It is well established that sensory perception becomes impaired with a
dvancing age and that, in parallel, dystrophy and degeneration of axon
s occur in sensory pathways. In this study, the impact of aging was ex
amined in the mystacial pad, which receives a large variety of sensory
nerve endings organized in a highly predictable pattern. Mystacial pa
d specimens from aged (30 months old) and young adult (2-3 months old)
female Sprague-Dawley rats were processed, in parallel. for immunohis
tochemical analyses with antibodies against human neuronal cytoplasmic
protein (protein gene product 9.5), transmitter enzymes, and several
neuropeptides. Several changes in cutaneous innervation including both
degenerative and regenerative processes were evident in the aged rat:
(1) the Merkel endings and lanceolate endings that emanate from large
-caliber afferents in the whisker follicles were reduced and shouted s
ig ns of degeneration. Furthermore, a reduction of piloneural complexe
s at the intervibrissal hairs were evident, but only in aged rats that
showed more severe behavioral sensorimotor disturbances. In contrast,
Ruffini endings as well as mechanoreceptors emanating: from medium-ca
liber axons, i.e., transverse lanceolate and reticular endings, appear
ed normal. (2) A reduction was evident among two sets of unmyelinated
epidermal endings; however, the epidermal innervation affiliated with
the intervibrissal hairs appeared normal in the aged rat. (3) A loss o
f sympathetic neuropeptide tyrosine (NPY) or tyrosine hydroxylase-immu
noreactive (IR) and somatosensory Calcitonin gene-related peptide (CGR
P)-IR perivascular axons was paralleled by an increase in presumed par
asympathetic NPY/CGRP-IR axons. (4) Two ''novel'' networks of fine-cal
iber axons were observed in the outer and inner root sheaths of the wh
isker follicles in the aged rat. (5) NPY was present in a population o
f small-caliber, somatosensory CGRP-IR axons in the aged rat. This may
represent a de novo synthesis, since, normally, NPY-like immunoreacti
vity is not observed in this set of axons. Our results suggest that th
e sensory impairments occurring with advancing age are part of a perip
heral process instigated by changes in nerve-target interactions and/o
r incapacitation of the neuronal machinery to sustain the axonal integ
rity.