We have studied the sprouting of intact high-threshold mechanosensory nerves into adjacent denervated trunk skin in adult rats behaviorally, histologically, and electrophysiologically. In the anesthetized animal, stimulation of high-threshold endings in back skin by localized pinching elicits a bilateral reflex excitation of the underlying skeletal muscle, the cutaneous trunci muscle (CTM), visible as a twitch-like puckering of the skin. The reflex was also evoked by electrical excitation of A delta and of C fibers in the dorsal cutaneous nerves (DCNs), with characteristic latencies of 7-20 msec and 40-60 msec, respectively; excitation of low-threshold (A alpha) fibers was ineffective. After cutting selected DCNs, the deprived skin became insensible, but pinch responsiveness gradually recovered over the following 2 weeks. Regeneration of cut axons was not responsible for this recovery; when neighboring intact DCNs were cut, however, all responses were abolished in the recovered skin that had been initially denervated. By 3-5 days after denervation, axons in the dermis were all histologically absent or degenerating; when pinch sensitivity was restored to such skin, silver-stainable axons reappeared in the formerly empty Schwann tubes. During the work we noticed that the periodic examination by pinching, used to follow the time course of recovery of function in individual animals, led to an earlier development of this recovery than in animals that were examined only once at a specified time after denervation. This apparent acceleration in the redevelopment of pinch sensitivity was correlated with the appearance of axons in the recovered skin, and was shown to be due to the impulse activity evoked in the remaining nerves by the periodic pinching; it did not occur when the nerves were blocked by tetrodotoxin (TTX), and it was mimicked by a brief (10-min) period of electrical excitation of the A delta fibers in a remaining nerve carried out at the time when the denervation of skin was done. The time course of the phenomenon suggested that the principal effect of the impulses was to shorten the latency to the onset of sprouting in the activated A delta axons; that is, they induced precocious sprouting. The impulses needed to be conducted centrally for the effect to occur, and precocious sprouting failed to occur if the impulses were allowed to proceed only distally toward the skin. It seems that a brief conditioning burst of impulses in A delta axons sensitizes the neurons to the influence of a sprouting stimulus that appears when skin is denervated.(ABSTRACT TRUNCATED AT 400 WORDS)
We have studied the collateral sprouting of intact low-threshold mechanosensory nerves into adjacent denervated skin in rats. An "isolated" field was produced by extensive denervations of the surrounding skin; sprouting of the remaining cutaneous nerve supplying the field was looked for in the form of field expansion into the surrounding denervated territory at various postoperative intervals. Such isolated fields failed to expand in the adult rat for periods up to at least 85 days. "Nonfunctional" sprouting is unlikely to explain this failure. However, similar experiments done in very young animals gave a different result. In rat pups aged less than 20 days, isolated fields did expand, but this ceased at about 20 days, and attempts to evoke it after this time were unsuccessful. There seems to be a critical period for sprouting of these touch-sensitive nerves into denervated skin, and our evidence suggests that it may not begin until about 15 days of age. Within this developmental window the sprouting that occurs is spatially constrained, an isolated field expanding preferentially into denervated skin of the parent dermatome; if only skin of neighboring dermatomes is available there is no expansion. In contrast, low-threshold nerves regenerated readily after a crush at all ages studied, and the mechanosensory fields established by regenerating nerves expanded progressively into denervated skin without apparent constraints at dermatomal boundaries. The temporal and spatial constraints found for the sprouting of intact low-threshold axons are in marked contrast to their absence for the well-described sprouting of high-threshold (nociceptive) nerves.
Parasympathetic neurons of the ciliary ganglion are innervated by preganglionic cholinergic neurons whose cell bodies lie in the brain stem; the ganglion cells in turn provide cholinergic innervation to the intrinsic muscles of the eye. Noradrenergic innervation of the iris is supplied by sympathetic neurons of the superior cervical ganglion. Using immunocytochemical and histochemical techniques, we have examined the ciliary ganglion of adult rats for the expression of cholinergic and noradrenergic properties. As expected, the postganglionic ciliary neurons possessed detectable levels of choline acetyltransferase immunoreactivity (ChAT-IR). Unexpectedly, many ciliary neurons also exhibited immunoreactivity for tyrosine hydroxylase (TH-IR). Some had dopamine beta-hydroxylase-like (DBH-IR) immunoreactivity, but none contained detectable catecholamines, even after treatment with nialamide and L-DOPA. A sparse plexus of fibers exhibiting faint TH-IR was present in the irises of acutely sympathectomized rats. The terminals of preganglionic axons in the ciliary ganglion exhibited not only immunoreactivity for ChAT, but also for TH and contained stores of endogenous catecholamine. Neither ciliary neurons nor their preganglionic innervation accumulated detectable stores of exogenous catecholamines. Rats sympathectomized as neonates by treatment with 6-hydroxydopamine subsequently had a greater proportion of neurons possessing detectable TH-IR in the ciliary ganglion; both the TH-IR perikarya and their axons in the iris were more intensely immunofluorescent. TH-IR was present in the ciliary neuron cell bodies of mouse, guinea pig, and ferret. These species, however, lacked detectable TH-IR or catecholamine stores in preganglionic terminals. These observations indicate that mature, functionally cholinergic neurons from 2 different embryonic origins, postganglionic ciliary neurons derived from the neural crest and preganglionic neurons derived from the neural tube, display several catecholaminergic properties.
The anatomical development of muscle sensory arbors and dendrites of brachial motoneurons in the spinal cord of the bullfrog was studied by labeling both types of cells with horseradish peroxidase. Sensory and motoneurons were labeled in tadpoles (stages XV-XVIII) by backfilling the triceps nerve in vivo with HRP throughout the stages in development when functional monosynaptic connections between these cells are first being formed. Individual triceps motoneurons were injected with HRP in other tadpoles at the same developmental stages. By stage XV, triceps sensory afferents already projected to and arborized in the ventral sensory neuropil region of the spinal cord where sensory-motor connections are made. In contrast, the dendrites of triceps motoneurons rarely were present in this region until stage XVI. By stage XVII, triceps dendrites in this region were common and they intermingled with the collaterals of muscle sensory axons. Thus, sensory axons supplying limb muscles grow into the future neuropil region well in advance of the arrival of motoneuronal dendrites. Electrophysiological studies have shown that the connections between triceps sensory and motor neurons are already specific at stage XVII, as soon as monosynaptic potentials between these cells can be detected (Frank and Westerfield: J. Physiol. (Lond.) 343:593-610, '83). The present anatomical results demonstrate that the processes of sensory and motor cells are not in close anatomical proximity before this time; thus the selection of appropriate synaptic partners must occur from the outset.
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