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Journal of Neuroscience, Vol 12, 1896-1905, Copyright © 1992 by Society for Neuroscience
On the role of nerve growth factor in the development of myelinated nociceptors
GR Lewin, AM Ritter and LM Mendell
Department of Neurobiology and Behavior, State University of New York, Stony Brook 11794.
We have previously demonstrated that administration of antisera against NGF
(anti-NGF) can have profound effects on developing primary afferents
(Ritter et al., 1991). Chronic administration of anti-NGF to rats beginning
on the day of birth results in a severe depletion of cutaneous A delta
high-threshold mechanoreceptors (HTMRs) from the sural nerve. Here we have
carried out further experiments in order to define the period of time over
which this change in the cutaneous afferent population can be produced, and
to investigate a possible mechanism for the change. Treatment with anti-NGF
from postnatal day (PND) 0-14 resulted in a depletion of cutaneous A delta
HTMRs from the sural nerve and also a 20% loss of sensory neurons. However,
treatment from PND 2-14 produced an identical deficit of HTMRs without any
accompanying cell death. Thus, the depletion of cutaneous A delta HTMRs can
be achieved in the absence of cell death induced by anti-NGF treatment. It
was also found that a 7 d treatment from PND 4-11 was sufficient to
reproduce this effect, but that 7 d treatments earlier (PND 2-9) or later
(PND 7-14) within the first 2 weeks were much less effective. This critical
period, PND 4-11, corresponds to a period of anatomical change in the
innervation of the skin, from epidermal innervation to primarily dermal
innervation (Fitzgerald, 1967; Reynolds et al., 1991). In every case where
anti-NGF treatment reduced the proportion of HTMRs, there was a reciprocal
increase in the proportion of sensitive A delta hair follicle (D-hair)
afferents. We hypothesize that in the absence of NGF, developing cutaneous
A delta HTMRs do not die but innervate novel targets in the dermis and
become D-hair afferents instead.
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