Functional evidence that gastroprotection can be induced by activation of central α2B-adrenoceptor subtypes in the rat

Dual Alpha2C/5HT1A Receptor Agonist Allyphenyline Induces Gastroprotection and Inhibits Fundic and Colonic Contractility

“…We demonstrated that clonidine and rilmenidine, when given either peripherally (per os, subcutaneously) or centrally (i.c.v. ), inhibited potently the direct necrotizing action of acidified ethanol on gastric mucosa in both rats and mice [12][13][14][15][16][17]. Our results also showed that the site of action is presumably within the CNS [16,17], where the activation of α2B-and α2C-ARs initiates a chain of events resulting in vagally mediated release of mucosal protective factors, such as prostaglandins and nitric oxide [13,16].…”

“…More importantly, our results clearly showed that this protective effect is mediated by α2B-and α2C-ARs localized in the brain, most probably in the dorsal vagal complex, and α2A-ARs do not have any significant role in it [12,14,17]. Accordingly, we proposed that selective α2B/C-AR agonists may represent a novel group of gastroprotective agents, which are devoid of several side effects mediated by the α2A-AR subtype, such as hypotension, bradycardia or sedation [17].…”

“…In the last two decades our research group demonstrated that α2-AR agonists induce a potent defensive effect in the stomach and reduce the extent of mucosal injury in both aciddependent (indomethacin) and independent (ethanol) ulcer models [12][13][14][15][16][17]. More importantly, our results clearly showed that this protective effect is mediated by α2B-and α2C-ARs localized in the brain, most probably in the dorsal vagal complex, and α2A-ARs do not have any significant role in it [12,14,17].…”

Involvement of β2-Adrenergic and μ-Opioid Receptors in Antinociception Produced by Intracerebroventricular Administration of α,β-Methylene-ATP

“…Furthermore, i.c.v. injections of propranolol (10 and 100 nmol/ rat) as a b -adrenergic receptor antagonist (27), atenolol (100 nmol /rat) as a b1-adrenergic receptor antagonist (28), butoxamine and ICI-118,551 (100 nmol/ rat, each) as b 2-adrenergic receptor antagonists (27,28), naloxone (10 and 30 nmol /rat) as an opioid receptor antagonist (29), naltrindole (30 nmol / rat) as a d-opioid receptor antagonist (30) and nor-BNI (30 nmol / rat) as a k-opioid receptor antagonist (31) were employed.…”

Age and monosodium glutamate treatment cause changes in the stimulation-induced [3H]-norepinephrine release from rat nucleus tractus solitarii-dorsal vagal nucleus slices

“…While investigating the central mechanisms involved in the maintenance of gastric mucosal integrity independently of the regulation of acid secretion, we have found recently that stimulation of alpha-2 B adrenoceptors (Gyires et al, 2000a) releases h-endorphin in the lower brainstem, most probably in the NTS-DVN region to produce a protective effect against acidified ethanol-induced mucosal damage in the rat stomach (Gyires et al, 2000b). Since releasable h-endorphin may originate either from a local neuronal pool or from a descending projection originating in the hypothalamic arcuate nucleus (Palkovits et al, 1987) we have used various forebrain transections (Rónai et al, 2002) or neonatal monosodium glutamate (MSG) treatment (Rónai et al, 2001) to eliminate (or reduce) the projection source.…”