Barbara K. Lipska Ph.D.
NIMH
Bldg 10 Room 4N306
Bethesda, MD 20892
FAX 301-402-2751
ph. 301-496-9501
lipskab@intra.nimh.nih.gov
For more detailed information
on research goals and bibliography, see Animal Models.
Dr. Lipska graduated with M.Sci. degree in chemistry from University of Warsaw in 1975
and a Ph.D. degree in neuropharmacology from Medical Academy in Warsaw, Poland, in
1989. She joined NIMH as a post-doctoral Fogarty fellow in 1989 and began her
independent research on animal modeling to reproduce multiple aspects of
schizophrenia. In 1997, she was promoted to a Staff Scientist in the
Clinical Brain Disorders Branch of NIMH. Dr Lipska's contributions include
serving on board of the Animal Care and Use Committee of NIMH and Institutional
Review Board of NIAAA, as a grant reviewer for Canadian NIH, Czech Government
Mental Health Center and the US Department of VA. She received National Alliance
for Research on Schizophrenia and Depression (NARSAD) Young Investigator Award
(1994-1995) and Theodore and Vada Stanley Foundation Research Award (1995-1996)
and signed 3 CRADA agreements with pharmaceutical companies. She is a patent
holder for "Rat or Mouse Exhibiting Behaviors Associated with
Human Schizophrenia" (No. 5,549,884 issued August 27, 1996
by the United States Patent & Trademark Office).
Research Interests
Dr. Lipska's major research theme is studying the etiology and pathophysiology of
schizophrenia at the level of animal neurobiology by developing heuristic animal
models that can be useful in development of new therapies, identifying candidate
genes and providing new insights about the disease. In a series of studies
described in over 50 published papers, Dr. Lipska demonstrated that some
behavioral abnormalities associated with neonatal hippocampal damage in
the rat remain quiet until a certain time in development while others appear
early after the lesion, that the profile of changes depends upon the age at
which damage is induced and that abnormalities can be reversed by neuroleptics.
This developmental lesion interacts with genetic and environmental factors that
vary the expression of the emergent phenomena. Subsequent studies showed that the
emergence of behavioral disruptions in adolescence is not dependent on the surge
of gonadal hormones at the time of puberty and that aberrant function of the
late maturing prefrontal cortex, to which the ventral hippocampus is connected,
is involved in the emergence of abnormal behaviors. Studies on the molecular
and electrophysiological properties of prefrontal neurons and their anatomical
characteristics indicate that the developmental lesion in the hippocampus
disrupts cortical function. Dr. Lipska initiated studies in the hippocampally
lesioned mice in order to enable testing genetic hypotheses by altering
hippocampal development and formation of hippocampal-prefrontal connections
by manipulations of genes that are implicated from post mortem or human
genetic studies, and is involved in designing and screening new treatments
for schizophrenia in many collaborative projects with pharmaceutical industry.