) but display functional somatostatin receptors mainly of the sstÔ and sstµ subtypes (Mounier et al. 1995). In keeping with these observations, both somatostatin and octreotide, a long-acting preferential agonist at sstµ receptor subtypes, inhibit basal GH release from GC cells (Mounier et al. 1995). In order to understand the mechanisms underlying the sustained release of GH by GC cells in the absence of external stimulation, we analysed their membrane activity and cytosolic Ca¥ concentration ([Ca¥] Ca¥ current activated at −33·6 ± 0·4 mV (holding potential (Vh), −40 mV), peaked at −1·8 ± 1·3 mV, was reduced by nifedipine and enhanced by S-(+)-SDZ 202 791. A TÏR_type Ca¥ current activated at −41·7 ± 2·7 mV (Vh, −80 or −60 mV), peaked at −9·2 ± 3·0 mV, was reduced by low concentrations of Ni¥ (40 ìÒ) or Cd¥ (10 ìÒ) and was toxin resistant. Parallel experiments revealed the expression of the class E calcium channel á1-subunit mRNA. 3. The K¤ channel blockers TEA (25 mÒ) and charybdotoxin (10-100 nÒ) enhanced spike amplitude andÏor duration. Apamin (100 nÒ) also strongly reduced the after-spike hyperpolarization. The outward K¤ tail current evoked by a depolarizing step that mimicked an action potential reversed at −69·8 ± 0·3 mV, presented two components, lasted 2-3 s and was totally blocked by Cd¥ (400 ìÒ). 4. The slow pacemaker depolarization (3·5 ± 0·4 s) that separated consecutive spikes corresponded to a 2-to 3-fold increase in membrane resistance, was strongly Na¤ sensitive but TTX insensitive. 5. Computer simulations showed that pacemaker activity can be reproduced by a minimum of six currents: an L-type Ca¥ current underlies the rising phase of action potentials that are repolarized by a delayed rectifier and Ca¥-activated K¤ currents. In between spikes, the decay of Ca¥-activated K¤ currents and a persistent inward cationic current depolarize the membrane, activate the TÏR-type Ca¥ current and initiate a new cycle.