STUDY OF CENTRAL NEUROTRANSMITTERS IN STRESS‐INDUCED GASTRIC ULCERATION IN ALBINO RATS

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Abstract
1 Restraint when combined with cold (4°C) consistently induces gastric ulceration in rats at 2 h. The cold-restraint ulcer (CRU) technique provides a suitable model for acute studies. 2 The peripheral mechanisms in CRU seem to be increased sympathetic and parasympathetic outflow since CRU was significantly reduced by prior spinal transection or vagotomy or by appropriate blocking agents. Since metiamide significantly reduced CRU, H2-histamine receptors are also involved. 3 Central catecholaminergic as well as cholinergic mechanisms seem to be responsible for the activation of peripheral sympathetic and parasympathetic outflow in CRU, since central administration of dibenamine, propranolol, 6-hydroxydopamine and atropine prevented the CRU. 4 Exogenous administration of putative neurotransmitters (adrenaline, noradrenaline and acetylcholine) into the cerebroventricular system produced gastric ulceration similar to CRU. However, dopamine, histamine and 5-hydroxytryptamine failed to induce gastric ulceration. 5 The results with intracerebroventricular adrenaline and acetylcholine indicate a central cholinergic link distal to adrenergic activation in the ulcerogenesis. 6 Intracerebroventricular adrenaline-induced gastric ulceration appears to be most akin to CRU. However, other central neurotransmitter mechanisms may also be involved.