Nuray Erin

Role of capsaicin-sensitive nerves in gastric and hepatic injury induced by cold-restraint stress.

The role of capsaicin-sensitive afferent fibers on cold-restraint stress-induced gastric and hepatic injury was examined at the macroscopic and ultrastructural levels. Wistar albino rats were treated with capsaicin either locally (intragastric, perivagal, and periceliac) or systemically (neonatal, intraperitoneal). Perineural and neonatal treatment with capsaicin was used to denervate afferent fibers, while intragastric capsaicin treatment would have activated mucosal afferent fibers just before the stress exposure. Capsaicin decreased significantly the formation of macroscopic gastric lesions caused by stress in all treatment groups. At the electron microscopic level, however, denervation of vagal afferent fibers with capsaicin was most effective in prevention of cellular injury in gastric mucosa. In the liver, systemic denervation of afferent fibers completely inhibited stress-induced cellular damage, while denervation of afferent fibers in vagus and splanchnic nerve was partially effective. Central neural pathways sensitive to capsaicin may mediate formation of both gastric and hepatic injury resulting from stress.

ROLE OF AFFERENT NEURONS IN STRESS INDUCED DEGENERATIVE CHANGES OF THE BLADDER

PURPOSE We investigated the role of afferent C fibers in morphological changes of the rat bladder during stress. MATERIALS AND METHODS Wistar albino rats were exposed to cold immobilization stress. Different routes of capsaicin administration before cold immobilization stress were studied. Capsaicin was given to neonates, around the vagus (perivagal) or celiac (periceliac), or perivagal plus periceliac. From each group samples of bladder were randomly chosen for morphological evaluation using electron microscopy. RESULTS Stress exposure led to pathological changes, including an increased number of mast cells, degenerated urothelium and dilated tight junctions, in the bladder. Capsaicin given neonatally and around the vagal and celiac ganglia prevented these stress induced degenerative bladder changes. CONCLUSIONS Activation of capsaicin sensitive afferent neurons locally and centrally may be involved in stress related pathological changes in the rat bladder.

The role of 5-HT3 receptors in the anti-ulcer effect of calcitonin

1. The aim of the present study was to determine the role of 5-HT3 receptors of the gastroprotective effect of salmon calcitonin (sCT) and sCT-induced changes in gastric, hepatic, brain and brainstem glutathione (GSH) and lipid-peroxidation (LP) levels in rats subjected to cold-immobilization stress. 2. Stress exposure resulted in ulcer formation and a decrease in GSH levels of the liver, brain and brainstem and an increase in gastric and hepatic LP (P < 0.05). 3. sCT prevented stress-induced gastric ulcer development (P < 0.01) and reversed the decrease in hepatic and brain GSH levels (P < 0.05). 4. In the present study, a 5-HT3 receptor antagonist, ICS 205,930 was used. Interestingly, the effect of the blocker on GSH and LP levels of the tissues studied was similar to those of sCT. 5. ICS 205,930 dose dependently reversed the anti-ulcer effect of sCT although it did not antagonize the effect of sCT on GSH and LP levels, but it seemed to show an additive interaction for brain and brainstem GSH and gastric LP levels with sCT.

Volume of Nerve Fibers in the Stress-Induced Bladder of Adult Rats following Capsaicin Treatment

Introduction: We have investigated the volume of nerve fibers in the rat urinary bladder following systematic exposure to cold-restraint stress and capsaicin treatment. Materials and Methods: Adult Wistar albino rats were either exposed to cold-restraint stress (vehicle group) or treated with capsaicin before exposure to cold-restraint stress (capsaicin group). In the control group, animals were neither exposed to cold-restraint stress nor given capsaicin. From each group, samples of bladder were prepared for morphological investigation and stereological evaluation of the volume of nerve fibers. Results: Stress exposure was associated with urothelial degeneration, a higher incidence and degranulation of mast cell profiles in the mucosa, and an increased volume of nerve fibers in the muscular layer of the bladder wall. Capsaicin treatment prevented the stress-induced degenerative changes. In the capsaicin group, the volume of nerve fibers in the muscular layer was also significantly smaller than that in the stress group. Conclusions: Exposure of adult rats to capsaicin prevented the stress-induced degeneration of the bladder and changed the volume of capsaicin-sensitive fibers in muscular layer. We conclude that capsaicin and related compounds may be useful in treating stress-induced bladder problems.

Alteration of cholinergic pressor and antinociceptive responses in rats pretreated with the cholinergic toxin AF64A.

1. In the present study, the pressor and antinociceptive effects of physostigmine and oxotremorine were investigated in rats injected with AF64A intracerebroventricularly. 2. Physostigmine (50-100 micrograms/kg, i.v.)-induced pressor responses were significantly lower in AF64A-injected rats compared with saline-injected animals, whereas oxotremorine (20-80 micrograms/kg, i.v.)-induced responses were found to be similar to those seen in the saline group. 3. The physostigmine (100 micrograms/kg, s.c.)-induced antinociceptive effect was totally abolished by AF64A treatment, but that of oxotremorine (30 micrograms/kg, s.c.) remained unchanged at the tail-flick test. 4. The results of this study present functional evidence for AF64A-produced substantial loss of cholinergic neurons involved in the regulation of blood pressure and nociception but not in postsynaptic muscarinic receptors.

The Protective Effect of 5-HT3 Receptor Antagonist in Thyrotropin Releasing Hormone-Induced Gastric Lesions

The present study examined 1) oxidative stress and gastric lesions induced by thyrotropin releasing hormone (TRH) 2) The effect of a 5-hydroxytryptamine3 (5-HT3) receptor antagonist, ICS 205930 on protective effect of calcitonin on gastric lesions produced by TRH. Calcitonin (5 micrograms/10 microliter) was injected i.c.v. 10 min before TRH (10 micrograms/10 microliter, i.c.v.) injection or ICS 0.5 mg/kg, (i.p.) was given 60 min prior to calcitonin or TRH to rats. Ulcer index, lipid peroxidation (LP) and glutathione (GSH) levels were quantified 3 h after TRH injection in the stomach, liver and brain. TRH caused mucosal lesions (UI: 10.0 +/- 2.0 mm) without changing gastric GSH and LP. JCS did not alter the protective effect of calcitonin against TRH-induced lesions but attenuated. TRH-induced lesion formation. The oxidative effects of calcitonin or ICS were similar to TRH but both drugs attenuated gastric lesion formation. Hence, oxidative changes in tissues studied are not directly involved in TRH-induced lesions.