Plasticity in expression of calcitonin gene-related peptide and substance P immunoreactivity in ganglia and fibres following guanethidine and/or capsaicin denervation

Mione, Marina; Cavanagh, J.F.R.; Kirkpatrick, Karen A.; Burnstock, Geoffrey

doi:10.1007/bf00319156

Cited by 34 publications

(13 citation statements)

References 37 publications

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“…This view suggests interplay between sympathetic and sensory nerves to and from WAT respectively, and is based on evidence for such interactions in other tissues. For example, global sympathectomy or surgical denervation markedly increases CGRP immunoreactivity in the mesenteric and other vascular beds, as well as in most organs (Mione et al 1992;Aberdeen et al 1990). Conversely, a reciprocal response occurs after global sensory denervation, resulting in increases in sympathetic activity measured electrophysiologically (Ralevic et al 1995 Fig.…”

Section: Does White Adipose Tissue Have Parasympathetic Nervous Systementioning

confidence: 99%

Brain–adipose tissue cross talk

et al. 2005

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While investigating the reversible seasonal obesity of Siberian hamsters, direct sympathetic nervous system (SNS) postganglionic innervation of white adipose tissue (WAT) has been demonstrated using anterograde and retrograde tract tracers. The primary function of this innervation is lipid mobilization. The brain SNS outflow to WAT has been defined using the pseudorabies virus (PRV), a retrograde transneuronal tract tracer. These PRV-labelled SNS outflow neurons are extensively co-localized with melanocortin-4 receptor mRNA, which, combined with functional data, suggests their involvement in lipolysis. The SNS innervation of WAT also regulates fat cell number, as noradrenaline inhibits and WAT denervation stimulates fat cell proliferation in vitro and in vivo respectively. The sensory innervation of WAT has been demonstrated by retrograde tract tracing, electrophysiological recording and labelling of the sensory-associated neuropeptide calcitonin gene-related peptide in WAT. Local injections of the sensory nerve neurotoxin capsaicin into WAT selectively destroy this innervation. Just as surgical removal of WAT pads triggers compensatory increases in lipid accretion by nonexcised WAT depots, capsaicin-induced sensory denervation triggers increases in lipid accretion of non-capsaicin-injected WAT depots, suggesting that these nerves convey information about body fat levels to the brain. Finally, parasympathetic nervous system innervation of WAT has been suggested, but the recent finding of no WAT immunoreactivity for the possible parasympathetic marker vesicular acetylcholine transporter (VAChT) argues against this claim. Collectively, these data suggest several roles for efferent and afferent neural innervation of WAT in body fat regulation.Sympathetic nervous system: Sensory nerves: Parasympathetic nervous system: Pseudorabies virus: Lipolysis A critical ability of all animals is to meet energy demands quickly with utilizable metabolic fuels. In mammals glycogen serves as a rapidly available, but extremely limited, carbohydrate energy source. Energy is predominately stored as lipid in white adipose tissue (WAT) in the form of triacylglycerol (Newsholme & Leech, 1983). Access to this energy in fat can be mediated by several means, principally by the sympathetic nervous system (SNS) innervation of WAT. The present review starts by discussing the SNS innervation of WAT and then considers its sensory innervation and possible parasympathetic nervous system (PSNS) innervation. As the title of the review suggests, the cross talk occurring between the brain and WAT, which use these innervations as conduits, will be highlighted. However, the provocative and interesting cross talk between WAT and the brain that occurs via humoral factors will not be discussed.Adrenal medullary catecholamines, once thought to be the principal stimulators of lipid mobilization, do not play a major role in lipolysisTraditionally, adrenal medullary secretion of catecholamines, primarily adrenaline, is thought to be the underlying means by whi...

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Section: Does White Adipose Tissue Have Parasympathetic Nervous Systementioning

confidence: 99%

Brain–adipose tissue cross talk

et al. 2005

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“…Similarly, the diminished low flow levels for ATP may represent a long-term effect of sensory denervation on endothelial synthesis and cytosolic levels. According ly, we have previously shown that endothelial cells iso lated from older rabbits release more ET and ATP than younger rabbits and also express more ET immunoreactivity [20], It is of particular interest that there was a greater per fusate flow-stimulated release of SP from the microvessels isolated from capsaicin-treated animals since SP is one of the neuropeptides found in sensory nerves [44], Capsaicin treatment thus leads to a depletion of the neural source of SP from the vasculature [25]. It is tempting to speculate that increased expression of SP in the endothelium of brain microvesseis may be a compensatory mechanism in vessels lacking sensory vasodilatory innervation.…”

Section: Discussionmentioning

confidence: 99%

“…On days 2 and 3 they were carried out under ice anesthesia. This treatment regime has been shown to lead to depletion of SPimmunoreactive nerves from the vasculature including cerebral ves sels [16,25],…”

Section: Capsaicin Treatmentmentioning

confidence: 99%

Interactions between Sensory Perivascular Nerves and the Endothelium in Brain Microvessels

Milner¹,

Bodin²,

Loesch³

et al. 1995

Int J Microcirc

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The purpose of our study was to see if selective denervation of sensory perivascular nerves leads to changes in release of vasoactive substances of endothelial origin from brain microvessels during increased flow. Male rats pups were treated with the neurotoxin, capsaicin, to destroy primary afferent sensory nerves. Three months later, brain microvessels were isolated, placed on a micro-pore filter and perfused with Krebs buffer. During the course of a 30-min experiment, the flow rate was increased from 0.5 to 3.0 ml/min for two 3-min periods. The levels of ATP, substance P, vasopressin and endothelin in the effluent were measured. Microvessels from 5 rats were pooled for each perfusion experiment. Data from 5 perfusion experiments showed that the release of substance P was significantly higher in the capsaicin-treated rats during the second period of increased flow (3.02 ± 1.04 pmol/min/mg protein) compared to the vehicle-treated controls (0.30 ± 0.21 pmol/min/mg protein; p < 0.02). In contrast, the release of ATP at low flow and during the second period of increased flow was significantly lower in the capsaicin-treated rats (0.21 ± 0.04 compared to 0.50 ± 0.03 pmol/min/mg protein for controls at low flow, p < 0.001; and 1.19 ± 0.15 compared to 2.11 ± 0.26 pmol/min/mg protein for controls during the second period of increased flow, p < 0.01). The release patterns of endothelin and vasopressin were similar in capsaicin-treated and vehicle-treated controls. In conclusion, chronic depletion of sensory innervation leads to altered release of two endothelium-dependent vasodilators, ATP and substance P from the brain microvasculature. These changes may be compensatory and suggest that there is an ongoing interaction between sensory perivascular nerves and the endothelium in brain microvessels.

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“…3, 5. 7 and 14 of life) [19]. The treatment was in accordance with statutory regulations for the use of animals in scientific procedures.…”

Section: In Vivo Capsaicin Treatmentmentioning

confidence: 99%

Long-Term Sensory Denervation Does Not Modify Endothelial Function or Endothelial Substance P and Nitric Oxide Synthase in Rat Mesenteric Arteries

Ralevic

Dikranian²,

Burnstock³

1995

J Vasc Res

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Mesenteric endothelial cell function and immunoreactivity for substance P and nitric oxide synthase (NOS) were examined in control rats and rats treated with capsaicin as neonates to destroy primary afferent nerves. Endothelial vasodilator function was examined pharmacologically in the methoxamine raised-tone isolated perfused mesenteric arterial bed. Endothelial immunoreactivity for substance P and NOS was examined at the ultrastructural level by electron-microscopic immunocytochemistry. The endothelium-dependent vasodilators acetylcholine and adenosine 5’-triphosphate elicited dose-dependent relaxations which were not different between control and capsaicin-treated rats. Dose-dependent relaxations to endothelium-independent vasodilators, calcitonin gene-related peptide and sodium nitroprusside, were also unchanged by capsaicin treatment. Positive staining for substance P was detected in 25% of endothelial cells in both control and capsaicin-treated rats. Positive staining for NOS was detected in 50% of endothelial cells in control rats, and this was not changed by capsaicin treatment. These results confirm that endothelial substance P is independent of substance P contained in sensory nerves. Long-term sensory denervation does not produce changes in endothelium-dependent or -independent relaxation, or in the number of endothelial cells showing positive labelling for substance P and NOS in rat mesenteric arteries.

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Plasticity in expression of calcitonin gene-related peptide and substance P immunoreactivity in ganglia and fibres following guanethidine and/or capsaicin denervation

Cited by 34 publications

References 37 publications

Brain–adipose tissue cross talk

Brain–adipose tissue cross talk

Interactions between Sensory Perivascular Nerves and the Endothelium in Brain Microvessels

Long-Term Sensory Denervation Does Not Modify Endothelial Function or Endothelial Substance P and Nitric Oxide Synthase in Rat Mesenteric Arteries

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