Potential role of neonatal rat chromaffin cells as glucosensors

Abstract

In mammals, a decrease in blood glucose (hypoglycemia) results in a number of complex autonomic responses that protect vital organs, e.g. the brain. Though central hypothalamic neurons are known to act as glucosensors, there is good evidence that peripheral glucosensors are the physiologically important ones. For example, carotid body (CB) chemoreceptors have recently been implicated as one of several peripheral sites thought to be involved in low glucose sensing and the initiation of counter-regulatory neuroendocrine responses (Nat. Neurosci. 5: 197ndash;198, 2002). In the present study, we tested the hypothesis that neonatal adrenomedullary chromaffin cells (AMC), which share several properties with CB chemoreceptors including the ability to sense PO2, may also act as peripheral glucosensors. Exposure of neonatal AMC to low glucose (0 – 3.3 mM; at different PO2 (140 - 90 mmHg)) caused an inhibition of outward current under voltage clamp, as well as membrane depolarization under current clamp. Additionally low glucose caused a Ca2+-dependent increase in catecholamine (CA) secretion as detected by carbon fiber amperometry. These findings raise the possibility that neonatal AMC can act as peripheral glucosensors and contribute to the critical CA surge that occurs at birth in response to ischemic stress. Funded by: The Heart and Stroke Foundation of Ontario and the Heart and Stroke Foundation of Canada