderbilt University and completed residency training in psychiatry at the University of Chicago.  She served on the University of Chicago faculty from 1975 to 1979 and moved to the NINDS for training in Neurology in 1978.   After joining the faculty at the University of Maryland Medical School in 1979, she practiced research, clinical care and teaching there until joining the faculty at UT Southwestern Medical School in 2003.
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      <br />Dr. Tamminga is currently a member of NIMHs National Advisory Board and has served on the Board of Scientific Counselors of the National Institute of Mental Health and the National Institute of Drug Abuse, as Council member and President of the American College of Neuropsychopharmacology, as a Member and Chair of the Psychopharmacological Drugs Advisory Committee of the FDA, as well as consultant for the Orphan Products Development Review Group, FDA.&nbsp; She is a member of the Advisory Board of the Brain and Behavioral Research Foundation (NARSAD).&nbsp;&nbsp; She is currently the Deputy Editor of the American Journal of Psychiatry and on the editorial board of several other journals in the field.&nbsp;&nbsp; Dr. Tamminga was elected to the Institute of Medicine of the National Academies of Sciences in 1998 and has served on several IOM committees in that capacity.
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    The hippocampal formation is one of the most extensively studied regions of the brain, with well described anatomy and basic physiology; moreover, aspects of human memory mediated by hippocampus are well characterized. In schizophrenia, alterations in hippocampal anatomy, perfusion and activation are consistently reported; impairments in declarative memory function, especially in the flexible use of event memories (e.g., in the service of memory-based inference), are common. Postmortem molecular changes suggest a selective reduction in glutamate transmission in the dentate gyrus (DG) and in its efferent fibers, the mossy fiber pathway. A reduction in DG glutamatergic output and in its information processing functions could generate two co-occurring outcomes in hippocampus: (a) a change in homeostatic plasticity processes in CA3, accompanied by increased activity due to reduced afferent stimulation from DG onto CA3 neurons, a process that could increase the ‘pattern completion’ functions of CA3; and (b) the loss of DG-specific mnemonic functions, namely ‘pattern separation’, a change that could increase the prevalence of illusory pattern completion and reduce discrimination between present and past experiences in memory. The resulting increase in ‘runaway’ CA3-mediated pattern completion could result in cognitive ‘mistakes’, generating psychotic associations and resulting in memories with psychotic content. Tests of this model could result in novel approaches to the treatment of psychosis and declarative memory alterations, and novel animal preparations for basic schizophrenia research.

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