Thyrotropin-releasing hormone causes a tonic excitatory postsynaptic current and inhibits the phasic inspiratory inhibitory inputs in inspiratory-inhibited airway vagal preganglionic neurons

Hou, Lili; Zhou, Xujiao; Chen, Y.; Qiu, Dong; Zhu, Liangliang; Wang, J.

doi:10.1016/j.neuroscience.2011.12.003

Cited by 11 publications

(19 citation statements)

References 25 publications

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“…The eNA area, from which IA‐AVPNs were identified in the present study, is within the range of the pre‐Bötzinger complex (PBC), a primary region that may generate respiratory rhythm in mammals (Smith et al 1991; Rekling & Feldman, 1998; Koshiya & Smith, 1999; Smith et al 2000). Previous studies have demonstrated that the cellular composition of the PBC is complex, containing heterogeneous phenotypes of neurons, including rhythm‐generating pacemaker neurons (Smith et al 2000; Del Negro et al 2001, 2002; Koizumi & Smith, 2008), hypoglossal premotoneurons (Koizumi & Smith, 2008), bulbospinal phrenic and intercostal premotoneurons (Bianchi et al 1995; Richter, 1996), rhythmically active GABAergic and glycinergic inhibitory neurons (Kuwana et al 2006; Winter et al 2009) and tracheobronchial‐projecting IA‐AVPNs and II‐AVPNs (Chen et al 2007, 2012; Qiu et al 2011; Hou et al 2012). The nicotine‐mediated modulation of medullary respiratory rhythm via activation of the α4β2 type of nAChR has previously been proved both at the network level and at the neuronal level in the ‘inspiratory’ neurons of the PBC, in both rats (Shao & Feldman, 2001, 2002, 2005) and mice (Shao et al 2008).…”

Section: Discussionmentioning

confidence: 99%

“…In the ventrolateral medulla, those AVPNs in the eNA predominate in the control of the trachea and bronchi; only the AVPNs in the eNA are labelled after finely controlled tracer application directly to the tracheobronchial (pulmonary) branch of the vagus (Kc et al 2004); and only the AVPNs in the cNA are labelled after finely controlled tracer application directly to the laryngeal nerves (Irnaten et al 2001 a , b ; Barazzoni et al 2005; Okano et al 2006; Chen et al 2007). The AVPNs in the eNA include inspiratory‐activated AVPNs (IA‐AVPNs) and inspiratory‐inhibited AVPNs (II‐AVPNs; Chen et al 2007,2012; Qiu et al 2011; Hou et al 2012); and the former far surpass the latter in number (Chen et al 2012). Likewise, peripherally in the paratracheobronchial parasympathetic ganglion, the postganglionic neurons also include ‘phasic’ neurons and ‘tonic’ neurons.…”

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confidence: 99%

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Nicotine enhances both excitatory and inhibitory synaptic inputs to inspiratory‐activated airway vagal preganglionic neurons

Zhou

Chen

et al. 2012

Experimental Physiology

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New Findings r What is the central question of this study?Airway vagal preganglionic neurons (AVPNs) supply the essential excitatory drive to the postganglionic neurons, which dominate the neural control of the airway physiologically and play critical roles in the pathogenesis of some common airway disorders. AVPNs express multiple subunits of nicotinic acetylcholine receptors (nAChRs), but the influences of exogenous nicotine or endogenous acetylcholine are unknown. r What is the main finding and its importance?Nicotine and endogenous acetylcholine both cause a postsynaptic excitatory current in inspiratory-activated AVPNs, and enhance both the excitatory and inhibitory synaptic inputs. The overall effect of nicotine on inspiratory-activated AVPNs is excitatory. The nicotinic effects on inspiratory-activated AVPNs are mediated presynaptically by activation of α4β2 type of nAChRs and postsynaptically by activation of multiple nAChRs including α7 and α4β2 types.The airway vagal preganglionic neurons (AVPNs) supply the essential excitatory drive to the postganglionic neurons and dominate the neural control of the airway both physiologically and pathophysiologically. The AVPNs express multiple subunits of nicotinic acetylcholine receptors (nAChRs), but the influences of exogenous nicotine and endogenous acetylcholine are unknown. This study examined the effects of nicotine and endogenous acetylcholine on retrogradely labelled, functionally identified inspiratory-activated AVPNs (IA-AVPNs) using the patchclamp technique. Nicotine (10 μmol l −1 ) significantly increased the frequency and amplitude of the spontaneous EPSCs of IA-AVPNs, and these effects were insensitive to methyllycaconitine (MLA, 100 nmol l −1 ), an antagonist of the α7 type of nAChR, but was prevented by dihydro-β-erythroidine (DHβE, 3 μmol l −1 ), an antagonist of the α4β2 type of nAChR. Nicotine caused a tonic inward current in IA-AVPNs, which was reduced by MLA or DHβE alone, but was not abolished by co-application of MLA and DHβE. Nicotine caused a significant increase in the frequency of GABAergic and glycinergic spontaneous IPSCs and significantly increased the amplitude of glycinergic spontaneous IPSCs, all of which were prevented by DHβE. Nicotine had no effects on the miniature EPSCs or miniature IPSCs following pretreatment with TTX. Under current clamp, nicotine caused depolarization and increased the firing rate of IA-AVPNs during inspiratory intervals. Neostigmine (10 μmol l −1 ), an acetylcholinesterase inhibitor, mimicked the effects of nicotine. These results demonstrate that nicotine and endogenous ACh enhance the excitatory and inhibitory synaptic inputs of IA-AVPNs and cause a postsynaptic excitatory

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Nicotine enhances both excitatory and inhibitory synaptic inputs to inspiratory‐activated airway vagal preganglionic neurons

Zhou

Chen

et al. 2012

Experimental Physiology

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“…Three to five day-old Sprague-Dawley rats (Shanghai General Hospital affiliated to Shanghai Jiao Tong University) were anesthetized by inhalation of halothane (0.5 ml) and hypothermia, and then the AVPNs were labeled, as described in our previous work [20,21]. 48-52 h after the labeling, the animal was deeply anesthetized with halothane again and then decapitated.…”

Section: Retrogradely Fluorescent Labelling Of the Avpns And Slice Prmentioning

confidence: 99%

“…Additionally, gap junctions [8,19]and endogenous cholinergic mechanisms mediated by activation of the α7 and α4β2 nicotinic acetylcholine receptors (nAChRs) are also involved in the regulation of IA-AVPNs [10,40]. For example, thyrotropin-releasing hormone (TRH) evoked a distinct oscillatory pattern mediated by gap junctions in IA-AVPNs [20], but not in II-AVPNs [21]. However, the roles of NMDA receptors, gap junctions and nACh receptors in the synaptic activation of IA-AVPNs by central activity remain unclear.…”

Section: Introductionmentioning

confidence: 99%

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Central inspiratory activity rhythmically activates synaptic currents of airway vagal preganglionic neurons in neonatal rats

Hou

Bellingham

Huang

et al. 2019

Neuroscience Letters

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This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. Central inspiratory activity rhythmically activates synaptic currents of airway vagal preganglionic neurons in neonatal rats

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Are thyrotropin‐releasing hormone (TRH) and analog taltirelin viable reversal agents of opioid‐induced respiratory depression?

Algera

Cotten

Velzen

et al. 2022

Pharmacology Res & Perspec

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Opioid‐induced respiratory depression (OIRD) is a potentially life‐threatening complication of opioid consumption. Apart from naloxone, an opioid antagonist that has various disadvantages, a possible reversal strategy is treatment of OIRD with the hypothalamic hormone and neuromodulator thyrotropin‐releasing hormone (TRH). In this review, we performed a search in electronic databases and retrieved 52 papers on the effect of TRH and TRH‐analogs on respiration and their efficacy in the reversal of OIRD in awake and anesthetized mammals, including humans. Animal studies show that TRH and its analog taltirelin stimulate breathing via an effect at the preBötzinger complex, an important respiratory rhythm generator within the brainstem respiratory network. An additional respiratory excitatory effect may be related to TRH’s analeptic effect. In awake and anesthetized rodents, TRH and taltirelin improved morphine‐ and sufentanil‐induced respiratory depression, by causing rapid shallow breathing. This pattern of breathing increases the work of breathing, dead space ventilation, atelectasis, and hypoxia. In awake and anesthetized humans, a continuous infusion of intravenous TRH with doses up to 8 mg, did not reverse sufentanil‐ or remifentanil‐induced respiratory depression. This is related to poor penetration of TRH into the brain compartment but also other causes are discussed. No human data on taltirelin are available. In conclusion, data from animals and human indicate that TRH is not a viable reversal agent of OIRD in awake or anesthetized humans. Further human studies on the efficacy and safety of TRH’s more potent and longer lasting analog taltirelin are needed as this agent seems to be a more promising reversal drug.

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Thyrotropin-releasing hormone causes a tonic excitatory postsynaptic current and inhibits the phasic inspiratory inhibitory inputs in inspiratory-inhibited airway vagal preganglionic neurons

Cited by 11 publications

References 25 publications

Nicotine enhances both excitatory and inhibitory synaptic inputs to inspiratory‐activated airway vagal preganglionic neurons

Nicotine enhances both excitatory and inhibitory synaptic inputs to inspiratory‐activated airway vagal preganglionic neurons

Central inspiratory activity rhythmically activates synaptic currents of airway vagal preganglionic neurons in neonatal rats

Are thyrotropin‐releasing hormone (TRH) and analog taltirelin viable reversal agents of opioid‐induced respiratory depression?

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