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Development of functional units within trigeminal ganglia correlates with increased expression of proteins involved in neuron–glia interactions

Published online by Cambridge University Press:  16 December 2010

Paul L. Durham*
Affiliation:
Center for Biomedical and Life Sciences, Missouri State University, Springfield, MO, USA
F.G. Garrett
Affiliation:
Center for Biomedical and Life Sciences, Missouri State University, Springfield, MO, USA
*
Correspondence should be addressed to: Paul L. Durham, Missouri State University, 524 N Boonville Avenue, Springfield, MO 65806, USA phone: 417-836-4869 fax: 417-836-7602 email: [email protected]

Abstract

Cell bodies of trigeminal nerves, which are located in the trigeminal ganglion, are completely surrounded by satellite glial cells and together form a functional unit that regulates neuronal excitability. The goals of this study were to investigate the cellular organization of the rat trigeminal ganglia during postnatal development and correlate those findings with expression of proteins implicated in neuron–glia interactions. During postnatal development there was an increase in the volume of the neuronal cell body, which correlated with a steady increase in the number of glial cells associated with an individual neuron from an average of 2.16 at birth to 7.35 on day 56 in young adults. Interestingly, while the levels of the inwardly rectifying K+ channel Kir4.1 were barely detectable during the first week, its expression in satellite glial cells increased by day 9 and correlated with initial formation of functional units. Similarly, expression of the vesicle docking protein SNAP-25 and neuropeptide calcitonin gene-related peptide was readily detected beginning on day 9 and remained elevated throughout postnatal development. Based on our findings, we propose that the expression of proteins involved in facilitating neuron–glia interactions temporally correlates with the formation of mature functional units during postnatal development of trigeminal ganglion.

Type
Research Article
Copyright
Copyright © Cambridge University Press 2010

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References

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