The Journal of Neuroscience, January 1, 1999, 19(1):258-273
Absence of the p75 Neurotrophin Receptor Alters the Pattern of
Sympathosensory Sprouting in the Trigeminal Ganglia of Mice
Overexpressing Nerve Growth Factor
Gregory S.
Walsh,
Karmen M.
Krol, and
Michael D.
Kawaja
Department of Anatomy and Cell Biology, Queen's University,
Kingston, Ontario, Canada K7L 3N6
Sympathetic axons invade the trigeminal ganglia of mice
overexpressing nerve growth factor (NGF) (NGF/p75+/+
mice) and surround sensory neurons having intense NGF immunolabeling; the growth of these axons appears to be directional and specific (). In this investigation, we provide new insight into
the neurochemical features and receptor requirements of this
sympathosensory sprouting. Using double-antigen immunohistochemistry, we demonstrate that virtually all (98%) trigeminal neurons that exhibit a sympathetic plexus are trk tyrosine kinase
receptor (trkA)-positive. In addition, the majority (86%) of
those neurons enveloped by sympathetic fibers is also calcitonin
gene-related peptide (CGRP)-positive; a smaller number of plexuses
(14%) surrounded other somata lacking this neuropeptide. Our results
show that sympathosensory interactions form primarily between
noradrenergic sympathetic efferents and the trkA/CGRP-expressing
sensory somata. To assess the contribution of the p75 neurotrophin
receptor (p75NTR) in sympathosensory sprouting, a
hybrid strain of mice was used that overexpresses NGF but lacks
p75NTR expression (NGF/p75
/
mice). The trigeminal ganglia of NGF/p75
/
mice,
like those of NGF/p75+/+ mice, have increased levels
of NGF protein and display a concomitant ingrowth of sympathetic axons.
In contrast to the precise pattern of sprouting seen in the ganglia of
NGF/p75+/+ mice, sympathetic axons course randomly
throughout the ganglionic neuropil of NGF/p75
/
mice, forming few perineuronal plexuses. Our results indicate that
p75NTR is not required to initiate or sustain the
growth of sympathetic axons into the NGF-rich trigeminal ganglia but
rather plays a role in regulating the directional patterns of axon growth.
Key words:
p75 neurotrophin receptor; transgenic; nerve growth
factor; axon growth; sympathetic; trigeminal
Copyright © 1999 Society for Neuroscience 0270-6474/99/191258-16$05.00/0