Noradrenaline regulates substance P release from rat dorsal root ganglion neurons in vitro

Wang, Yanjie; Li, Xing-Fu; Ding, Feng; Shu, Qiang; Song, Lijun; Yu, Xiao; Liu, Huaxiang

doi:10.1007/s12264-011-1034-4

Cited by 6 publications

(5 citation statements)

References 32 publications

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“…The α-adrenoceptors include α 1A , α 1B , α 1D , α 2A , α 2B , and α 2C subtypes, and β-adrenoceptors into β 1 , β 2 , and β 3 subtypes [ 21 ]. They have been reported to be expressed in primary sensory neurons with their cell bodies located in the dorsal root ganglia (DRGs) [ 22 , 23 ]. Previous studies have suggested that the β 1 and β 2 subtypes are involved in the adrenergic activation [ 24 ] that may play a role in colonic transit.…”

Section: Introductionmentioning

confidence: 99%

Neonatal Maternal Deprivation Followed by Adult Stress Enhances Adrenergic Signaling to Advance Visceral Hypersensitivity

et al. 2018

Neurosci. Bull.

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The pathophysiology of visceral pain in patients with irritable bowel syndrome remains largely unknown. Our previous study showed that neonatal maternal deprivation (NMD) does not induce visceral hypersensitivity at the age of 6 weeks in rats. The aim of this study was to determine whether NMD followed by adult stress at the age of 6 weeks induces visceral pain in rats and to investigate the roles of adrenergic signaling in visceral pain. Here we showed that NMD rats exhibited visceral hypersensitivity 6 h and 24 h after the termination of adult multiple stressors (AMSs). The plasma level of norepinephrine was significantly increased in NMD rats after AMSs. Whole-cell patch-clamp recording showed that the excitability of dorsal root ganglion (DRG) neurons from NMD rats with AMSs was remarkably increased. The expression of β2 adrenergic receptors at the protein and mRNA levels was markedly higher in NMD rats with AMSs than in rats with NMD alone. Inhibition of β2 adrenergic receptors with propranolol or butoxamine enhanced the colorectal distention threshold and application of butoxamine also reversed the enhanced hypersensitivity of DRG neurons. Overall, our data demonstrate that AMS induces visceral hypersensitivity in NMD rats, in part due to enhanced NE-β2 adrenergic signaling in DRGs.

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Section: Introductionmentioning

confidence: 99%

Neonatal Maternal Deprivation Followed by Adult Stress Enhances Adrenergic Signaling to Advance Visceral Hypersensitivity

et al. 2018

Neurosci. Bull.

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“…On the other hand, a positive loop between NA and SP has been previously described, in which NA promotes SP release by binding to α-adrenoceptor. 50 , 52 , 53 In this vein, it is reasonable to hypothesize that despite blocking the β-receptors located on inflammatory cells, NA can still favor SP release through α-adrenoceptor. Therefore, blocking NK1R would inhibit the inflammatory response by preventing SP effects on both the afferent and efferent pathways.…”

Section: Discussionmentioning

confidence: 99%

A Hypothalamic-Controlled Neural Reflex Promotes Corneal Inflammation

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Fonteyne

Chaabane³

et al. 2021

Invest. Ophthalmol. Vis. Sci.

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Purpose To test whether an acute corneal injury activates a proinflammatory reflex, involving corneal sensory nerves expressing substance P (SP), the hypothalamus, and the sympathetic nervous system. Methods C57BL6/N (wild-type [WT]) and SP-depleted B6.Cg-Tac1tm1Bbm/J (TAC1-KO) mice underwent bilateral corneal alkali burn. One group of WT mice received oxybuprocaine before alkali burn. One hour later, hypothalamic neuronal activity was assessed in vivo by magnetic resonance imaging and ex vivo by cFOS staining. Some animals were followed up for 14 days to evaluate corneal transparency and inflammation. Tyrosine hydroxylase (TH), neurokinin 1 receptor (NK1R), and neuronal nitric oxide synthase (nNOS) expression was assessed in brain sections. Sympathetic neuron activation was evaluated in the superior cervical ganglion (SCG). CD45 + leukocytes were quantified in whole-mounted corneas. Noradrenaline (NA) was evaluated in the cornea and bone marrow. Results Alkali burn acutely induced neuronal activation in the trigeminal ganglion, paraventricular hypothalamus, and lateral hypothalamic area (PVH and LHA), which was significantly lower in TAC1-KO mice ( P < 0.05). Oxybuprocaine application similarly reduced neuronal activation ( P < 0.05). TAC1-KO mice showed a reduced number of cFOS + /NK1R + /TH + presympathetic neurons ( P < 0.05) paralleled by higher nNOS expression ( P < 0.05) in both PVH and LHA. A decrease in activated sympathetic neurons in the SCG and NA levels in both cornea/bone marrow and reduced corneal leukocyte infiltration ( P < 0.05) in TAC1-KO mice were found. Finally, 14 days after injury, TAC1-KO mice showed reduced corneal opacity and inflammation ( P < 0.05). Conclusions Our findings suggest that stimulation of corneal sensory nerves containing SP activates presympathetic neurons located in the PVH and LHA, leading to sympathetic activation, peripheral release of NA, and corneal inflammation.

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“…Recordings from the dorsal root attached to an excised DRG preparation taken from rats with chronic constriction injury of the sciatic nerve revealed that C, Aδ, and Aβ neurons responded to NE and to an α 2 receptor agonist applied topically to the DRG (Zhang et al, 1997). NE activation of α receptors in peptidergic nociceptors has also been reported to enhance the release of substance P (Wang et al, 2011c). Note that these studies rarely distinguished direct effects of NE from indirect effects mediated by other cell types in the ganglion or possibly even in the culture dish.…”

Section: Interactions Among Sympathetic Activity Innate Immune Fumentioning

confidence: 99%

How is chronic pain related to sympathetic dysfunction and autonomic dysreflexia following spinal cord injury?

Walters

2018

Autonomic Neuroscience

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Autonomic dysreflexia (AD) and neuropathic pain occur after severe injury to higher levels of the spinal cord. Mechanisms underlying these problems have rarely been integrated in proposed models of spinal cord injury (SCI). Several parallels suggest significant overlap of these mechanisms, although the relationships between sympathetic function (dysregulated in AD) and nociceptive function (dysregulated in neuropathic pain) are complex. One general mechanism likely to be shared is central sensitization - enhanced responsiveness and synaptic reorganization of spinal circuits that mediate sympathetic reflexes or that process and relay pain-related information to the brain. Another is enhanced sensory input to spinal circuits caused by extensive alterations in primary sensory neurons. Both AD and SCI-induced neuropathic pain are associated with spinal sprouting of peptidergic nociceptors that might increase synaptic input to the circuits involved in AD and SCI pain. In addition, numerous nociceptors become hyperexcitable, hypersensitive to chemicals associated with injury and inflammation, and spontaneously active, greatly amplifying sensory input to sensitized spinal circuits. As discussed with the aid of a preliminary functional model, these effects are likely to have mutually reinforcing relationships with each other, and with consequences of SCI-induced interruption of descending excitatory and inhibitory influences on spinal circuits, with SCI-induced inflammation in the spinal cord and in DRGs, and with activity in sympathetic fibers within DRGs that promotes local inflammation and spontaneous activity in sensory neurons. This model suggests that interventions selectively targeting hyperactivity in C-nociceptors might be useful for treating chronic pain and AD after high SCI.

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Noradrenaline regulates substance P release from rat dorsal root ganglion neurons in vitro

Abstract: NA may significantly increase CAP-evoked SP release through activation of α-adrenoreceptors, which may contribute to noradrenergic pain modulation.

Cited by 6 publications

References 32 publications

Neonatal Maternal Deprivation Followed by Adult Stress Enhances Adrenergic Signaling to Advance Visceral Hypersensitivity

Neonatal Maternal Deprivation Followed by Adult Stress Enhances Adrenergic Signaling to Advance Visceral Hypersensitivity

A Hypothalamic-Controlled Neural Reflex Promotes Corneal Inflammation

How is chronic pain related to sympathetic dysfunction and autonomic dysreflexia following spinal cord injury?

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