Volume 274, Issue 1 pp. 142-150
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Opioid peptide gene expression in rat trigeminal nucleus caudalis neurons: Normal distribution and effects of trigeminal deafferentation

Toshikazu Nishimori

Toshikazu Nishimori

Departments of Neurology, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts 02114

Gene Neuroscience Unit, ARC, NIDA, Baltimore, Maryland 21224

Departments of Neurology and Neuroscience, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205

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Michael A. Moskowitz

Michael A. Moskowitz

Departments of Neurology, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts 02114

Departments of Neurosurgery, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts 02114

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George R. Uhl

George R. Uhl

Departments of Neurology, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts 02114

Gene Neuroscience Unit, ARC, NIDA, Baltimore, Maryland 21224

Departments of Neurology and Neuroscience, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205

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First published: 1 August 1988
Citations: 28

Abstract

Preproenkephalin (preproenkephalin A) and preprodynorphin (preproenkephalin B) are the opioid peptide genes expressed in neurons of the nucleus caudalis of the trigeminal nuclear complex. We have used recently developed techniques for quantitative in situ hybridization to identify the neurons in laminae I and II of the nucleus caudalis that display the mRNA products of each of these genes. The specificity of these hybridization patterns is supported by several biochemical features, and by qualitative and quantitative parallels with previous immunohistochemical results. In animals killed 4 days after unilateral lesions of the trigeminal ganglion, neuronal expression of both preproenkephalin and preprodynorphin is altered in the nucleus caudalis. Decreases in preproenkephalin mRNA are due to a decline in the number of neurons that appear to express this gene. Conversely, preprodynorphin mRNA increases by adding a significant population of expressing neurons. These deafferentation-induced changes in gene expression may provide clues to the role of primary afferent information in modulating the functions of nucleus caudalis neurons containing opioid peptides.

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