Drexel
Home | Faculty | Research | Postdocs | Residents | Students | Seminars | Education | Fellowships | Resources
Neurobiology facebook | Office | Departmental directory |  

Douglas H. Baird, Ph.D.

Assistant Professor
Developmental Neurobiology

TECHNICIAN POSITION OFFERED: Research Assistant desired for image processing and histology projects in neurobiology laboratories. Experience in microscopy, digital image acquisition and processing, and simple programming essential. Annual salary $23,000 - $30,000+ depending on experience. Contact Dr. Jonathan Nissanov (yoni@cbis.ece.drexel.edu; 215 991-8410 or Dr. Douglas Baird (Douglas.Baird@Drexel.edu; 215 991-8481) Dept. of Neurobiology and Anatomy, MCP Hahnemann University, 2900 Queen Lane, Philadelphia, PA 19129; Fax 215 843-9082.

Email, Douglas.Baird@drexel.edu

My laboratory is devoted to the study of how axonal growth is regulated in central nervous system (CNS) target regions. Our work specifically concerns the development of the CNS and neural regeneration after injury. If the factors that prevent regeneration of CNS axons can be overcome, the next challenges in devising therapies for CNS disease and injury will be encouraging regenerating axons to enter their proper target region, and to make synaptic connections with appropriate target neurons. We have taken a cell biological approach to these problems of specificity, and devised in vitro models of axonal growth using purified populations of cerebellar neurons and glia.

One set of studies involves characterizing the arrest of mossy fiber extension after contact with their granule cell targets. This "stop-growing" signal is observed by quantifying axon lengths and by directly observing the interruption of neurite extension using time-lapse video microscopy. The stop-growing signal is both axon and target cell specific, resides on the target cell surface, and is regulated by NMDA receptors. Our working hypothesis is that the stop-growing signal is involved in the transformation of a growth cone to a synaptic terminal, and is involved in the specificity of synaptic connections. Studies in progress will further characterize the stop-growing signal at the cellular and molecular levels. Specific questions to be addressed include assessing the ability of target cell membranes to provide a stop-growing signal to growing axons, and determining whether the site of NMDA sensitivity is presynaptic, postsynaptic, or both.

Most recently, we have begun to examine previously characterized molecules that are known to inhibit or repel the growth of axons, including members of the collapsin/semaphorin family of proteins. We have found that Sema3A (formerly semaphorin III/D/collapsin-1) is expressed in cerebellar Purkinje cells during the postnatal development of the cerebellum. In addition, in vitro studies indicate that mossy fibers arrest their extension or retract if exposed to Sema3A. These results suggest that Sema3A may act during cerebellar development to prevent mossy fibers from contacting an inappropriate target cell, the Purkinje cell, and thereby promote specificity of synaptic connections within the cerebellar cortex.

In a third set of studies, the role of neurotrophins and their receptors, the trks, in the development and maintenance of an identified CNS synapse is being analyzed in vitro. Target granule neurons express both brain-derived neurotrophic factor (BDNF) and its receptor, trkB. Mossy fiber neurons which make synapses onto granule neurons also express trkB, and respond to BDNF with increased neurite outgrowth. Further analysis of the development of the mossy fiber-granule neuron synapse should further our understanding of how neurotrophins are involved in the development and maintenance of synaptic connections in the CNS, and suggest how and when neurotrophins could be best be applied in therapeutic approaches to degenerative brain disease and injury.

Biography

Douglas Baird received his undergraduate degree in Life Sciences from M.I.T. followed by graduate studies at Yale University in the Neurobiology Division of the Biology Department. His thesis topic was the neurobiology of Drosophila and he received his Ph.D. in 1988. Following training as an N.I.H. postdoctoral fellow at Columbia University and a Howard Hughes Postdoctoral Associate at Rockefeller University, Dr. Baird joined the faculty at MCP Hahnemann University in 1993.

Selected Publications

Baird, D.H., Trenkner, E., Mason, C.A. (1996) Arrest of afferent axon extension by target neurons in vitro is regulated by the NMDA receptor. J. Neurosci. 16:2642-2648.

Mason, C.A., Morrison, M.E., Ward, M.S., Zhang, Q., Baird, D.H. (1997) Axon-target interactions in the developing cerebellum. Perspectives on Developmental Neurobiology 5:69-82 (special issue: The Cerebellum: a Model For Construction of a Cortex).

Rabacchi, S., J. Solowska, B. Kruk, Y. Luo, J. A. Raper and D.H. Baird (1999) Collapsin-1/Semaphorin-III/D is regulated developmentally in Purkinje cells and collapses pontocerebellar mossy fiber neuronal growth cones. J. Neurosci. 19:4437-4448.

Rabacchi, S.A., Hamilton, J., Carney, C., Hoffman, J., Kruk, B., Meyer, S.L., Springer, J.E., Baird, D.H. (1999) BDNF and NT4/5 increase survival, neurite outgrowth and trkB RNA of pontocerebellar mossy fiber neurons J. Neurobiol. 40:254-269.