Systemic administration of leptin potentiates the response of neurons in the nucleus of the solitary tract to chemoreceptor activation in the rat

The Carotid Body Does Not Mediate the Acute Ventilatory Effects of Leptin

“…To explore direct effects of leptin in the CB, we studied in vitro the time course of the release of 3 H-CA using intact CBs, and we observed that leptin at concentrations ×4 basal endogenous levels does not affect the release of 3 H-CA either in basal conditions or during hypoxic or high external K + . Owing that the release of CA is very reliable index of chemoreceptor cell activation (González et al 1992 ) data would indicate that leptin must exert its ventilatory effects acting centrally, probably at the nucleus of the tractus solitarious where the sensory nerve of the CB projects and where Ciriello and Moreau ( 2013 ) have demonstrated the existence a set of neurons that expressing leptin receptors receive inputs from CB chemoreceptors. It is worth noting, that these neurons expressing leptin receptors project to the vasopressor sites of the rostroventrolateral medulla, and thereby contribute with the hypothalamic nuclei with neurons (arcuate, ventromedial, paraventricular and dorsomedial nuclei) to control sympathetic activity (particularly renal sympathetic activity; Ciriello and Moreau 2012 ), heart rate and blood pressure (Harlan and Rahmouni 2013 ).…”

Leptin dependent changes in the expression of tropomyosin receptor kinase B protein in nucleus of the solitary tract to acute intermittent hypoxia

“…Although leptin does not appear to be involved in the reduction in synaptophysin during exposure to IH, leptin does play an important role in mediating chemoreceptor reflex responses as injections of leptin into the caudal medial NTS potentiates the cardiovascular and sympathetic reflex responses to activation of the chemoreceptor reflex [11]. Furthermore, the response of NTS neurons to chemoreceptor reflex activation has been shown to be facilitated by leptin [12].…”

“…In addition, during each acute exposure to IH the leptin levels within the circulation have been shown to be elevated [35,36,40]. Changes in circulatory levels of leptin have been reported to not only exacerbate the effects of chemoreceptor reflex activation on the cardiovascular system, but also potentiate the neuronal responses in NTS to chemoreflex activation [12] while inhibiting the neuronal responses to baroreflex activation [9]. These affects are not observed in leptin receptor deficient Zucker obese rats [9,11].…”

Links between Autonomic Dysfunction and Metabolic Syndrome

“…Interestingly, the long form of the leptin receptor (Ob-Rb) has been detected in NTS of Sprague-Dawley rats and leptin injection in NTS elicits sympathoexicitatory responses through the stimulation of Ob-Rb and mediate chemoreceptor afferent information to specific areas of the rostral ventrolateral medulla (RVLM) which are involved in the reflex control of arterial blood pressure [41]. Hyperleptinemia is associated with increased fat mass and human obesity.…”