Release of calcitonin gene-related peptide from the jugular–nodose ganglion complex in rats – A new model to examine the role of cardiac peptidergic and nitrergic innervation

Strecker, Thomas; Koulchitsky, Stanislav; Dieterle, Anne; Neuhuber, Winfried; Weyand, Michael; Meßlinger, Karl

doi:10.1016/j.npep.2008.08.002

Cited by 8 publications

(5 citation statements)

References 41 publications

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“…The intragangionic release of CGRP within JNC has not been demonstrated so far in vivo. Previous study on rat has reported about the release of CGRP from isolated JNC after stimulation with different substances such as capsaicin, nitric oxide donor sodium nitroprusside [41]. Our findings showed an increase of CGRP-positive neurons in JNC, but a release of CGRP from the neuron into the ganglia could not be demonstrated in the present study.…”

Section: Discussioncontrasting

confidence: 92%

Allergic airway inflammation induces the migration of dendritic cells into airway sensory ganglia

Rochlitzer

Fischer

et al. 2014

Respir Res

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BackgroundA neuroimmune crosstalk between dendritic cells (DCs) and airway nerves in the lung has recently been reported. However, the presence of DCs in airway sensory ganglia under normal and allergic conditions has not been explored so far. Therefore, this study aims to investigate the localisation, distribution and proliferation of DCs in airway sensory ganglia under allergic airway inflammation.MethodsUsing the house dust mite (HDM) model for allergic airway inflammation BALB/c mice were exposed to HDM extract intranasally (25 μg/50 μl) for 5 consecutive days a week over 7 weeks. With the help of the immunohistochemistry, vagal jugular-nodose ganglia complex (JNC) sections were analysed regarding their expression of DC-markers (MHC II, CD11c, CD103), the neuronal marker PGP 9.5 and the neuropeptide calcitonin gene-related peptide (CGRP) and glutamine synthetase (GS) as a marker for satellite glia cells (SGCs). To address the original source of DCs in sensory ganglia, a proliferation experiment was also carried in this study.ResultsImmune cells with characteristic DC-phenotype were found to be closely located to SGCs and vagal sensory neurons under physiological conditions. The percentage of DCs in relation to neurons was significantly increased by allergic airway inflammation in comparison to the controls (HDM 51.38 ± 2.38% vs. control 28.16 ± 2.86%, p < 0.001). The present study also demonstrated that DCs were shown to proliferate in jugular-nodose ganglia, however, the proliferation rate of DCs is not significantly changed in the two treated animal groups (proliferating DCs/ total DCs: HDM 0.89 ± 0.38%, vs. control 1.19 ± 0.54%, p = 0.68). Also, increased number of CGRP-positive neurons was found in JNC after allergic sensitisation and challenge (HDM 31.16 ± 5.41% vs. control 7.16 ± 1.53%, p < 0.001).ConclusionThe present findings suggest that DCs may migrate from outside into the ganglia to interact with sensory neurons enhancing or protecting the allergic airway inflammation. The increase of DCs as well as CGRP-positive neurons in airway ganglia by allergic airway inflammation indicate that intraganglionic DCs and neurons expressing CGRP may contribute to the pathogenesis of bronchial asthma. To understand this neuroimmune interaction in allergic airway inflammation further functional experiments should be carried out in future studies.

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Section: Discussioncontrasting

confidence: 92%

Allergic airway inflammation induces the migration of dendritic cells into airway sensory ganglia

Rochlitzer

Fischer

et al. 2014

Respir Res

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“…The loss of nitrergic nerve varicosities within the musculature is probably reflecting both primarily intrinsic enteric nitrergic motor neurons and vagal afferent nNOS positive neurons 42 but likely not vagal efferent neurons, as no alterations in the numbers of vagal efferent nNOS neurons were noted in the vagal motor nucleus (dorsal motor nucleus and nucleus ambiguous) between control and diabetic tissues in a study on STZ‐DM rat model. 43 Interestingly, in the nodose ganglion of STZ‐DM rats, an increased number of nNOS positive neurons without an accompanying increase in nNOS mRNA was attributed to a diabetes‐induced inhibition of axonal transport that either caused a build up of protein in the cell body, interrupted neurotrophic support to the neurons, or both, 43 suggesting less nNOS in nerve endings.…”

Section: Discussionmentioning

confidence: 94%

Loss of intramuscular and submuscular interstitial cells of Cajal and associated enteric nerves is related to decreased gastric emptying in streptozotocin‐induced diabetes

Huizinga

Diamond

et al. 2009

Neurogastroenterology Motil

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Interstitial cells of Cajal (ICC) are associated with afferent innervation and peristalsis of the stomach suggestive of a key role in the pathophysiology of gastroparesis. We studied changes in the density and ultrastructure of ICC and enteric nerves in the streptozotocin-induced diabetes mellitus (STZ-DM) in Wistar rats using immunohistochemistry and electron microscopy. Gastric emptying was studied in vivo by single-photon emission computed tomography. In the STZ-DM antrum, a marked reduction was observed in the density of the intramuscular ICC (ICC-IM) and ICC located at the submucosal border of the circular muscle layer of the antrum (ICC-SM). The surviving ICC showed lamellar bodies and partial vacuolation of the cytoplasm content, loss of connections between ICC-IM and nerves; it appeared that injured ICC-IM developed into fibroblast-like ICC. ICC associated with Auerbach's plexus (ICC-AP) in the antrum and ICC in the fundus were not affected significantly except for a loss of connections with nerve structures. Marked reduction in nerve tissue (Protein Gene Product-9.5 positivity) was also restricted to the muscle layers including nitrergic nerves (neuronal nitric oxide synthase positivity). In vivo assessed gastric emptying was markedly reduced in STZ-DM rats. Our data demonstrate in the STZ-DM rat stomach a decreased density of ICC limited to the antrum and to ICC-IM and ICC-SM, and structural degeneration in ICC-IM and associated nerves with a special emphasis on loss of synaptic connections, accompanied by a decrease in gastric emptying. Hence, in this model of gastroparetic diabetes, regional injury to subsets of ICC and nerves are associated with gastric motor dysfunction.

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“…Hitherto investigations revealed the CGRP expression in sensory spinal ganglia and distal ganglia of the vagus of the pig (Bulc et al., ) and rat (Strecker et al., ). Our study additionally confirmed co‐expression of CGRP in 30% of PACAP‐IR neurons of the porcine distal ganglion of the vagus.…”

Section: Discussionmentioning

confidence: 99%

Co-expression of PACAP with VIP, SP and CGRP in the Porcine Nodose Ganglion Sensory Neurons

Rytel

Palus

Całka

2014

Anat. Histol. Embryol.

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Our previous study revealed the expression of substance P (SP) and calcitonin gene-related peptide (CGRP) in sensory distal ganglion of the vagus (nodose ganglion) neurons in the pig. As these neuropeptides may be involved in nociception, the goal of these investigations was to determine possible expression of vasoactive intestinal polypeptide (VIP), SP and CGRP in the pituitary adenylate cyclase-activating polypeptide-immunoreactive (PACAP-IR) porcine nodose perikarya. Co-expression of these substances was examined using a double-labelling immunofluorescence technique. To reveal the ganglionic cell bodies, the pan-neuronal marker protein gene product 9.5 (PGP 9.5) was used. Quantitative analysis of the neurons revealed that 67.25% of the PGP 9.5+ somata in the right-side ganglion and 66.5% in the left side, respectively, co-expressed PACAP-IR. Moreover, 60.6% of the PACAP-IR cells in the right-side ganglion and 62.1% in the left, respectively, co-expressed VIP. SP-IR was observed in 52.2 and 39.9% of the right and left ganglia, respectively. CGRP was found in 27.7 and 34.1% of the right and left distal ganglion of the vagus, respectively. High level of co-expression of PACAP with VIP, SP and CGRP in the distal ganglia of the vagus sensory perikarya directly implicates studied peptides in their functional interaction during nociceptive vagal transduction.

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Release of calcitonin gene-related peptide from the jugular–nodose ganglion complex in rats – A new model to examine the role of cardiac peptidergic and nitrergic innervation

Cited by 8 publications

References 41 publications

Allergic airway inflammation induces the migration of dendritic cells into airway sensory ganglia

Allergic airway inflammation induces the migration of dendritic cells into airway sensory ganglia

Loss of intramuscular and submuscular interstitial cells of Cajal and associated enteric nerves is related to decreased gastric emptying in streptozotocin‐induced diabetes

Co-expression of PACAP with VIP, SP and CGRP in the Porcine Nodose Ganglion Sensory Neurons

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