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E K Matthews

Publications and source records attributed to E K Matthews.

8 recordsLinked to original sources
PubMed1979

Dynamic oscillations in the membrane potential of pancreatic islet cells.

Glucose and other metabolizable sugars which elicit insulin release from the beta-cell of the pancreatic islet induce repetitive oscillations in the beta-cell transmembrane potential. Upon each phasic depolarization are superimposed rapid fluctuations in potentials, i.e. 'action potentials' or 'spikes' which occur as bursts of electrical activity; the duration and frequency of each burst is a function of glucose concentration. These established electrophysiological features of glucose-islet cell interaction are described in detail together with a consideration of their possible molecular and ionic basis. Based on these observations, a dynamic mathematical computer model of the beta-cell membrane electrical behaviour is presented which utilizes the Goldman equation extended to include divalent ions. The model illustrates how the ionic mechanisms deduced from experimental observations can account for the electrical patterns produced by the beta-cells in the presence of D-glucose; it also allows systematic changes to be made in a number of state variables in order to assess their relative importance and possible contribution to the integrated processes actually observed. Finally, distinction is made between aspects of the model which are well supported by experimental results and those areas which require further analysis.

Animals↗
PubMed1978

Developmental changes in rat adrenocortical cell membrane potential.

Resting membrane potentials of zona fasciculata-reticularis cells of the rat adrenal gland varied with age. The mean membrane potentials of newborn rat adrenal cells was -56.4 +/- 0.7 mV in the first week of life. The mean potential increased slightly to -61.9 +/- 0.8 mV in the second week and then decreased with age to a mean of -38.5 +/- 0.8 mV in 25--50 week old rats and of -25.9 +/- 1.9 mV in 100 week old rats. The changes in membrane potential may correlate with the indices of adrenocortical growth and activity.

Adrenal Cortex↗
PubMed1975

Electrical characteristics of pancreatic islet cells.

1. The electrical properties of mouse pancreatic islet cells have been explored in vitro using a single intracellular micro-electrode for both voltage recording and current injection. 2. The frequency of spontaneous electrical activity induced in islet cells by concentrations of D-glucose greater than 2-8 mM was enhanced by depolarizing, and reduced by hyperpolarizing, current injection. Post-stimulus inhibition and facilitation were also observed. 3. Intracellular current injection evoked a spike potential in Krebs solution containing a low D-glucose concentration (2-8mM), and in glucose-free, but not Ca-free solution. Evoked spikes were observed in approximately 10% of the cell population impaled. 4. The relationship between the rate of rise of an evoked spike and membrane potential displacement by intracellular current injection a sigmoid curve suggesting the presence of an inactivation process in spike potential genesis. 5. High [K]o, 30-50mM, induced electrical activity rarely, and then only transiently, thereafter blocking it; conditioning hyperpolarizing current tended to restore spike activity. 6. D-600, 5 times 10-minus 5M, blocked the electrical activity induced by D-glucose, tolbutamide or current injection; these inhibitory effects were reversed by a threefold increase in [Ca]o to 7-68 mM. 7. From these results it is concluded that the electrical activity induced in islet cells by Dglucose, tolbutamide and current injection is due mainlu to Ca-2+ influx and is dependent on the level of the membrane potential

Action Potentials↗
PubMed1975

Pancreatic islet cells: effects of monosaccharides, glycolytic intermediates and metabolic inhibitors on membrane potential and electrical activity.

1. The effects of monosaccharides, glycolytic intermediates, metabolic inhibitors and anxia, have been studied on the membrane electrical activity of mouse pancreatic islet cells in vitro using a single intracellular micro-electrode for both voltage recording and current injection. 2. In addition to D-glucose (28mM), D-mannose (16-6mM), and L-leucin (10mM), the substances D-glyceraldehyde (11mM), and acetoacetate (20 mM), induced action potentials in islet cells but other glucos analogues and metabolic intermediates including L-glucose dod not. 3. Mannoheptulose 20 mM), but not D-galactose or 2-deoxy-D-glucose, antagonized the electrical activity induced in islet cells by D-glucose, 28mM. Prior treatment of the cells with mannoheptulose caused them to hyperpolarize and completely prevented the appearance of electrical activity on subsequent exposure to D-glucose. 4. Electrical activity induced by D0glucose 28mM, was progressively inhibited by phloridzin, 10mM, if the cells were exposed to D-glucose and inhibitor simultaneously, and abolished on pretreatment with inhibitor for 30-60 min. Phloridzin also caused depolarization of the islet cells which was independent of extracellular glucose. 5. Anoxia completely blocked the electrical activity induced by glucose but not that evoked by D-glyceraldehyde, L-leucine, tolbutamide or glibenclamide. 6. Iodoacetic acid, 5 mM, rapidly blocked glucose-induced electrical activity whilst that elicited by tolbutamide was relatively resistant to inhibition. 7. The nature and possible location of the glucoreceptor in pancreatic islet cells is discussed in relation to the origin and functional significance of glucose-induced electrical activity and insulin secretion.

Acetoacetates↗