| First Author | Yu H | Year | 2022 |
| Journal | Neurosci Bull | Volume | 38 |
| Issue | 2 | Pages | 149-165 |
| PubMed ID | 34212297 | Mgi Jnum | J:354261 |
| Mgi Id | MGI:7730946 | Doi | 10.1007/s12264-021-00742-4 |
| Citation | Yu H, et al. (2022) A Neural Circuit Mechanism Controlling Breathing by Leptin in the Nucleus Tractus Solitarii. Neurosci Bull 38(2):149-165 |
| abstractText | Leptin, an adipocyte-derived peptide hormone, has been shown to facilitate breathing. However, the central sites and circuit mechanisms underlying the respiratory effects of leptin remain incompletely understood. The present study aimed to address whether neurons expressing leptin receptor b (LepRb) in the nucleus tractus solitarii (NTS) contribute to respiratory control. Both chemogenetic and optogenetic stimulation of LepRb-expressing NTS (NTS(LepRb)) neurons notably activated breathing. Moreover, stimulation of NTS(LepRb) neurons projecting to the lateral parabrachial nucleus (LPBN) not only remarkably increased basal ventilation to a level similar to that of the stimulation of all NTS(LepRb) neurons, but also activated LPBN neurons projecting to the preBotzinger complex (preBotC). By contrast, ablation of NTS(LepRb) neurons projecting to the LPBN notably eliminated the enhanced respiratory effect induced by NTS(LepRb) neuron stimulation. In brainstem slices, bath application of leptin rapidly depolarized the membrane potential, increased the spontaneous firing rate, and accelerated the Ca(2+) transients in most NTS(LepRb) neurons. Therefore, leptin potentiates breathing in the NTS most likely via an NTS-LPBN-preBotC circuit. |
