People & Projects

Dr. James McCasland, Professor Cell and Developmental Biology
PhD., California Institute of Technology
Postdoctoral Fellow, Washington University, St. Louis
Email: mccaslaj@mail.upstate.edu
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Stacy Lynne Donovan, PhD Candidate
Edinboro University of Pennsylvania: Edinboro, PA
B.S. Biology (cum laude)
Email: briggss@mail.upstate.edu

My main interest in neuroscience is the formation of complex patterns within the brain. How do developing axons navigate to their appropriate target? Using the whisker-to-barrel pathway in rodents serves as a useful tool to approach this issue. The whisker pattern is preserved at each synaptic relay in the trigeminal system (brainstem, thalamus and cortex), and is visible using standard histological techniques, such as cytochrome oxidase or cresylviolet. Our lab reported the loss of the cortical barrel pattern in mice deficient for the presynaptic protein, growth associated protein 43 (GAP-43) (Maier et al. 1999). Using serotonin transporter (SERT) immunohistochemistry, a marker for thalamocortical afferents, we discovered a very disorganized barrel map, with widely spread thalamocortical arbors. GAP-43 knockout mice also show region specific deficits of the serotonergic system in early postnatal life (Donovan et al. 2002). Defects in the corpus callosum and anterior commissure have also been observed in the same mouse line (Shen et al. 2002).

Jacob G. Dubroff, MD PhD Candidate
University of Pennsylvania: Philadelphia, PA
B.A.S. Biomedical Engineering, B.A. History and Sociology of Science
Email: dubroffj@upstate.edu

Every year stroke and cerebral vascular disease drastically alter the lives of over half a million Americans. I am interested in how pharmacological therapies either retard or assist recovery after a cortical ischemic insult. The human neocortex can be generalized as a series of internal maps representing the eternal world. I am interested in cortical plasticity, the capacity of these maps to change. We use the rodent barrel whisker barrel cortex as our model of cortical maps. I am able to observe such changes in cortical representation of rodent whisker through two methods. First, as developed by Dr. James McCasland, I use 2DG in combination with GAD immunohistochemistry to label and classify neuronal excitatory and inhibitory cells. In association with the cortical plasticity division of Dr. C.J. Hodge Jr.'s Neurosurgery research laboratory. The functional whisker representation of an individual barrel can be mapped using intrinsic signal imaging before and after a lesion. Such representation can also be visualized in 3-dimensions using the signal change as the amplitude in the Z axis. Both central (cortical) and peripheral lesions (eg whisker trimming/sparing or whisker ablation) can profoundly changes in the whisker representation.

Ginny Grieb, Chief Lab Technician
State University of New York at Oswego
B.S. Zoology
Email: graczykg@mail.upstate.edu

Emily A. Kelly, PhD Candidate
Bates College, Lewiston Maine
B.S. Biopsychology
Email: orre@mail.upstate.edu

Our lab, as a whole, is interested in the effects of the growth associated protein, GAP-43, during development in the rodent somatosensory cortex. By using a genetically manipulated mouse line, the levels of GAP-43 have been reduced or eliminated, allowing us to discern the role of this protein during important steps in synapse development. Our specific interests are in the establishment of whisker related barrels in the rodent somatosensory cortex. Barrel development in thought to involve a close communication between both pre- and postsynaptic cells, yielding a refined and strengthened synaptic connection. GAP-43, a presynaptic protein, is thought to play a role in neurotransmission, axonal pathfinding and synaptic plasticity and has been shown to be regulated by the activity of a postsynaptic receptor NMDA.
My current projects investigate these synaptic interactions. Using immunohistochemistry and fluorescence, I am currently looking at the changes in both NMDAR and AMPAR distribution in the barrel cortex (see figure) as a result of decreasing GAP-43 levels. Using image analysis techniques, I am able to assess the degree of colocalization between these two receptors across different ages and genotypes during development. Additionally, I am also interested in potential changes in metabolic activity within this mouse line. I use a cytochrome oxidase stain to determine whether decreasing the level of GAP-43 alters the degree of neurotransmission. Presumably, if GAP-43 is playing a role in neurotransmission, reducing its levels should subsequently effect activity and possibly alter the communication between pre- and postsynaptic cells.

Vera McIlvain, PhD Candidate
State University of New York at Binghamton
B.S. Biology
Email: perzovav@upstate.edu

My thesis research focuses on the role of Growth Associated Protein (GAP-43) in development and plasticity of sensory maps, specifically whisker/barrels. Cortical whisker/barrels are the clearest example of a visible cortical map. Each whisker on a rodent's face has a one-to-one correspondence to the barrel on the contralateral side of the brain. We use the transgenic GAP-43 mouse to study the effect of reduced amount of GAP-43 on map development. The knockout mice from this line do not form barrels, while heterozygous (+/-) mice still have a clearly identifiable, however distorted barrel map. I am interested in (+/-) mice because in spite of the abnormalities, the distorted map provides important clues for identifying the mechanism underlying the formation of the barrel cortex. I have found a number of pathfinding abnormalities among the pathway of thalamocortical afferents (Fig. 1) as well as decrease in arborization and branching in layer IV (Fig. 2) in (+/-) mice. In addition, I found that the development of cortical barrels in (+/-) mice is delayed. Our findings suggest that reduced GAP-43 expression can significantly alter the fine-tuning of a cortical map through a combination of pathfinding and synaptic plasticity mechanisms.




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