Ph.D., Wayne State University, 1986
Department of Psychology
Phone: (302) 831-4209: Office
Office: Room 243 Wolf Hall: (302) 831-3645: Fax
I joined the University of Delaware Biopsychology Program in 1995 after
conducting research for several years at the National Institutes of Health.
I am very excited about being at Delaware: The Psychology Department has
a number of experts in the field of emotion research and is a great place
for cross-fertilization of ideas from people working on various aspects
of emotion. My interests in emotion research are in understanding the physiological,
neuroanatomical and molecular bases of fear and anxiety. To approach these
problems, we study fear-related behaviors that have defined neuroanatomical
circuits, such as fear-potentiated startle and fear-induced freezing or
immobility in rats. Experiments are designed to study the pharmacology,
biochemistry and molecular biology of fear within the neural circuits that
mediate these fear-related behaviors. We use numerous techniques including
brain stimulation and lesions, anatomical tracing, administration of drugs,
and detection of proteins and messenger RNA using in situ hybridization,
immunohistochemistry, and Northern and Western blotting.
I am also interested in understanding how pathological anxiety may develop
from normal, adaptive fear. I think one of the key elements in this process
is the development of hyperexcitability in brain circuits that mediate
fear, so that responses to threatening stimuli become exaggerated. To experimentally
investigate this hypothesis, we induce hyperexcitability in the brain by
repeated electrical stimulation (kindling) or drug administration. As a
result of these procedures animals become more sensitive to further stimulation.
Because the brain structures involved in this hyperexcitability are also
those that mediate fear, we are finding that hyperexcitability produces
exaggerated fear responses (see Rosen et al. 1996 in the publication list
below). Determining the neurobiology of hyperexcitability and exaggeration
of fear should have important implications for our understanding of how
anxiety disorders may develop.
Post, R. M., Weiss, S. R. B., Smith, M. A., Rosen, J. B., & Frye, M.
(1995). Stress, conditioning, and the temporal aspects of affective disorders.
Annals of the New York Academy of Sciences, 771, 677-696.
Weiss, S. R. B., Clark, M., Rosen, J. B., Smith, M. A., & Post, R.
M. (1995). Contingent tolerance to the anticonvulsant effects of carbamazepine:
Relationship to loss of endogenous adaptive mechanisms. Brain Research
Reviews, 20, 305-325.
Weiss, S. R. B., Li, X.-L., Rosen, J. B., Li, H., Heynan, T., & Post,
R. M. (1995). Quenching: Inhibition of development and expression of amygdala
kindled seizures with low frequency stimulation. Neuroreport, 6,
Rosen, J. B., Hamerman, E., Sitcoske, M., Glowa, J., & Schulkin, J.
(1996). Hyperexcitability: Exaggerated fear-potentiated startle produced
by partial amygdala kindling. Behavioral Neuroscience, 110,
Kim, S.-Y., Post, R. M., & Rosen, J. B. (1996). Differential regulation
of basal and kindling-induced TRH mRNA expression by thyroid hormone in
hypothalamic and limbic structures. Neuroendocrinology, 63,
Zhang, L. X., Smith, M. A., Rosen, J. B., Massenburg, G., Weiss, S. R.
B., & Post, R. M. (1996). Changes in cholecystokinin mRNA expression
after amygdala kindled seizures. Molecular Brain Research, 35,