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Patricia M. Whitaker-Azmitia, Ph.D.
University of Toronto (1979)
Professor, Neuropharmacology
Office: Psychology B-312
Office Hours: Monday and Friday 11-12
Phone Number: (631) 632-9899
e-mail: patricia.whitaker@stonybrook.edu


Areas of Interest:
Animal models of human developmental illnesses.

Current Research:

Dr. Whitaker-Azmitia is a neuropharmacologist interested in brain development, in particular what is different in development which leads to disorders such as autism. Neurotransmitters such as serotonin and hormones such as progesterone and cortisol play a role. Although past work has focused almost entirely on animal models (including the rat model of developmental hyperserotonemia developed in this lab) currently Dr. Whitaker-Azmitia is working more with human subjects and using that information to develop better animal models.

In human illnesses such as autism, animal models can not only verify etiologies, they can also be used to test treatments Continuously modifying models is essential to new discoveries. For example, research on obstetrical factors has led to our recently published hypothesis that low levels of progesterone during development will lead to an increased incidence of autism. To further test this hypothesis, an animal model of lowered progesterone will be developed. Furthermore, women who perceive more stress during pregnancy are also more likely to give birth to a child with autism and a model of prenatal stress will be used in animals to determine whether or not autism-like behaviors and neurochemistry result

Representative Publications:

Whitaker-Azmitia, P.M. Lobel, M. and Moyer, A (2013) Low maternal progesterone may be a single factor contributing to both obstetrical complications and autism Medical Hypothesis, in press.

Aiello TP, Whitaker-Azmitia PM. (2011) Sexual differentiation and the neuroendocrine hypothesis of autism. Anat Rec . 294(10):1663-70.

Azmitia EC, Singh JS, Whitaker-Azmitia PM. (2011) Increased serotonin axons (immunoreactive to 5-HT transporter) in postmortem brains from young autism donors. Neuropharmacology.;60(7-8):1347-54.

Bialowas-McGoey LA, Lesicka A, Whitaker-Azmitia PM. (2008) Vitamin E increases S100B-mediated microglial activation in an S100B-overexpressing mouse model of pathological aging. Glia.;56(16):1780-90.

Whitaker-Azmitia, P.M. (2005) Behavioral and cellular consequences of increased serotonin during development. Int. J. Dev. Neurosci, 23, 75-83.

Shapiro, L. and Whitaker-Azmitia, P.M. (2004) Expression levels of cytoskeletal proteins indicate accelerated aging of S100B transgenic mice. Brain Res, 1019, 39-46.

Kahne, D., Tudorica, A., Borella, A., Shapiro, L., Johnstone, F., Huang, W. and Whitaker-Azmitia, P.M. (2002) Behavioral and magnetic resonance spectroscopic studies in the rat hyperserotonemic model of autism. Physiology and Behavior, 75, 403-410.

Whitaker-Azmitia, P.M. (2001) Serotonin dysfunction and human developmental disorders. Brain Res. Bull. 56: 479-486.

Current Research Support:

National Alliance for Autism Research
Serotonin, Oxytocin and Social Behaviors
6/2005 - 5/2007
Patricia M. Whitaker-Azmitia (Principle Investigator)

National Institute for Neurological Disease and Stroke
S100B in the Phenotype of Down Syndrome
12/2000 - 1/2006
Patricia M. Whitaker-Azmitia (Principle Investigator)