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Cheryl F. Harding

Ph.D., Rutgers University, Psychobiology

Contact Information:
Dr.Cheryl F. Harding
Department of Psychology
Hunter College
695 Park Avenue Room 631N
New York, NY 10021
Tel: (212) 772-5047
Fax:(212) 650-3647

Current Areas of Research:

I have recently switched my research area from behavioral neuroendocrinology in birds to behavioral neuroimmunology in mice.  Over the last few years, evidence has mounted that exposure to mold causes a broad range of health problems. According to most estimates, about 33-40% of American buildings are moldy.  As a neuroscientist, I am particularly intrigued by the effects of mold exposure on neural function and cognition.  Recent research has documented that people who lived or worked in moldy buildings had multiple cognitive problems.  Compared to controls, mold-exposed individuals in one study scored below the 10th percentile on a number of cognitive tests. In other studies, mold-exposed patients demonstrated neurological deficits that correlated with their cognitive problems. Perhaps one of the most striking findings was that multiple studies concluded that individuals exposed to mold suffered cognitive deficits that could not be distinguished from those of patients suffering from traumatic brain injury. In addition, about 20% of Americans appear to be genetically-susceptible to long-term inflammation with resulting medical problems following mold exposure.

My current research seeks to develop a mouse model of the effects of mold exposure on neural and cognitive function.  No such animal research has been published to date.  My basic hypothesis is that exposure to mold activates an innate immune response in the brain just as it does in peripheral tissues like the lungs. Prolonged innate immune activation is known to cause adverse neurological consequences.  First, mice are given basic physiological and cognitive tests.  They are then exposed to control or mold stimuli and retested.  We compare individuals’ performances pre- and post-exposure and as well as looking for differences in performance between groups following mold or control exposures.  We then use immunohistochemical techniques to look for differences in brain structure and chemistry between groups following mold exposure.  We measure the number, size, and morphology of microglia, the primary immune cells found in the brain.  We quantify the production of several cytokines released by immune cells and neurons.  These chemicals are known to cause inflammation.  Finally, we quantify neuron birth and death in the hippocampus, since these processes can have a major impact on learning and memory in our cognitive tasks.  Finally, the animals’ performance on the cognitive tests following mold exposure is compared to their measures of neural function to determine possible relationships.

We have just begun this NIH-funded research and do not yet have any publications in this area.

Selected Publications:

Walters, M.J., Collado, D., and Harding, C.F. (1991) Oestrogenic modulation of singing in male zebra finches: Differential effects on directed and undirected songs. Animal Behaviour, 42, 445-452.

Barclay, S.R., Harding, C.F., and Waterman, S.A. (1996) Central DSP-4 treatment decreases norepinephrine levels and courtship behavior in male zebra finches. Pharmacology, Biochemistry Behavior, 53, 213-220.

Harding, C.F., Barclay, S.R., and Waterman, S.A. (1998) Changes in catecholamine levels and turnover rates in hypothalamic, vocal control, and auditory nuclei in male zebra finches during development. Journal of Neurobiology, 34, 329-346.

Harding, C.F. and Rowe, S.A. (2003) Vasotocin treatment inhibits courtship behavior in male zebra finches; Concomitant androgen treatment inhibits this effect. Under review.


Behavioral Endocrinology
Reproductive Physiology and Behavior
Behavioral Endocrinology of Primates
Sexual Differentiation
Hormonal Restructuring of the Adult Brain

Graduate Students:
Diane Bogdan
Akshat Vyas
Sharon Lukban

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