“…Indeed, opioid neuropeptides, which are massively released in shock conditions (Lang et al, 1982;Farrell et al, 1983;Elam et al, 1984;Bernton et al, 1985) and are considered important factors in the pathophysiology and evolution of shock (Holaday, 1983;Bernton et al, 1985), inhibit Ca2+ influx into target neurones and cells (Yamamoto et al, 1978;Guerrero-Munoz et al, 1979), and a number of studies have confirmed an antagonistic interaction between opioids and calcium in a variety of experimental systems (for reviews, see Ross & Cardenas, 1979;Chapman & Way, 1980;Huidobro-Toro & Way, 1983). Conversely, melanocortin peptides increase intracellular calcium concentration in target neurones (for reviews see: Jolles et al, 1980;O'Donohue & Dorsa, 1982;De Wied & Jolles, 1982;Wiegant et al, 1986;Eberle, 1988), and melanocortin-induced behavioural symptoms are antagonized by w-conotoxin (Argiolas et al, 1990).…”