These slow oscillations appear at a threshold concentration of glucose characteristic for the individual β-cell, but unlike the classical bursts they are not modified by additional increases in the sugar concentration ( Hellman, Gylfe, Grapengiesser, Lund & Berts, 1992). Further investigations on individual pancreatic β-cells resulted in the discovery of large amplitude i oscillations with a frequency of 0.2-0.5 min −1 ( Grapengiesser, Gylfe & Hellman, 1988).

The burst pattern is precisely regulated by glucose, the burst duration increasing with the sugar concentration ( Meissner & Schmelz, 1974). This pattern, unfortunately often referred to as slow waves, represents fast oscillations (typically 3-5 min −1) in membrane potential, which were later found to be synchronized with i oscillations ( Santos, Rosario, Nadal, Garcia-Sancho, Soria & Valdeolmillos, 1991 Gilon & Henquin, 1992). The first type of oscillatory signalling observed in islets of Langerhans was repetitive bursts of action potentials ( Dean & Matthews, 1970 Meissner & Schmelz, 1974). However, there is much confusion about the nature of this i signalling, since oscillations with quite different properties have been observed. It is generally assumed that pulsatile insulin release is determined by oscillations in the cytoplasmic Ca 2+ concentration ( i) of the pancreatic β-cells ( Bergsten & Hellman, 1993 a, b Gilon, Shepherd & Henquin, 1993 Bergsten, Grapengiesser, Gylfe, Tengholm & Hellman, 1994 Bergsten, 1995 Gilon & Henquin, 1995 Martin, Sanchez-Andres & Soria, 1995). Insulin is released in a pulsatile fashion from the human pancreas ( Pørksen, Munn, Steers, Vore, Veldhuis & Butler, 1995), and this pulsatility is believed to be important for maintaining upregulation of the insulin receptors ( Lefèbvre, Paolisso, Scheen & Henquin, 1987).

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