Developmental Regulation of Glucosensing in Rat Adrenomedullary Chromaffin Cells: Potential Role of the KATP Channel

Livermore, Simon; Piskuric, Nikol A.; Salman, Shaima; Nurse, Colin A.

doi:10.1007/978-94-007-4584-1_27

Cited by 3 publications

(2 citation statements)

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“…In addition to the well-established role of central neurons in glucose control, numerous pieces of evidence indicate that glucose sensors also exist at the periphery and that they have an essential physiological role (Cane et al, 1986 ). In addition to α-cells of the pancreas, hypoglycemia-sensitive cells have also been suggested to exist in the liver (Hamilton-Wessler et al, 1994 ), near the portal vein (Hevener et al, 1997 ), and in the adrenal gland of the newborn (Livermore et al, 2012 ).…”

Section: Carotid Body and Glucose Sensingmentioning

confidence: 99%

Glucose sensing by carotid body glomus cells: potential implications in disease

et al. 2014

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The carotid body (CB) is a key chemoreceptor organ in which glomus cells sense changes in blood O2, CO2, and pH levels. CB glomus cells have also been found to detect hypoglycemia in both non-primate mammals and humans. O2 and low-glucose responses share a common final pathway involving membrane depolarization, extracellular calcium influx, increase in cytosolic calcium concentration, and neurotransmitter secretion, which stimulates afferent sensory fibers to evoke sympathoadrenal activation. On the other hand, hypoxia and low glucose induce separate signal transduction pathways. Unlike O2 sensing, the response of the CB to low glucose is not altered by rotenone, with the low glucose-activated background cationic current unaffected by hypoxia. Responses of the CB to hypoglycemia and hypoxia can be potentiated by each other. The counter-regulatory response to hypoglycemia by the CB is essential for the brain, an organ that is particularly sensitive to low glucose. CB glucose sensing could be altered in diabetic patients, particularly those under insulin treatment, as well as in other medical conditions such as sleep apnea or obstructive pulmonary diseases, where chronic hypoxemia presents with plastic modifications in CB structure and function. The current review will focus on the following main aspects: (1) the CB as a low glucose sensor in both in vitro and in vivo models; (2) molecular and ionic mechanisms of low glucose sensing by glomus cells, (3) the interplay between low glucose and O2 sensing in CB, and (4) the role of CB low glucose sensing in the pathophysiology of cardiorespiratory and metabolic diseases, and how this may serve as a potential therapeutic target.

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Section: Carotid Body and Glucose Sensingmentioning

confidence: 99%

Glucose sensing by carotid body glomus cells: potential implications in disease

et al. 2014

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“…Furthermore, they showed in denervation experiments that removal of the splanchnic innervation in mature or adult animals resulted in a gradual re-appearance of this non-neurogenic mechanism (Slotkin and Seidler, 1988). More recent studies in the rat suggest that adrenal responses to hypercapnia, acidity and hypoglycemia are also suppressed postnatally, in parallel with splanchnic innervation (Livermore et al, 2011;Livermore et al, 2012;Muñoz-Cabello et al, 2005;Rico et al, 2005). Interestingly, in mammals that are born relatively mature (e.g.…”

Section: Introductionmentioning

confidence: 99%

Ontogeny of O2 and CO2//H+ chemosensitivity in adrenal chromaffin cells: role of innervation

Salman

Buttigieg

Nurse

2014

Journal of Experimental Biology

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The adrenal medulla plays a key role in the physiological responses of developing and mature mammals by releasing catecholamines (CAT) during stress. In rodents and humans, the innervation of CATproducing, adrenomedullary chromaffin cells (AMCs) is immature or absent during early postnatal life, when these cells possess 'direct' hypoxia-and CO 2 /H + -chemosensing mechanisms. During asphyxial stressors at birth, these mechanisms contribute to a CAT surge that is critical for adaptation to extra-uterine life. These direct chemosensing mechanisms regress postnatally, in parallel with maturation of splanchnic innervation. Here, we review the evidence that neurotransmitters released from the splanchnic nerve during innervation activate signaling cascades that ultimately cause regression of direct AMC chemosensitivity to hypoxia and hypercapnia. In particular, we consider the roles of cholinergic and opioid receptor signaling, given that splanchnic nerves release acetylcholine and opiate peptides onto their respective postsynaptic nicotinic and opioid receptors on AMCs. Recent in vivo and in vitro studies in the rat suggest that interactions involving α7 nicotinic acetylcholine receptors (nAChRs), the hypoxia inducible factor (HIF)-2α signaling pathway, protein kinases and ATP-sensitive K + (K ATP ) channels contribute to the selective suppression of hypoxic chemosensitivity. In contrast, interactions involving μ-and/or δ-opiod receptor signaling pathways contribute to the suppression of both hypoxic and hypercapnic chemosensitivity, via regulation of the expression of K ATP channels and carbonic anhydrase (CA I and II), respectively. These data suggest that the ontogeny of O 2 and CO 2 /H + chemosensitivity in chromaffin cells can be regulated by the tonic release of presynaptic neurotransmitters.

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