A quantitative investigation of the effects of neonatal capsaicin treatment on vagal afferent neurons in the rat

Abstract

The sensory cells of the nodose and jugular ganglia of the rat have been quantitatively evaluated in longitudinal paraffin sections. The right vagal ganglia contain significantly more neurons than the left, particularly neurons with somata having sectioned areas 200-400 microm2 and longest diameters 15-25 microm. Such neurons appear to be homogenously distributed because sections of the right vagal ganglia did not show specific areas of neuronal density compared with those of the left. Neonatal capsaicin treatment reduced the number of neurons in both the left and right ganglia to about 30% of controls. Capsaicin destroyed neurons with sectioned areas of 100-600 microm2 and longest diameters of 15-35 microm, but had no statistically significant effects on larger neurons.

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

“…Taken together with our results, these data suggest that the adult NG reveal quantitatively comparable capsaicin-induced damage to the NG of neonates. In contrast to our results, however, Carobi (1996) found no restoration of neuronal number between the time of neonatal capsaicin treatment (2 days postnatal) and adulthood. Our finding that NG neuronal number is restored to control levels within 60 days after capsaicin treatment of adult rats suggests that the adult rat retains precursor cells capable of replacing lost neurons by a process involving DNA synthesis and cell division.…”

“…Our present data does not allow us to determine the degree to which these two mechanisms may contribute to the expression of VR1 in our system. The only previous quantification of capsaicin-induced destruction of NG neurons (Carobi, 1996) reported that adult rats injected with capsaicin as neonates sustained a 70% reduction in total NG neuronal number compared to untreated controls. Taken together with our results, these data suggest that the adult NG reveal quantitatively comparable capsaicin-induced damage to the NG of neonates.…”

“…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). We found that capsaicin administration to adult rats results in strong expression of cleaved cas-3 immunoreactivity by NG neurons within 24h after treatment.…”

Immune-Induced Flavor Aversion in Mice: Modification by Neonatal Capsaicin Treatment

“…In this regard, Carobi [18] showed that following neonatal capsaicin administration to rats, only a 30% reduction was observed in the number of nodose ganglion neurons, compared to the controls. In addition to that, although 99% of abdominal vagal fibers have been shown to be small unmyelinated c-fibers [19], Berthoud et al [20] reported the existence of capsaicin-resistant afferent vagal fibers in different areas of the gastrointestinal tract.…”

Percepção neural da alergia alimentar: envolvimento de mecanismos dependentes de IgE e das fibras nervosas do tipo C

“…Since the amygdala also receives afferent inputs from the NTS [32], this route could be involved in at least part of food allergy-induced cfos expression in the CeA, even considering the lower activation seen in the NTS of capsaicin-treated animals. Despite the fact that neonatal capsaicin has been shown to destroy only 30% of the number of vagal neurons in the nodose ganglia [7] and 41 -75% of unmyelinated fibers in spinal cord roots [19], the present results lead us to suggest that additional mechanisms, apart from the capsaicin-sensitive C-fibers, are involved in food allergy signaling to specific brain areas. This suggestion is in accordance with our previous data showing that, albeit diminishing the magnitude of food aversion in allergic mice, capsaicin treatment was not able to block its development [3].…”