Intranasal leptin improves survival after opioid overdose in a mouse model

Freire, Carla; Pho, Huy; Bevans‐Fonti, Shannon; Sennes, Luiz Ubirajara; Polotsky, Vsevolod Y.

doi:10.1186/s12967-021-02803-8

Cited by 5 publications

(1 citation statement)

References 11 publications

(19 reference statements)

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“…Future studies are needed to investigate whether the LEPR b positive CB cells project to LEPR b positive NTS neurons, and if this pathway is dependent on TRPM7 channel activity to up-regulate breathing in obese mice [58]. Intranasal administration of leptin did not affect leptin plasma levels [17], but delivered leptin to the medulla [59] and reversed OSA in leptin-resistant mice, which suggests that respiratory effects of leptin are independent of peripheral signaling in the CB and the CB-NTS axis.…”

Section: The Effect Of Activation Of Lepr B Positive Nts Neurons On Breathing During Sleepmentioning

confidence: 98%

The Effect of DREADD Activation of Leptin Receptor Positive Neurons in the Nucleus of the Solitary Tract on Sleep Disordered Breathing

Amorim

Dergacheva

Curado

et al. 2021

IJMS

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Obstructive sleep apnea (OSA) is recurrent obstruction of the upper airway due to the loss of upper airway muscle tone during sleep. OSA is highly prevalent, especially in obesity. There is no pharmacotherapy for OSA. Previous studies have demonstrated the role of leptin, an adipose-tissue-produced hormone, as a potent respiratory stimulant. Leptin signaling via a long functional isoform of leptin receptor, LEPRb, in the nucleus of the solitary tract (NTS), has been implicated in control of breathing. We hypothesized that leptin acts on LEPRb positive neurons in the NTS to increase ventilation and maintain upper airway patency during sleep in obese mice. We expressed designer receptors exclusively activated by designer drugs (DREADD) selectively in the LEPRb positive neurons of the NTS of Leprb-Cre-GFP mice with diet-induced obesity (DIO) and examined the effect of DREADD ligand, J60, on tongue muscle activity and breathing during sleep. J60 was a potent activator of LEPRb positive NTS neurons, but did not stimulate breathing or upper airway muscles during NREM and REM sleep. We conclude that, in DIO mice, the stimulating effects of leptin on breathing during sleep are independent of LEPRb signaling in the NTS.

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Section: The Effect Of Activation Of Lepr B Positive Nts Neurons On Breathing During Sleepmentioning

confidence: 98%