The present study examined contribution of mGluRs to the development and maintenance of changes in behavioural and clinical symptoms, blood concentrations of cortisol and catecholamines during visceral pain produced by descsending colonal distension (CD). Experiments were carried out in fourth stages (each of six sheep). Every experiment was performed simultaneously on two unfed animals, which were placed in two individual metabolic cages at one week intervals. Blood was collected 30 min prior to the experiment, at 0 time, and 5, 10, 15, 30, 60 and 120 min after intracerebroventricular (icv) administration of the mGluR1 antagonist: L-2-Amino-3-phosphonopropionic acid (L-AP3, 0.2, 0.4 and/or 0.8 mg in toto), 10 min before, blocked the development of visceral pain symptoms and neuroendocrine changes in the plasma of sheep. This data demonstrated that the development and maintenance of the visceral pain symptoms of CD is dependent on activation of mGluR1 in central nervous system (CNS) and that these receptors play a crucial role in modulating acute jejunal (colic) experimental pain It can be concluded that the mGluR1 antagonists prevent behavioural, clinical and neuroendocrine symptoms of visceral pain. They can be possibly used in cases of acute visceral pain, especially, in combination with opioid agonists. Their simultaneous administration allows to minimise dose of opioids and slows down dynamics of the development of tolerance. This knowledge can be also useful in paliative medicine.