Altered distribution of dorsal root fibers in the rat following neonatal capsaicin treatment

Réthelyi, M.; Salim, Misbah; Jancsó, Gábor

doi:10.1016/0306-4522(86)90067-9

Cited by 46 publications

(16 citation statements)

References 26 publications

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“…This notion is strongly supported by the observations that a similar deprivation of the spinal dorsal horn of its C-fibre afferent input by neonatal treatment with capsaicin (Jancso et al 1977 results in sprouting of the remaining intact primary afferent fibres and in synaptic reorganization (Nagy & Hunt, 1983;Rethelyi & Jancso, 1983;Rethelyi et al 1986; Beal & Knight, 1987;Shortland, Molander, Woolf & Fitzgerald, 1990). Similar changes in the receptive field properties of dorsal horn neurones and the disorganization of dorsal horn somatotopic maps have been documented both after perineural capsaicin and after nerve section (see above).…”

Section: Functional Implications Of C-fibre Transganglionic Degenerationsupporting

confidence: 67%

“…Nagy & Hunt, 1983;Rethelyi & Jancso, 1983;Rethelyi, Salim & Jancso, 1986). A substantial reorganization of muscle afferent projections has been demonstrated after lesions of rat hindlimb nerves (Brushart, Henry & Mesulam, 1981).…”

Section: Functional Implications Of C-fibre Transganglionic Degenerationmentioning

confidence: 99%

“…Electrophysiological and functional studies revealed that the action of capsaicin can be clearly separated into three phases (Jancso & Such, 1983). The first phase involves a selective activation of Ad-and C-fibres (Jancso & Such, 1983;Such & Jancso, 1986;Marsh, Stansfeld, Brown, Davey & McCarthy, 1987), which may evoke cardiovascular reflexes, antidromic vasodilatation (Gamse & Saria, 1987) and cutaneous plasma extravasation (G. Jancso, unpublished observations). The second phase is characterized by a blockage of impulse conduction in C-and, to a lesser extent, A-fibres (Jancso & Such, 1983;Petsche, Fleischer, Lembeck & Handwerker, 1983; 1985 a; Such & Jancso, 1986;Lynn et al 1987;Waddell & Lawson, 1989;Pini et al 1990).…”

Section: Peptide Histochemistry Of Injured Primary Sensory Neuronesmentioning

confidence: 99%

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Pathobiological reactions of C‐fibre primary sensory neurones to peripheral nerve injury

Jancsó

1992

Experimental Physiology

101

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Mammalian primary sensory neurones display profound anatomical and chemical changes in response to injury of their peripheral processes. Peripheral nerve damage results in transganglionic degeneration of central terminals of A‐fibre primary afferent neurones terminating in the deeper layers of the medullary or spinal dorsal horn. The depletion of neuropeptides and other neurone‐specific macromolecules from neurones in sensory ganglia and from the superficial dorsal horn, the known central projection area of C‐fibre primary afferents, is a salient phenomenon commencing after peripheral nerve lesions. A recently devised new experimental procedure, termed the capsaicin‐gap method, permitted evaluation of the transganglionic degenerative phenomena which develop in C‐fibre primary sensory neurones after a lesion is inflicted upon their peripheral branches. The experimental findings indicated that C‐fibre primary afferent terminals underwent transganglionic degeneration following a perineural treatment with capsaicin, and that this was associated with, and probably resulted from, ganglionic cell degeneration. Studies on the effects of peripheral nerve section yielded similar results. It has therefore been suggested that the observed depletion of specific macromolecules, including sensory peptides, specific glycoconjugates and sensory neurone specific acid phosphatase, may be accounted for, at least in part, by an irreversible loss of sensory ganglion neurones. In contrast, many injured neurones express peptides, including vasoactive intestinal polypeptide, peptide histidine‐isoleucine and galanin, which can be demonstrated in only a few neurones under normal conditions. These seem to be involved in dorsal horn regenerative and/or compensatory processes following peripheral nerve damage. There is suggestive evidence that the partial deafferentation caused by the transganglionic degeneration of C‐fibre primary afferents creates favourable circumstances for an anatomical rearrangement of neuronal connections within the spinal cord dorsal horn. These changes may provide a morphological substrate of some of the functional alterations demonstrated after peripheral nerve lesions.

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Section: Functional Implications Of C-fibre Transganglionic Degenerationsupporting

confidence: 67%

Section: Functional Implications Of C-fibre Transganglionic Degenerationmentioning

confidence: 99%

Section: Peptide Histochemistry Of Injured Primary Sensory Neuronesmentioning

confidence: 99%

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Pathobiological reactions of C‐fibre primary sensory neurones to peripheral nerve injury

Jancsó

1992

Experimental Physiology

101

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“…Neonatal capsaicin treatment has been shown to result not only in irreversible destruction of the C-fiber primary afferent neurons and their spinal terminations [4,8], but also in a compensatory/ regenerative sprouting of the A-fiber afferents, as revealed by both histochemical [11,14] and classical silver impregnation techniques [2]. Surprisingly, this could not be clearly observed in the present study when CTB-HRP was utilized as a neuronal tracer with the highly sensitive TMB technique for the demonstration of HRP activity; faint labelling of a few presumed sprouting A-fiber afferents was detected only after nerve transection in the capsaicinpretreated rats.…”

Section: Discussionmentioning

confidence: 99%

“…The results of light microscopy and the quantitative data on the increase in the proportion of labelled large spinal ganglion cells after nerve transection support this assumption. It should be mentioned in this respect that in previous studies which showed the sprouting of myelinated afferents into the substantia gelatinosa in capsaicin-pretreated rats, HRP was either injected directly into the spinal ganglia [11] or applied to the cut central end of the dorsal root [14], presumably producing optimum labelling of the dorsal root fibers.…”

Section: Discussionmentioning

confidence: 99%

Morphological and phenotypic changes of nociceptive primary afferent neurons following neurotmesis and perineural capsaicin treatment

Szigeti¹

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Effect of neonatal capsaicin and infraorbital nerve section on whisker-related patterns in the rat trigeminal nucleus

Waite

Permentier

1997

J. Comp. Neurol.

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In the present study, we investigated the effect of neonatally administered capsaicin on whisker-related pattern formation in the rat trigeminal complex. Both normal whisker-related patterns of barrelettes and the modified patterns seen after neonatal section of the infraorbital nerve were assessed. Capsaicin caused no change in the pattern or size of cytochrome oxidase (CO) barrelettes in the principal trigeminal nucleus (Vp) or trigeminal nucleus interpolaris (Vi) or caudalis (Vc). Injections of horseradish peroxidase (HRP) or wheatgerm agglutinin conjugated to HRP (WGA-HRP) into the posteroorbital (PO) whisker follicle in vehicle-treated animals showed that WGA labelled a larger number of trigeminal ganglion cells than HRP (203 +/- 23; cf. 158 +/- 19), with an increased labelling of small-diameter neurons (HRP: 25.9 +/- 7.7 microm; WGA: 23.2 +/- 7.2 pm). Capsaicin caused a loss of smaller diameter cells but had no effect on the location, cross-sectional area, or rostrocaudal extent of the transganglionically labelled HRP terminations in Vp, Vi, Vc, and cervical dorsal horn. WGA-HRP labelling revealed similar, but less dense, central terminal areas as HRP and an additional area of superficial terminals in the caudal medulla; these were also unaffected by capsaicin treatment. After infraorbital nerve section, CO patches and transganglionically labelled afferent terminations, corresponding to innervated nonmystacial whiskers, were approximately doubled in size. Capsaicin had no effect on the increased size of these spared whisker patches or their afferent terminal areas. These results suggest that barrelette formation is not dependent on unmyelinated afferents and that the changes in response properties seen after capsaicin, such as increased receptive fields, reflect functional changes rather than anatomical expansion of afferent terminal areas.

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Altered distribution of dorsal root fibers in the rat following neonatal capsaicin treatment

Cited by 46 publications

References 26 publications

Pathobiological reactions of C‐fibre primary sensory neurones to peripheral nerve injury

Pathobiological reactions of C‐fibre primary sensory neurones to peripheral nerve injury

Morphological and phenotypic changes of nociceptive primary afferent neurons following neurotmesis and perineural capsaicin treatment

Effect of neonatal capsaicin and infraorbital nerve section on whisker-related patterns in the rat trigeminal nucleus

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