Distribution of capsaicin-sensitive nerve fibres containing immunoreactive substance P in cutaneous and visceral tissues of the rat

Holzer, Peter; Bucsics, A.; Lembeck, Fred

doi:10.1016/0304-3940(82)90029-5

Cited by 128 publications

(34 citation statements)

References 22 publications

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“…In the bladder, capsaicin-sensitive fibers constitute a large proportion (60%) of both sensory and most of the substance-P-containing fibers (Holzer et al, 1982;Hu-Tsai et al, 1992). Our finding therefore agrees with previous observations of a contribution of peptidergic unmyelinated primary afferents to neurogenic inflammation (Ahluwalia et al, 1994;Baluk, 1997;McDonald et al, 1996).…”

Section: Discussionsupporting

confidence: 93%

Activation for CNS Circuits Producing a Neurogenic Cystitis: Evidence for Centrally Induced Peripheral Inflammation

et al. 1999

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We present a model of neurogenic cystitis induced by viral infection of specific neuronal circuits of the rat CNS. Retrograde infection by pseudorabies virus (PRV) of neuronal populations neighboring those that innervate the bladder consistently led to a localized immune response in the CNS and bladder inflammation. Infection of bladder circuits themselves or of circuits distant from these rarely produced cystitis. Absence of virus in bladder and urine ruled out an infectious cystitis. Total denervation of the bladder, selective C-fiber deafferentation, or bladder sympathectomy prevented cystitis without affecting the CNS disease, indicating a neurogenic component to the inflammation. The integrity of central bladder-related circuits is necessary for the appearance of bladder inflammation, because only CNS lesions affecting bladder circuits, i.e., bilateral dorsolateral or ventrolateral funiculectomy, as well as bilateral lesions of Barrington's nucleus/locus coeruleus area, prevented bladder inflammation. The close proximity in the CNS of noninfected visceral circuits to infected somatic neurons would thus permit a bystander effect, leading to activation of the sensory and autonomic circuits innervating the bladder and resulting in a neurogenic inflammation localized to the bladder. The present study indicates that CNS dysfunction can bring about a peripheral inflammation.

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Section: Discussionsupporting

confidence: 93%

Activation for CNS Circuits Producing a Neurogenic Cystitis: Evidence for Centrally Induced Peripheral Inflammation

et al. 1999

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“…Additionally, capsaicin induces degeneration of peripheral afferents in skin, cornea, urinary bladder and gut (Holzer et al, 1982;Fujita et al, 1987;Hiura et al, 1999). Although there are numerous reports of capsaicin-induced primary afferent terminal degeneration, there are only a few reports of effects of capsaicin treatment on primary afferent perikarya, and without exception these have involved capsaicin administration in neonates (Carobi, 1996;Szoke et al, 2002;Hiura et al, 2002).…”

Section: Discussionmentioning

confidence: 99%

Capsaicin-induced neuronal death and proliferation of the primary sensory neurons located in the nodose ganglia of adult rats

2008

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To evaluate the potential for neuronal replacement following destruction of vagal afferent neurons, we examined nodose ganglia following intraperitoneal capsaicin treatment of adult rats. Rats received capsaicin or vehicle followed by a regimen of 5'-bromo-2'-deoxyuridine injections (BrdU) to reveal DNA replication. Nodose ganglia were harvested at various times post-treatment and processed for DAPI nuclear staining and immunofluorescence to estimate neuronal numbers and to determine vanilloid receptor, cleaved caspase 3, TUNEL, BrdU, the neuron-selective marker PGP-9.5 and neurofilament-M-immunoreactivity. Twenty-four hours after capsaicin approximately 40% of nodose ganglion neurons expressed cleaved caspase 3-immunoreactivity and 16% revealed TUNEL staining, indicating that primary sensory neurons are killed by the capsaicin treatment of adult rats. The occurrence of neuronal death was confirmed by counts of DAPI-stained neuronal nuclei, which revealed ≥50% reduction of nodose neuron number by 30 days post-capsaicin. However, by 60 days post-capsaicin, the total numbers of neuronal nuclei in nodose ganglia from capsaicin-treated rats were not different from controls, suggesting that new neurons had been added to the nodose ganglia. Neuronal proliferation was confirmed by significant BrdU incorporation in nuclei of nodose ganglion cells immunoreactive for the neuron-specific antigen PGP-9.5 revealed 30 and 60 days postcapsaicin. Collectively, these observations suggest that in adult rats massive scale neurogenesis occurs in nodose ganglia following capsaicin-induced neuronal destruction. The adult nodose ganglion, therefore, provides a novel system for studying neural plasticity and adult neurogenesis after peripheral injury of primary sensory neurons.

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“…In this model, permanent injury to the afferent fibers occurs indistinctly in the extrinsic nervous system (vagus nerve and fibers of spinal projection) (7,10). If we assume that the afferent stimulus, which determines the effect of these three drugs on GE, originates in the digestive tract, it is not possible to determine the pathway it follows.…”

Section: Discussionmentioning

confidence: 99%

Phenylpyrazolone derivatives inhibit gastric emptying in rats by a capsaicin-sensitive afferent pathway

Vinagre

Collares

2009

Braz J Med Biol Res

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Dipyrone (Dp), 4-aminoantipyrine (AA) and antipyrine (At) administered iv and Dp administered icv delay gastric emptying (GE) in rats. The participation of capsaicin (Cps)-sensitive afferent fibers in this phenomenon was evaluated. Male Wistar rats were pretreated sc with Cps (50 mg/kg) or vehicle between the first and second day of life and both groups were submitted to the eye-wiping test. GE was determined in these animals at the age of 8/9 weeks (weight: 200-300 g). Ten minutes before the study, the animals of both groups were treated iv with Dp, AA or At (240 μmol/kg), or saline; or treated icv with Dp (4 μmol/animal) or saline. GE was determined 10 min after treatment by measuring % gastric retention (GR) of saline labeled with phenol red 10 min after orogastric administration. Percent GR (mean ± SEM, N = 8) in animals pretreated with Cps and treated with Dp, AA or At (35.8 ± 3.2, 35.4 ± 2.2, and 35.6 ± 2%, respectively) did not differ from the GR of saline-treated animals pretreated with vehicle (36.8 ± 2.8%) and was significantly lower than in animals pretreated with vehicle and treated with the drugs (52.1 ± 2.8, 66.2 ± 4, and 55.8 ± 3%, respectively). The effect of icv administration of Dp (N = 6) was not modified by pretreatment with Cps (63.3 ± 5.7%) compared to Dp-treated animals pretreated with vehicle (62.3 ± 2.4%). The results suggest the participation of capsaicin-sensitive afferent fibers in the delayed GE induced by iv administration of Dp, AA and At, but not of icv Dp

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Distribution of capsaicin-sensitive nerve fibres containing immunoreactive substance P in cutaneous and visceral tissues of the rat

Cited by 128 publications

References 22 publications

Activation for CNS Circuits Producing a Neurogenic Cystitis: Evidence for Centrally Induced Peripheral Inflammation

Activation for CNS Circuits Producing a Neurogenic Cystitis: Evidence for Centrally Induced Peripheral Inflammation

Capsaicin-induced neuronal death and proliferation of the primary sensory neurons located in the nodose ganglia of adult rats

Phenylpyrazolone derivatives inhibit gastric emptying in rats by a capsaicin-sensitive afferent pathway

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