Keifer Lab

Joyce Keifer, Ph.D.


Neuroscience Group

Division of Basic Biomedical Sciences

University of South Dakota

Sanford School of Medicine

Vermillion, SD  57069-2390

  tel:   (605)  658-6355

  fax:  (605)  677-6381




Ph.D. in Neuroscience,  University of Wisconsin - Madison, 1987     

B.S. in Physiological Psychology, Arizona State University, 1980



Northwestern University Medical School, Department of Physiology, 1987 - 1991

Professor, University of South Dakota Sanford School of Medicine; Division of Basic Biomedical Sciences, 2003 - present

DirectorNIH COBRE on Neural Mechanisms of Adaptive Behavior, USD, 2000 - 2011

Associate Professor, University of South Dakota School of Medicine; Division of Basic Biomedical Sciences, 1997 - 2003

Assistant Professor, University of South Dakota School of Medicine; Department of Anatomy and Structural Biology, 1993 - 1997

Research Assistant Professor, Northwestern University Medical School; Department of Physiology, 1991—1993


Research Interests

The Keifer lab is interested in the cellular and molecular mechanisms that underlie learning and memory and adaptive motor control. We use an isolated brainstem preparation from the turtle as a model system that provides a unique opportunity to study large-scale neural circuits for a period of hours or days in vitro thereby allowing studies of learning "in a dish". Our research program is focused on examining the in vitro classically conditioned eyeblink response. Instead of using sensory stimuli like a tone or airpuff, a neural correlate of learned blink responses can be generated simply by pairing electrical stimulation of the pontine cranial nerves and recording the output of nerves controlling blinking. Current studies are aimed at examination of learning mechanisms related to several key questions:  1) Signal transduction for coincidence detection – how paired stimuli are detected to generate associative learning while unpaired stimuli do not result in learning.  2) How scaffolding proteins are coordinated for the appropriately timed and subunit-specific delivery of AMPAR subunits GluA1 and GluA4 during conditioning.  3) Epigenetic mechanisms that control BDNF expression during conditioning, including DNA methylation/demethylation and transcriptional control by DNA binding proteins (MeCP2, Tet1) and transcription factors (CREB, BHLHB2), as well as alternative splicing. The insights gained into these basic processes of learning and memory have fundamental implications for understanding the cellular basis of learning and cognitive disorders such as Alzheimer's disease and Rett Syndrome.