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GAP‐43 mRNA in Rat Spinal Cord and Dorsal Root Ganglia Neurons: Developmental Changes and Re‐expression Following Peripheral Nerve Injury
Author(s) -
Chong M. S.,
Fitzgerald M.,
Winter J.,
HuTsai M.,
Emson P. C.,
Wiese U.,
Woolf C. J.
Publication year - 1992
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1111/j.1460-9568.1992.tb00115.x
Subject(s) - sciatic nerve , spinal cord , dorsal root ganglion , gap 43 protein , motor neuron , anatomy , gdf7 , ganglion , biology , messenger rna , neuroscience , medicine , embryonic stem cell , immunohistochemistry , biochemistry , gene
The expression of growth‐associated protein GAP‐43 mRNA in spinal cord and dorsal root ganglion (DRG) neurons has been studied using an enzyme linked in situ hybridization technique in neonatal and adult rats. High levels of GAP‐43 mRNA are present at birth in the majority of spinal cord neurons and in all dorsal root ganglion cells. This persists until postnatal day 7 and then declines progressively to near adult levels (with low levels of mRNA in spinal cord motor neurons and 2000–3000 DRG cells expressing high levels) at postnatal day 21. A re‐expression of GAP‐43 mRNA in adult rats is apparent, both in sciatic motor neurons and the majority of L4 and L5 dorsal root ganglion cells, 1 day after sciatic nerve section. High levels of the GAP‐43 mRNA in the axotomized spinal motor neurons persist for at least 2 weeks but decline 5 weeks after sciatic nerve section, with the mRNA virtually undetectable after 10 weeks. The initial changes after sciatic nerve crush are similar, but by 5 weeks GAP‐43 mRNA in the sciatic motor neurons has declined to control levels. In DRG cells, after both sciatic nerve section or crush, GAP‐43 mRNA re‐expression persists much longer than in motor neurons. There was no re‐expression of GAP‐43 mRNA in the dorsal horn of the spinal cord after peripheral nerve lesions. Our study demonstrates a similar developmental regulation in spinal cord and DRG neurons of GAP‐43 mRNA. We show moreover that failure of re‐innervation does not result in a maintenance of GAP‐43 mRNA in axotomized motor neurons.