![]() ![]() Thus, the satiety signal conferred by PSK acts antagonistically to the hunger signal, provided by the adipokinetic hormone (AKH): PSK depresses the electrical activity of DUM neurons by inhibiting the pTRPĪ³ channel that is activated by AKH under conditions of food shortage. PSK increased the intracellular cAMP level while decreasing the intracellular Ca 2+ concentration in DUM neurons. Application of PSK to DUM neurons attenuated the spiking frequency (EC 50=11pM) due to reduction of a pacemaker Ca 2+ current through cAMP-inhibited pTRPĪ³ channels. It occurs only in a few neurons, among them are the dorsal unpaired median (DUM) neurons which release octopamine thereby regulating the general level of activity. To correlate the distributions of PSK and its receptor (PSKR), we cloned the gene coding for PSKR and provide evidence for its expression within the nervous system. PSK is found in the neurohemal organ of the brain and in nerve endings throughout the central nervous system. We identified the sources of PSK which is used both as hormone and as paracrine messenger. The aim of this study was to resolve the mechanism by which the antifeedant activity of perisulfakinin (PSK) in Periplaneta americana is mediated. The counterpart to the mammalian satiety signal cholecystokinin (CCK) in insects are the sulfakinins. Satiety is related to resting or sleep whereas hunger correlates to wakefulness and activity. The metabolic state is one of the determinants of the general activity level. ![]()
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