Richard W. Burry, Ph.D.

Associate Professor
Department of Neuroscience

Degree: University of Colorado, Health Sciences Center
Postdoctoral Training: University of Tennessee, Center for Health Sciences, Dr. John G. Wood

Phone: (614) 292-2814
Fax: (614) 688-8742
Email: burry.1@osu.edu

Link to NLM PubMed publications list for Richard W. Burry (last 10 years)

Research Area:

Signal transduction pathways leading to development and regeneration of neurons.

Current Research:

A special property of nerve cells is the ability to extend cellular processes, which develop specialized endings, synaptic terminals. The neuron has the ability to communicate electrical activity to other neurons through chemical synapses. Considerable information has been accumulated about the function of the synapse, little is known of the signaling which stimulate these events.

We have examined the distribution of a developmentally regulated neuronal protein, GAP-43. In cultured cerebellar neurons, GAP-43 is found at high levels in growth cones and filopodia, but is seen at low levels in older cultures. Presynaptic terminals have a decreasing amount of GAP-43 and it is only associated with the plasma membrane. GAP-43 is seen at highest levels in the growth cones and distal axons of developing neurons, and is lost from both the soma and proximal axons. The distribution of GAP-43 in developing neurons suggests it is involved in growth cone activity and possibility in growth cone functions. These results were obtained with a new immunocytochemical technique developed in my laboratory. This procedure utilizes incubations of tissue with 1 nanometer gold particles and subsequent silver enhancement prior to embedding for standard EM.

More recently we have examined the signaling leading to the expression of GAP-43. Neuronal differentiation is dependent on protein growth factors, which bind to receptor proteins on the surface of developing neurons. As a result of this binding a cascade of signaling is activated which changes the cell from a dividing neuroblast to a differentiating neuron. Nerve growth factor (NGF) is one factor, which binds to a high affinity receptor, trkA, and starts a signaling cascade leading to transcription of new proteins, and activation of other signaling enzymes. The neuroendocrine cell line, PC12, differentiate into sympathetic-like neurons with long neurites following stimulation with NGF. NGF activated signal cascade induces expression of many proteins from cytoskeletal to enzymes that synthesize neurotransmitters. The observation of neurite outgrowth is an indication that these events have been signaled in an appropriate order and that the correct proteins have been expressed.

An additional interest is in the corticotrophin releasing factor (CRF) as a growth factor in the developing cerebellum. CRF has been extensively studied in the stress pathway, but it is also a peptide neuromodulator in the adult cerebellum changing the excitability of Purkinje cells. In developing cerebellum, CRF has been seen in afferents at early stages of development prior to synapse formation, and the CRF receptors are present on granule cells in the external granule cell layer. The early appearance of CRF in the developing cerebellum has lead to the suggestion that CRF has a role in signaling differentiation. Current Experiments are determining the role CRF plays in signaling neuronal differentiation. The initial experiments are examining the signaling pathways activated by the CRF in a cultured neuronal cell PC12 cell line transfected with CRF receptors. Specifically, we are looking for the activation or expression of transcription factors. To transfer this information to the developing cerebellum, we are testing the previously identified CRF signaling pathways in primary cultures of rat cerebellar granule cells. With this information about signaling of CRF on rat granule cells, the actions of CRF on differentiation we will examine the responses of neurite growth and levels of expression of GAP-43.

Collaborations: Understanding the role of CRF in development is a goal of Drs. James S. King and Gerogia A. Bishop of the Department of Neuroscience and our lab works extensively with these labs. The collaboration has taken the form a shared working on each others grants and papers.

Interests in cellular signaling are shared with Drs. Allan Yates, Arfaan Rampersaud, and James Van Brocklyn in the Department of Pathology, Division of Neuropathology. Currently, we are jointly working on the interactions of the ganglioside GM1 on NGF signaling through trkA.

Techniques:

Biochemistry and Molecular Biology: SDS-PAGE, 2D gel electrophoresis, immunoprecipitation, cell fractionation, western blot, preparation of plasmids, transfection, retroviral production and retroviral infection.

Cell Culture: primary cell cultures of CNS neurons, PC12 cells, neuroblastoma, glial and fibroblast cell lines, mutant cell cloning, generation of monoclonal and polyclonal antibodies.

Microscopy: silver enhanced gold probe for electron microscopy immunocytochemistry, light microscopic immunocytochemistry, scanning laser confocal microscopy, time lapse microscopy, scanning electron microscopy, computer based image analysis.