Activation of α1-adrenoceptors facilitates excitatory inputs to medullary airway vagal preganglionic neurons

Ge, Daochuan; Yan, Xianxia; Guo, Yuhong; Chen, Xingxin; Guan, Ruijuan; Chen, Yonghua; Qiu, Dong; Wang, Ji‐Jiang

doi:10.1152/japplphysiol.00045.2015

Cited by 8 publications

(11 citation statements)

References 34 publications

(45 reference statements)

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“…However, we report that A61603, an α1A agonist, increased sEPSC but did not alter the frequency of sIPSC. Such an excitation effect through α1A receptors has been reported in other CNS regions (11,31).…”

Section: Synaptic Current Modulation Of Nasupporting

confidence: 70%

Noradrenergic effects in rat sacral autonomic nucleus using in vitro slice patch-clamp recordings

et al. 2017

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Noradrenergic modulation has been frequently discussed in the context of neural activities that are related to pelvic organs. The sacral preganglionic nucleus (SPN) is a spinal nucleus containing parasympathetic preganglionic neurons that send fibers to pelvic nerves. In spite of the abundant presence of noradrenergic fibers around the SPN, the effects of noradrenaline (NA) remain obscure. To explore this issue, NA (50 μM) was applied to parasympathetic preganglionic neurons in the SPN during whole-cell patch clamp recording. The SPN was labeled with the retrograde tracer, DiI. These neurons demonstrated two classes of firing patterns (delayed and regular) in terms of initiation of firing. Independent of these firing patterns, NA induced inward (56%) or outward (32%) currents in labeled SPN neurons. Phenylephrine, an α1 receptor agonist, induced an inward current, and clonidine, an α2 receptor agonist, induced an outward current, indicating the existence of both α1 and α2 adrenoreceptors in DiI-labeled SPN neurons. NA also modulated synaptic currents according to the firing patterns. In delayed firing neurons, NA inhibited both spontaneous excitatory post-synaptic currents (sEPSCs) and spontaneous inhibitory post-synaptic currents (sIPSCs). Hence, NA facilitated sEPSCs and sIPSCs in about a half of regular firing neurons. Bath application of phenylephrine facilitated sEPSCs and sIPSCs, and clonidine inhibited them. These results support the hypothesis of multiple effects of NA in the SPN, and may suggest functional differences among SPN neurons.The sacral parasympathetic nerve controls the functions of pelvic organs such as the urinary bladder, distal end of the colon, and penis. Preganglionic neurons in the sacral parasympathetic nucleus (SPN), which constitutes the pelvic nerve, are located in the lateral edge and/or medial part of laminae V-VII of L6-S1 in the spinal cord of the rat. These neurons receive input from several brainstem nuclei and spinal interneurons. Retrograde tracers such as fast blue and fast DiI are frequently used to distinguish parasympathetic preganglionic neurons (PGNs) within the SPN, because the SPN also contains interneurons, which show similar membrane properties to the PGNs (6). Induced firing of retrogradely labeled SPN neurons in the rat shows several distinct properties (4,19). One type of neurons show delayed firing in response to injected current pulse, and the other type of neurons show regular firing as a response. Various neurotransmitters and chemicals modulate SPN neuronal activities. However, differences in neurochemical modulation of these two types of neurons have not been fully studied. Noradrenaline (NA) is a well-known neurotransmitter in the central nervous system (CNS) and is present in descending pathways from brainstem nuclei A5 and A6 (locus coeruleus) to the spinal cord (27). NAergic modulation of spinal regions has been extensively studied. NA directly depolarizes motor

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Section: Synaptic Current Modulation Of Nasupporting

confidence: 70%

Noradrenergic effects in rat sacral autonomic nucleus using in vitro slice patch-clamp recordings

et al. 2017

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“…One study found that thyrotropin-releasing hormone significantly suppressed the inspiratory outward currents of II-AVPNs while has no effect on their sIPSCs (Hou et al, 2012 ). Another found that an agonist of α 1 -adrenoceptors significantly enhanced the inspiratory outward currents of II-AVPNs but had no effect on their pharmacologically isolated GABAergic or glycinergic sIPSCs (Ge et al, 2015 ). Therefore, it is more possible that the inspiratory-related inhibitory inputs of II-AVPNs, which are primarily glycinergic (Hou et al, 2012 ), are somewhat different from the spontaneous inhibitory inputs in respect of the origin, and their inspiratory-related activity may be modulated distinctively.…”

Section: Discussionmentioning

confidence: 99%

“…AVPNs were retrogradely labeled as we have previously described (Chen et al, 2007 , 2012 ; Ge et al, 2015 ). In brief, the 2- to 3-day-old Sprague–Dawley rat was anesthetized with halothane and hypothermia.…”

Section: Methodsmentioning

confidence: 99%

“…These AVPNs are intrinsically silent, and their spontaneous or phase-locked inspiratory activity depends completely on the balance between the excitatory, mainly glutamatergic, and the inhibitory, mainly γ-aminobutyric acidergic (GABA) and glycinergic, inputs that they receive. Alterations in this equilibrium are thought to be associated with dysregulation of pulmonary vagal functions (Haxhiu et al, 2005 ; Chen et al, 2007 , 2012 ; Hou et al, 2012 ; Zhou et al, 2013 ; Ge et al, 2015 ).…”

Section: Introductionmentioning

confidence: 99%

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Arginine Vasopressin Alters Both Spontaneous and Phase-Locked Synaptic Inputs to Airway Vagal Preganglionic Neuron via Activation of V1a Receptor: Insights into Stress-Related Airway Vagal Excitation

Yan

Chen

Guo

et al. 2017

Front. Cell. Neurosci.

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The airway vagal preganglionic neurons (AVPNs) in the external formation of the nucleus ambiguus (eNA) play a major role in the vagal control of tracheobronchial smooth muscle tone and maintenance of airway resistance. The eNA receives vasopressinergic projection from the hypothalamic paraventricular nucleus (PVN), the key node for the genesis of psychological stress. Since airway vagal excitation is reportedly to be associated with the psychological stress-induced/exacerbated airway hyperresponsiveness in asthmatics, arginine vasopressin (AVP) might be involved in stress-related airway vagal excitation. However, this possibility has not been validated. This study aimed to test whether and how AVP regulates AVPNs. In rhythmically active medullary slices of newborn rats, retrogradely labeled AVPNs were identified as inspiratory-activated and inspiratory-inhibited AVPNs (IA- and II-AVPNs) using patch-clamp techniques according to their inspiratory-related firing behavior and synaptic activities. The results show that under current clamp, AVP depolarized both IA- and II-AVPNs, and significantly increased their spontaneous firing rate. Under voltage clamp, AVP elicited a slow inward current, and significantly increased the frequency of spontaneous excitatory postsynaptic currents (sEPSCs) in both types of AVPNs. In addition, AVP significantly enhanced the phase-locked excitatory inspiratory inward current in inspiratory-activated airway vagal preganglionic neurons (IA-AVPNs), but significantly suppressed the phase-locked inhibitory inspiratory outward current in II-AVPNs. In both types AVPNs, AVP significantly increased the frequency and amplitude of pharmacologically isolated spontaneous GABAergic and glycinergic inhibitory postsynaptic currents (IPSCs). All of the AVP-induced effects were prevented by SR49059, an antagonist of V1a receptors, but unaffected by SSR149415, an antagonist of V1b receptors. AVP did not cause significant changes in the miniature excitatory postsynaptic currents (mEPSCs), miniature inhibitory postsynaptic currents (mIPSCs) and membrane input resistance of either type of AVPNs. These results demonstrate that AVP, via activation of V1a receptors, enhanced the spontaneous excitatory and inhibitory inputs similarly in the two types of AVPNs, but differentially altered their phase-locked inspiratory excitatory and inhibitory inputs. The overall effects of AVP are excitatory in both types AVPNs. These results suggest that increased central AVP release may be involved in the stress-induced augmentation of airway vagal activity, and, consequently, the induction or exacerbation of some airway diseases.

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“…Airway vagal preganglionic neurons have been mainly found in the external compact of nucleus ambiguus (eNA) via application of fluorescent tracer to the extrathoracic tracheal wall ( Haselton et al, 1992 ; Haxhiu and Loewy, 1996 ; Kc et al, 2004 ; Chen Y. et al, 2007 ; Qiu et al, 2011 ; Chen et al, 2012a , b ; Hou et al, 2012 , 2015 ; Zhou et al, 2013 ; Ge et al, 2015 ; Guo et al, 2017 ; Yan et al, 2017 ). AVPNs in the eNA function as the main neurons which modulate cholinergic tone of airway smooth muscles as well as control the intrapulmonary airway resistance and tracheobronchial caliber ( Haselton et al, 1992 ; Canning and Fischer, 2001 ; Yan et al, 2017 ).…”

Section: Introductionmentioning

confidence: 99%

Inspiratory-Activated Airway Vagal Preganglionic Neurones Excited by Thyrotropin-Releasing Hormone via Multiple Mechanisms in Neonatal Rats

Hou

Zhang

et al. 2018

Front. Physiol.

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The airway vagal preganglionic neurons (AVPNs) providing projections to intrinsic tracheobronchial ganglia are considered to be crucial to modulation of airway resistance in physiological and pathological states. AVPNs classified into inspiratory-activated AVPNs (IA-AVPNs) and inspiratory-inhibited AVPNs (II-AVPNs) are regulated by thyrotropin-releasing hormone (TRH)-containing terminals. TRH causes a direct excitatory current and attenuates the phasic inspiratory glycinergic inputs in II-AVPNs, however, whether and how TRH influences IA-AVPNs remains unknown. In current study, TRH regulation of IA-AVPNs and its mechanisms involved were investigated. Using retrogradely fluorescent labeling method and electrophysiology techniques to identify IA-AVPNs in brainstem slices with rhythmic inspiratory hypoglossal bursts recorded by a suction electrode, the modulation of TRH was observed with patch-clamp technique. The findings demonstrate that under voltage clamp configuration, TRH (100 nM) caused a slow excitatory inward current, augmented the excitatory synaptic inputs, progressively suppressed the inhibitory synaptic inputs and elicited a distinctive electrical oscillatory pattern (OP). Such a current and an OP was independent of presynaptic inputs. Carbenoxolone (100 μM), a widely used gap junction inhibitor, fully suppressed the OP with persistence of TRH-induced excitatory slow inward current and augment of the excitatory synaptic inputs. Both tetrodotoxin (1 μM) and riluzole (20 μM) functioned to block the majority of the slow excitatory inward current and prevent the OP, respectively. Under current clamp recording, TRH caused a slowly developing depolarization and continuously progressive oscillatory firing pattern sensitive to TTX. TRH increased the firing frequency in response to injection of a square-wave current. The results suggest that TRH excited IA-AVPNs via the following multiple mechanisms: (1) TRH enhances the excitatory and depresses the inhibitory inputs; (2) TRH induces an excitatory postsynaptic slow inward current; (3) TRH evokes a distinctive OP mediated by gap junction.

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Activation of α₁-adrenoceptors facilitates excitatory inputs to medullary airway vagal preganglionic neurons

Cited by 8 publications

References 34 publications

<b>Noradrenergic effects in rat sacral autonomic nucleus using in vitro slice patch-clamp r</b><b>ecordings </b>

<b>Noradrenergic effects in rat sacral autonomic nucleus using in vitro slice patch-clamp r</b><b>ecordings </b>

Arginine Vasopressin Alters Both Spontaneous and Phase-Locked Synaptic Inputs to Airway Vagal Preganglionic Neuron via Activation of V1a Receptor: Insights into Stress-Related Airway Vagal Excitation

Inspiratory-Activated Airway Vagal Preganglionic Neurones Excited by Thyrotropin-Releasing Hormone via Multiple Mechanisms in Neonatal Rats

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