Local capsaicin application to the stellate ganglion and stellatectomy attenuate neurogenic inflammation in rat bronchi

Tseng, Wen-Yen; Tsao, Chiung-Fang; Ko, Chun-Chuan; Huang, Hung‐Tsai

doi:10.1016/s1566-0702(01)00361-7

Cited by 6 publications

(4 citation statements)

References 18 publications

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“…The respiratory tract is another major peripheral site of SP synthesis and release (Lecci et al, 2000). Here, SP containing sensory fibers have been identified in the smooth muscle layers of the bronchi and trachea, airway epithelium, and larynx (Kraneveld & Nijkamp, 2001; Mazzone, 2004; Tseng, Tsao, Ko, & Huang, 2001). SP-immunoreactive nerve fibers have also been shown to surround blood vessels of the lower airways (Martling, Matran, Alving, Hökfelt, & Lundberg, 1990).…”

Section: The Basics Of Spmentioning

confidence: 99%

“…Permanent or reversible long-term loss of SP-containing afferent fibers can be achieved through pretreatment with high doses of capsaicin (Scheerens, Buckley, Muis, Van Loveren, & Nijkamp, 1996). Loss of sensory fibers, in this respect or as a consequence of severing the thoracic branch of the vagus nerve, blocks the development of airway hypersensitivity and neurogenic inflammation in the lower airways (Buckley & Nijkamp, 1994; Ladenius & Nijkamp, 1993; Tseng et al, 2001). Selective antagonists to the NK-1r have also been shown to prevent development of airway hyperresponsivity, airway obstruction, and cough (reviewed in Advenier et al, 1997).…”

Section: Role Of Sp In Diseases Of Chronic Inflammatory Diseasementioning

confidence: 99%

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Substance P at the nexus of mind and body in chronic inflammation and affective disorders.

Rosenkranz

2007

Psychological Bulletin

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For decades, research has demonstrated that chronic diseases characterized by dysregulation of inflammation are particularly susceptible to exacerbation by stress and emotion. Likewise, rates of depression and anxiety are overrepresented in individuals suffering from chronic inflammatory disease. In recent years, substance P has been implicated in both the pathophysiology of inflammatory disease and the pathophysiology of depression and anxiety by 2 parallel fields of study. This review integrates the literature from these 2 parallel fields and examines the possibility that substance P dysregulation may be a point of convergence underlying the overlap of chronic inflammatory disease and mood and anxiety disorders. First, the involvement of substance P in peripheral inflammation and in the immune events associated with chronic inflammatory disease is discussed, with a focus on inflammatory bowel disease and asthma. Next, the function of substance P in the communication of peripheral inflammation to the brain is considered. Finally, to complete the bidirectional loop of brain-immune interactions, substance P expression in anxiety and depression as well as its potential role in the neural regulation of peripheral inflammation is reviewed.

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Section: The Basics Of Spmentioning

confidence: 99%

Section: Role Of Sp In Diseases Of Chronic Inflammatory Diseasementioning

confidence: 99%

Substance P at the nexus of mind and body in chronic inflammation and affective disorders.

Rosenkranz

2007

Psychological Bulletin

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“…Characterization of activation of non-vagal C-fibers might be more complicated. It probably represents a collection of unmylinated sensory C-fibers innervating most visceral organs, such as heart [25,26,39], lung [5,37], and the upper airways [7,23]. Increases in neural amplitude caused by non-vagal C-fiber activation would override part of the inhibition evoked by vagal C-fibers.…”

Section: Changes In Cardiopulmonary Functions With Pulmonary C-fiber mentioning

confidence: 99%

Response of Respiratory-Related Hypoglossal Nerve Activity to Capsaicin-Induced Pulmonary C-Fiber Activation in Rats

Lee

et al. 2003

J Biomed Sci

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This study was designed to examine respiratory-related hypoglossal nerve activity in response to activation of pulmonary C-fibers by capsaicin. Rats were anesthetized with urethane (1.2 g/kg, i.p.). Tracheostomy was performed. Catheters were introduced into the femoral vein and artery. Another catheter was placed near the entrance of the right atrium via the right jugular vein. Rats were paralyzed with gallamine triethiodide (5 mg/kg, i.v.), and ventilated artificially. Activities of the phrenic nerve (PNA) and the hypoglossal nerve (HNA) were recorded simultaneously. Varied doses of capsaicin (0.625, 1.25, and 5 µg/kg) were delivered into the right atrium to activate pulmonary C-fibers. Before bilateral vagotomy, apnea, decreases in PNA and HNA were observed in response to pulmonary C-fiber activation by the low and moderate doses of capsaicin. The high dose of capsaicin evoked an increase in PNA, an immediate tonic discharge of the hypoglossal nerve, and a decrease in phasic HNA. The onset time of HNA preceding PNA was abolished and replaced by a time lagged pattern as pulmonary C-fibers were activated. Raising CO₂ concentration did not attenuate the inhibitory effect of pulmonary C-fiber activation upon PNA and HNA. After bilateral sectioning of the vagi, administration of the moderate dose of capsaicin to activate non-vagal C-fibers produced increases in PNA and HNA. These results suggest that pulmonary vagal C-fiber activation may narrow the diameter at the oropharyngeal level by a decrease in phasic HNA, which may be disadvantageous for the maintenance of a patent upper airway.

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“…Five adult male Sprague-Dawley rats (60–70 days postnatal, ~225g, Harlan) were anesthetized (60 mg/kg ketamine, 8 mg/kg xylazine, and 0.4mg/kg atropine, intraperitoneal injection), intubated, respired mechanically and a unilateral thoracotomy (2 nd rib) carried out. The subclavian artery was identified and followed inferiorly where it branches into the costocervical artery and internal thoracic artery; the stellate ganglion lies in a cleft between the latter vessels (Hansson et al, 1998; Tseng et al, 2001). The superior and inferior branches were cut and the ganglia were removed bilaterally.…”

Section: Methodsmentioning

confidence: 99%

Modulation of rat parasympathetic cardiac ganglion phenotype and NGF synthesis by adrenergic nerves

Hasan

Smith

2009

Autonomic Neuroscience

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Cardiac function is regulated by interactions among intrinsic and extrinsic autonomic neurons, and the mechanisms responsible for organizing these circuits are poorly understood. Parasympathetic neurons elsewhere synthesize the neurotrophin NGF, which may promote postganglionic axonal associations where parasympathetic axons inhibit sympathetic transmitter release. Previous studies have shown that parasympathetic NGF content and neurochemical phenotype are regulated by sympathetic innervation. In this study we assessed contributions of sympathetic input on cardiac ganglion neuronal phenotype and NGF expression. Because cardiac ganglia are reported to contain putative noradrenergic neurons, we eliminated sympathetic input both surgically (extrinsic) and chemically (extrinsic plus intrinsic). In controls, most cardiac ganglion neurons expressed vesicular acetylcholine transporter, frequently colocalized with vesicular monoamine transporter, but lacked catecholamine histofluorescence. Most cardiac ganglion neurons expressed NGF transcripts, and 40% contained mature and 47% proNGF immunoreactivity. Guanethidine treatment for 7 days decreased numbers of neurons expressing vesicular acetylcholine transporter, NGF transcripts and NGF immunoreactivity, but did not affect proNGF or vesicular monoamine transporter immunoreactivity. Stellate ganglionectomy had comparable effects on neurochemical phenotype and mature NGF immunoreactivity, but proNGF expression was additionally reduced.These findings show that individual cardiac ganglion neurons display markers of both cholinergic and noradrenergic transmission. Sympathetic noradrenergic innervation maintains levels of cholinergic but not noradrenergic marker protein. Sympathetic innervation also promotes cardiac ganglion neuronal NGF synthesis. Because chemical blockade of all noradrenergic transmission is no more effective than extrinsic sympathectomy, local intrinsic noradrenergic transmission is not a factor in regulating ganglion neuron phenotype.

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Local capsaicin application to the stellate ganglion and stellatectomy attenuate neurogenic inflammation in rat bronchi

Cited by 6 publications

References 18 publications

Substance P at the nexus of mind and body in chronic inflammation and affective disorders.

Substance P at the nexus of mind and body in chronic inflammation and affective disorders.

Response of Respiratory-Related Hypoglossal Nerve Activity to Capsaicin-Induced Pulmonary C-Fiber Activation in Rats

Modulation of rat parasympathetic cardiac ganglion phenotype and NGF synthesis by adrenergic nerves

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