Neuropeptide messenger plasticity in the CNS neurons following axotomy |
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Authors: | Miklós Palkovits |
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Institution: | (1) Laboratory of Neuromorphology, Semmelweis Medical University, Budapest, Hungary;(2) Laboratory of Cell Biology, NIMH, NIH, Bldg. 36, Rm. 3A17, Bethesda, MD |
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Abstract: | Neuronal peptides exert neurohormonal and neurotransmitter (neuromodulator) functions in the central nervous system (CNS).
Besides these functions, a group of neuropeptides may have a capacity to create cell proliferation, growth, and survival.
Axotomy induces transient (1–21 d) upregulation of synthesis and gene expression of neuropeptides, such as galanin, corticotropin
releasing factor, dynorphin, calcitonin gene-related peptide, vasoactive intestinal polypeptide, cholecystokinin, angiotensin
II, and neuropeptide Y. These neuropeptides are colocalized with “classic” neurotransmitters (acetylcholine, aspartate, glutamate)
or neurohormones (vasopressin, oxytocin) that are downregulated by axotomy in the same neuronal cells. It is more likely that
neuronal cells, in response to axotomy, increase expression of neuropeptides that promote their survival and regeneration,
and may downregulate substances related to their transmitter or secretory activities. |
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Keywords: | Neuropeptides neuropeptide mRNA axotomy central nervous system neuronal plasticity |
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