Role of the nucleus tractus solitarii in the protection of pre-moxibustion on gastric mucosal lesions

Previous studies have shown that somatic sensation by acupuncture and visceral nociceptive stimulation can converge in the nucleus tractus solitarii where neurons integrate signals impact- ing on the function of organs. To explore the role of the nucleus tractus solitarii in the protective mechanism of pre-moxibustion on gastric mucosa, nucleus tractus solitarii were damaged in rats and pre-moxibustion treatment at the Zusanli （ST36） point followed. The gastric mucosa was then damaged by the anhydrous ethanol lavage method. Morphological observations, enzyme linked immunosorbent assays, and western immunoblot analyses showed that gastric mucosa surface lesion and the infiltration of inflammatory cells were significantly ameliorated after pre-moxibustion treatment. Furthermore, the gastric mucosal damage index and somatostatin level were reduced, and epidermal growth factor content in the gastric mucosa and heat-shock protein-70 expression were increased. These results were reversed by damage to the nucleus tractus solitarii. These findings suggest that moxibustion pretreatment at the Zusanli point is protective against acute gastric mucosa injury, and nucleus tractus solitarii damage inhibits these responses. Therefore, the nucleus tractus solitarii may be an important area for regulating the signal transduction of the protective effect of pre-moxibustion on gastric mucosa.

Circuit-Specific Control of Blood Pressure by PNMT‑Expressing Nucleus Tractus Solitarii Neurons

The nucleus tractus solitarii(NTS)is one of the morphologically and functionally defined centers that engage in the autonomic regulation of cardiovascular activity.Phenotypically-characterized NTS neurons have been implicated in the differential regulation of blood pressure(BP).Here,we investigated whether phenylethanolamine N-methyltransferase(PNMT)-expressing NTS(NTS^(PNMT))neurons contribute to the control of BP.We demonstrate that photostimulation of NTS^(PNMT)neurons has variable effects on BP.A depressor response was produced during optogenetic stimulation of NTS^(PNMT)neurons projecting to the paraventricular nucleus of the hypothalamus,lateral parabrachial nucleus,and caudal ventrolateral medulla.Conversely,photostimulation of NTS^(PNMT)neurons projecting to the rostral ventrolateral medulla produced a robust pressor response and bradycardia.In addition,genetic ablation of both NTS^(PNMT)neurons and those projecting to the rostral ventrolateral medulla impaired the arterial baroreflex.Overall,we revealed the neuronal phenotype-and circuit-specific mechanisms underlying the contribution of NTS^(PNMT)neurons to the regulation of BP.

A Neural Circuit Mechanism Controlling Breathing by Leptin in the Nucleus Tractus Solitarii

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-ex-pressing 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^pRb neurons projecting to the LPBN notably eliminated the enhanced respiratory effect induced by NTSLepRb neuron stimulation.In brainstem slices,bath application of leptin rapidly depolarized the membrane potential,increased the spontaneous firing rate,and accelerated the Ca2+transients in most NTSLepRb neurons.Therefore,leptin potentiates breathing in the NTS most likely via an NTS-LPBN-preBdtC circuit.