GAP-43 EXPRESSION IN PRIMARY SENSORY NEURONS FOLLOWING CENTRAL AXOTOMY

Citation
Ms. Chong et al., GAP-43 EXPRESSION IN PRIMARY SENSORY NEURONS FOLLOWING CENTRAL AXOTOMY, The Journal of neuroscience, 14(7), 1994, pp. 4375-4384
Citations number
87
Categorie Soggetti
Neurosciences
Journal title
ISSN journal
02706474
Volume
14
Issue
7
Year of publication
1994
Pages
4375 - 4384
Database
ISI
SICI code
0270-6474(1994)14:7<4375:GEIPSN>2.0.ZU;2-7
Abstract
Primary sensory neurons are capable of successful regenerative growth in response to peripheral nerve but not dorsal root injury. The presen t study is concerned with the differential expression of the mRNA for GAP-43, a growth-associated protein, in these sensory neurons, in resp onse to injury of their central or peripheral axonal branches. Periphe ral axotomy resulted in an elevation in message detectable within 24 h r, using Northern blot and in situ hybridization, which was maintained for 30 d, whereas dorsal root section produced no change except a tra nsient and small increase if the axotomy was immediately adjacent to t he dorsal root ganglia (DRG). Dorsal root section had no effect on GAP -43 mRNA levels in the dorsal horn or in neighboring intact DRG. It al so failed to alter the laminar boundaries of the GAP-43 central termin al labeling produced by peripheral nerve section, even though vacant s ynaptic sites were produced in unstained laminae by this procedure. Th is indicates that the location of GAP-43 immunolabeling in the central terminals of primed sensory cells may not depend only on the location of vacant synaptic sites. We conclude that distinct control mechanism s regulate the response of DRG neurons to peripheral nerve and dorsal root injury, and these may be related both to the glial environment an d the particular target influences exerted on the central and peripher al branches of the primary sensory neuron. Central denervation alone i s insufficient to upregulate GAP-43 levels, and this may explain the r elative absence of collateral sprouting after the production of centra l vacant synaptic sites. The failure of dorsal root section to increas e GAP-43 expression may contribute to the poor regenerative response i nitiated by such lesions.