Department of Biology and Wildlife

University of Alaska Fairbanks

PO Box 75700

Fairbanks, AK 99775-7000

After completing her undergraduate work in Marine Biology at the University of British Columbia, Canada, Barbara Taylor received a M.S. in Marine Biology in 1990 and a Ph.D. in Marine Biology from the University of of British Columbia in 1997.  Following postdoctoral positions at the University of Calgary and Dartmouth Medical School, she moved to the University of Alaska Fairbanksas an Assistant Professor in 2003.

(907) 474-2487

ffbet@uaf.edu

Taylor Homepage

 

 

 

 

 

 

 

 

 

RESEARCH INTERESTS OF THE TAYLOR LABORATORY

Sudden infant death syndrome (SIDS) is a leading cause of post-neonatal infant mortality in North America, and has a disproportionately high incidence in Alaska and among Alaska Natives. The causes of SIDS are unknown, but it is characterized by ventilatory failure. In all vertebrates, ventilation is controlled by the brainstem. A medullary serotonin (5-HT) network resides within the brainstem, and consists of serotonergic neurons and their synaptic targets, which express 5-HT receptors. This medullary 5-HT network acts as a gain-modulating system by influencing the intensity of responses in a wide variety of behaviors, including ventilation. Functional deficits in the medullary 5-HT network have been implicated in a subset of SIDS. These deficits are proposed to compromise reflex ventilatory responses to hypercapnia and hypoxia, which are common, but potentially life-threating, ventilatory stressors. Fetal exposure to ethanol or nicotine has also been implicated in SIDS and the development of these deficits. The consequences of 5-HT- signaling deficits and the causative roles of ethanol and nicotine in the development of these deficits have not been elucidated.  My laboratory is employing the amphibian brainstem model for its simplicity and robustness for in vitro approaches providing a unique opportunity to investigate medullary 5-HT-signaling during development and to manipulate the developmental environment.  We are using this model to define ventilation-related functions of medullary 5-HT-signaling at different stages of development, and the disruption of 5-HT-signaling by developmental exposure to ethanol and nicotine. Our working hypothesis is that an undisturbed neuromodulation by the medullary 5-HT neuronal network is pivotal throughout development for proper modulation of ventilation and ventilatory responses to hypercapnia and hypoxia.

        

SELECTED PUBLICATIONS

Taylor BE, Harris MB, Leiter JC, and Gdovin MJ (2003). Ontogeny of central CO2 chemoreception: chemosensitivity in the ventral medulla of developing bullfrogs. Am. J. Physiol. Regul. Integr. Comp. Physiol. 285:R1461-1472.

Taylor BE, Harris MB, Coates EL, Gdovin MJ, and Leiter JC, (2003). Central respiratory CO2 chemoreception in developing bullfrogs: Anomalous response to acetazolamide. J. Appl Physiol 94:1204-1212.

Taylor BE, Harris MB, Burk M, Smith K, Lukowaik K,and Remmers JE (2003). Nitric oxide mediates metabolism as well as respiratory and cardiac responses to hypoxia in the snail Lymnaea stagnalis. J Exp Zool 295:37-46

Harris MB, Wilson RJA, Vasilakos K, Taylor BE, and Remmers JE (2002) Nitric oxide modulates central respiratory activity in the in vitro brainstem of the tadpole. Am J Physiol 283:R417-428

Taylor BE, Smyth K, Remmers JE, and Lukowiak K (2001) Metabolic consequences of hypoxic conditioning in Lymnea Stagnalis, pp 225-230. In: Adv Exp Med Biol: Frontiers in Modeling and Control of Breathing.