As is the case with microglial cells, there are two possible origins for enteric glial cells; however, each theory has enteric glia originating in the neural crest. The first theory is that enteric glial cells migrate to the bowel within the original population of vagal and sacral crest-derived cells that also form enteric neurons. The second theory is that enteric glial cells enter the gut later in development. In order to investigate the first theory, portions of fetal gut were isolated before innervation by extrinsic nerves occurred. When these portions were grown in vitro, it was found that GFAP-positive cells developed, indicating that enteric glial precursors are present in the gut at the time when the explants were removed. Thus, cells capable of producing glial cells are present in the gut before extrinsic innervation arrives and proves that glial cells can be derived from the original wave of neural crest cells that colonize the gut. A similar type of study was carried out in which explants of the cells of presumptive ganglion cells were removed from ls/ls mice. In these mice, the terminal colon is aganglionic because it is not infiltrated by enteric glial precursors from the neural crest. However, this region is not denervated as extrinsic nerves grow into the region from the ganglia in more proximal regions. These nerves exhibit GFAP immunoreactivity. The mutation in ls/ls mice is due to the inability of the tissue to support inward migration of neural crest-derived neuroglial cells. Explants of ls/ ls bowel give rise to cultures that contain neither neurons nor glia as these segments of gut are devoid of precursor cells. It appears that the supporting cells in this area are derived from Schwann cells. Thus, glial components may be derived from separate lineages of cells, of which one is the crest-derived precursors that colonize the gut early and the other is the Schwann cell population that reaches the bowel later in development.
Enteric glial cells possess a variety of surface receptors that can be used to distinguish them from nonmyeli-nating Schwann cells, with which they can be easily confused. These include reacting to the marker RAN-1, although it is only seen in cultured enteric glial cells, not in situ. The enzyme plasmalemmal 5'-nucleotidease is found on the surface of enteric glial cells but not on Schwann cells.
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Dawson, M. R., Levine, J. M., and Reynolds, R. (2000). NG2-expressing cells in the central nervous system: Are they oligodendroglial progenitors? J. Neurosci. Res. 61, 471-479. Eder, C. (1998). Ion channels in microglia (brain macrophages). Am. J. Physiol. 275, C327-342.
Fedoroff, S., Zhai, R., and Novak, J. P. (1997). Microglia and astroglia have a common progenitor cell. J. Neurosci. Res. 50, 477-486.
Gershon, M. D. (1998). Genes, lineages, and tissue interactions in the development of the enteric nervous system. Am. J. Physiol. 275, G869-G873.
Gershon, M. D., and Rothman, T. P. (1991). Enteric glia. Glia 4, 195-204.
Hansen, A. J. (1985). Effect of anoxia on ion distribution in the brain. Physiol. Rev. 65, 101-148.
Izumi, Y., Benz, A. M., Katsuki, H., and Zorumski, C. F. (1997). Endogenous monocarboxylates sustain hippocampal synaptic function and morphological integrity during energy deprivation. J. Neurosci. 17, 9448-9457.
Kamholz, J., Menichella, D., Jani, A., Garbern, J., Lewis, R. A., Krajewski, K.M., Lilien, J., Scherer, S.S., and Shy, M. E. (2000). Charcot-Marie-Tooth disease type 1: Molecular pathogenesis to gene therapy. Brain 123, 222-233.
Mirsky, R., and Jessen, K.R. (1999). The neurobiology of Schwann cells. Brain Pathol. 9, 293-311.
Raisman, G. (1997). Use of Schwann cells to induce repair of adult CNS tracts. Rev. Neurol. (Paris) 153, 521-525.
Rothman, T. P., Tennyson, V. M., and Gershon, M. D. (1986). Colonization of the bowel by the precursors of enteric glia: studies of normal and congenitally aganglionic mutant mice. J. Comp. Neurol. 252, 493-506.
Sontheimer, H., Trotter, J., Schachner, M., and Kettenmann, H. (1989). Channel expression correlates with differentiation stage during the development of oligodendrocytes from their precursor cells in culture. Neuron 2, 1135-1145.
Stoll, G., and Jander, S. (1999). The role of microglia and macrophages in the pathophysiology of the CNS. Prog. Neurobiol. 58, 233-247.
Wiesinger, H., Hamprecht, B., and Dringen, R. (1997). Metabolic pathways for glucose in astrocytes. Glia 21, 22-34.
Wender, R., Brown, A. M., Fern, R., Swanson, R. A., Farrell, K., and Ransom, B. R. (2000). Astrocytic glycogen influences axon function and survival during glucose deprivation in central white matter. J. Neurosci. 20, 6804-6810.
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