This study associates cholinergic stimulation of the pancreatic β‐cell electrical activity with a short‐term memory phenomenon. Glucose pulses applied to a basal glucose concentration induce depolarizing waves which are used to estimate the evolution of the β‐cell glucose sensitivity. Exposure to carbamoylcholine (carbachol) increases the size of the glucose‐induced depolarizing waves. This change appears after carbachol withdrawal and implies a temporal potentiation of sensitivity (TPS) lasting up to one hour. TPS induction requires the simultaneous action of carbachol and glucose. The substitution of glucose with the secretagogues glyceraldehyde or 2‐ketoisocaproate mimics glucose‐induced TPS, while palmitate does not. TPS is not produced if the membrane is kept hyperpolarized by diazoxide. Glucose can be replaced by tolbutamide, suggesting a role of depolarization and a subsequent increase in intracellular calcium concentration. A role for kinases is suggested because staurosporine prevents TPS induction. Cycloheximide does not impair TPS induction, indicating that de novo protein synthesis is not required. The fact that the two inputs acting simultaneously produce an effect that lasts up to one hour without requiring de novo protein synthesis suggests that TPS constitutes a case of short‐term associative conditioning in non‐neural tissue. The convergence of basal glucose levels and muscarinic activation happens physiologically during the cephalic phase of digestion, in order to later absorb incoming fuels. Our data reveals that the role of the cephalic phase may be extended, increasing nutrient sensitivity during meals while remaining low between them.

We studied the emergence of oscillatory electrical activity after addition of glucose to insulin secreting cells. In the physiological glucose range (7-20 mM), these cells show a typical square-wave bursting pattern when they are coupled in the islet. Islet of Langerhans consists of some thousands of beta cells, coupled through gap-junctions. When these cells are isolated they also become more excitable in presence of glucose, spiking continuously, but they fail to oscillate. We have hypothesized a role of cell coupling in the generation of oscillatory activity in this system. Now, we examine the phase of continuous activity that appears after a glucose challenge to check our hypothesis. Both experimental data and computer simulations of a small network of I~ cells, further supports our hypothesis on a role of intercellular coupling in the emergence of oscillatory patterns. I N T R O D U C T I O NWe have already described that an optimal range of input resistance is necessary to keep the oscillatory behavior of the pancreatic beta cell (1,2). Inside this range, input resistance oscillates between two levels in a clear correlation with membrane potential. The absence of phase lag between the oscillations of the membrane potential and the input resistance of the cell points to the possibility of input resistance determining the appropriate balance of conductances allowing the cell to behave as an oscillator.In a coupled network , input resistance reflects, not only the state of the cell conductances (non-junctional conductances) but also the contribution of the neighbor coupled cells:through the coupling conductances (junctional conductance). A careful study of coupling changes (3) along the oscillatory phases, as well as in the silent periods, and continuous spiking periods, can help to understand the behavior of the input resistance for different glucose concentrations and thus to understand the electrical requirements of these cells to be able to show such a variety of electrical patterns. Besides, coupling seems to be crucial for this system to have a proper electrical response as far as isolated cells are unable to oscillate (4,5,6)

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