The insulin receptor is differentially expressed in somatic and visceral primary sensory neurons

Lázár, Bence András; Jancsó, Gábor; Nagy, I.; Horváth, Viktor J.; Stella, Péter

doi:10.1007/s00441-018-2868-0

Cited by 4 publications

(10 citation statements)

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“…The neurochemical phenotypes of InsR-expressing PSNs innervating different organs have also been revealed. It has been demonstrated that about one-quarter of somatic (cutaneous and muscle) and about half of visceral (urinary bladder and pancreatic) PSNs express the InsR [24]. In addition, it has been demonstrated that the differences between the two subpopulations (somatic and visceral) were significant [24].…”

Section: Neurochemical Characterization Of Somatic and Visceral Psns mentioning

confidence: 99%

“…It has been demonstrated that about one-quarter of somatic (cutaneous and muscle) and about half of visceral (urinary bladder and pancreatic) PSNs express the InsR [24]. In addition, it has been demonstrated that the differences between the two subpopulations (somatic and visceral) were significant [24]. However, about 60% of InsR-expressing PSNs innervating the dorsal hind paw skin, the gastrocnemius muscle, the urinary bladder and the pancreas showed TRPV1 receptor immunoreactivity [24].…”

Section: Neurochemical Characterization Of Somatic and Visceral Psns mentioning

confidence: 99%

“…In addition, it has been demonstrated that the differences between the two subpopulations (somatic and visceral) were significant [24]. However, about 60% of InsR-expressing PSNs innervating the dorsal hind paw skin, the gastrocnemius muscle, the urinary bladder and the pancreas showed TRPV1 receptor immunoreactivity [24]. These observations suggest that the majority of InsR-expressing PSNs are nociceptive in nature.…”

Section: Neurochemical Characterization Of Somatic and Visceral Psns mentioning

confidence: 99%

“…In recent years, electrophysiological, immunohistochemical and functional studies demonstrated the localization and functional significance of InsRs in primary sensory neurons (PSNs), in particular nociceptive PSNs expressing the transient receptor potential vanilloid type 1 (TRPV1) receptor [19][20][21][22][23][24][25]. The present review attempts to summarize experimental data on the diverse roles of insulin and InsRs in physiological and pathophysiological processes involving PSNs.…”

Section: Introductionmentioning

confidence: 99%

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Modulation of Sensory Nerve Function by Insulin: Possible Relevance to Pain, Inflammation and Axon Growth

Lázár

Jancsó

Stella

2020

IJMS

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Insulin, besides its pivotal role in energy metabolism, may also modulate neuronal processes through acting on insulin receptors (InsRs) expressed by neurons of both the central and the peripheral nervous system. Recently, the distribution and functional significance of InsRs localized on a subset of multifunctional primary sensory neurons (PSNs) have been revealed. Systematic investigations into the cellular electrophysiology, neurochemistry and morphological traits of InsR-expressing PSNs indicated complex functional interactions among specific ion channels, proteins and neuropeptides localized in these neurons. Quantitative immunohistochemical studies have revealed disparate localization of the InsRs in somatic and visceral PSNs with a dominance of InsR-positive neurons innervating visceral organs. These findings suggested that visceral spinal PSNs involved in nociceptive and inflammatory processes are more prone to the modulatory effects of insulin than somatic PSNs. Co-localization of the InsR and transient receptor potential vanilloid 1 (TRPV1) receptor with vasoactive neuropeptides calcitonin gene-related peptide and substance P bears of crucial importance in the pathogenesis of inflammatory pathologies affecting visceral organs, such as the pancreas and the urinary bladder. Recent studies have also revealed significant novel aspects of the neurotrophic propensities of insulin with respect to axonal growth, development and regeneration.

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Section: Neurochemical Characterization Of Somatic and Visceral Psns mentioning

confidence: 99%

Section: Neurochemical Characterization Of Somatic and Visceral Psns mentioning

confidence: 99%

Section: Neurochemical Characterization Of Somatic and Visceral Psns mentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Modulation of Sensory Nerve Function by Insulin: Possible Relevance to Pain, Inflammation and Axon Growth

Lázár

Jancsó

Stella

2020

IJMS

Self Cite

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“…Insulin exerts its neural actions through the insulin receptor (InsR), a member of the receptor tyrosine kinases family ( Ward and Lawrence, 2009 ) present in nerve tissue ( Havrankova et al, 1978 ; Unger et al, 1989 ). Further, it has also been revealed that a relatively high proportion of dorsal root ganglion (DRG) neurons express the InsR ( Baiou et al, 2007 ; Lázár et al, 2018a , b ).…”

Section: Introductionmentioning

confidence: 99%

Insulin Confers Differing Effects on Neurite Outgrowth in Separate Populations of Cultured Dorsal Root Ganglion Neurons: The Role of the Insulin Receptor

et al. 2018

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Apart from its pivotal role in the regulation of carbohydrate metabolism, insulin exerts important neurotrophic and neuromodulator effects on dorsal root ganglion (DRG) neurons. The neurite outgrowth-promoting effect is one of the salient features of insulin’s action on cultured DRG neurons. Although it has been established that a significant population of DRG neurons express the insulin receptor (InsR), the significance of InsR expression and the chemical phenotype of DRG neurons in relation to the neurite outgrowth-promoting effect of insulin has not been studied. Therefore, in this study by using immunohistochemical and quantitative stereological methods we evaluated the effect of insulin on neurite outgrowth of DRG neurons of different chemical phenotypes which express or lack the InsR. Insulin, at a concentration of 10 nM, significantly increased total neurite length, the length of the longest neurite and the number of branch points of cultured DRG neurons as compared to neurons cultured in control medium or in the presence of 1 μM insulin. In both the control and the insulin exposed cultures, ∼43% of neurons displayed InsR-immunoreactivity. The proportions of transient receptor potential vanilloid type 1 receptor (TRPV1)-immunoreactive (IR), calcitonin gene-related peptide (CGRP)-IR and Bandeiraea simplicifolia isolectin B4 (IB4)-binding neurons amounted to ∼61%, ∼57%, and ∼31% of DRG neurons IR for the InsR. Of the IB4-positive population only neurons expressing the InsR were responsive to insulin. In contrast, TRPV1-IR nociceptive and CGRP-IR peptidergic neurons showed increased tendency for neurite outgrowth which was further enhanced by insulin. However, the responsiveness of DRG neurons expressing the InsR was superior to populations of DRG neurons which lack this receptor. The findings also revealed that besides the expression of the InsR, inherent properties of peptidergic, but not non-peptidergic nociceptive neurons may also significantly contribute to the mechanisms of neurite outgrowth of DRG neurons. These observations suggest distinct regenerative propensity for differing populations of DRG neurons which is significantly affected through insulin receptor signaling.

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Insulin enhances acid-sensing ion channel currents in rat primary sensory neurons

Xu,

Liu,

Qin

et al. 2024

Sci Rep

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Insulin has been shown to modulate neuronal processes through insulin receptors. The ion channels located on neurons may be important targets for insulin/insulin receptor signaling. Both insulin receptors and acid-sensing ion channels (ASICs) are expressed in dorsal root ganglia (DRG) neurons. However, it is still unclear whether there is an interaction between them. Therefore, the purpose of this investigation was to determine the effects of insulin on the functional activity of ASICs. A 5 min application of insulin rapidly enhanced acid-evoked ASIC currents in rat DRG neurons in a concentration-dependent manner. Insulin shifted the concentration-response plot for ASIC currents upward, with an increase of 46.2 ± 7.6% in the maximal current response. The insulin-induced increase in ASIC currents was eliminated by the insulin receptor antagonist GSK1838705, the tyrosine kinase inhibitor lavendustin A, and the phosphatidylinositol-3 kinase antagonist wortmannin. Moreover, insulin increased the number of acid-triggered action potentials by activating insulin receptors. Finally, local administration of insulin exacerbated the spontaneous nociceptive behaviors induced by intraplantar acid injection and the mechanical hyperalgesia induced by intramuscular acid injections through peripheral insulin receptors. These results suggested that insulin/insulin receptor signaling enhanced the functional activity of ASICs via tyrosine kinase and phosphatidylinositol-3 kinase pathways. Our findings revealed that ASICs were targets in primary sensory neurons for insulin receptor signaling, which may underlie insulin modulation of pain.

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The insulin receptor is differentially expressed in somatic and visceral primary sensory neurons

Cited by 4 publications

References 44 publications

Modulation of Sensory Nerve Function by Insulin: Possible Relevance to Pain, Inflammation and Axon Growth

Modulation of Sensory Nerve Function by Insulin: Possible Relevance to Pain, Inflammation and Axon Growth

Insulin Confers Differing Effects on Neurite Outgrowth in Separate Populations of Cultured Dorsal Root Ganglion Neurons: The Role of the Insulin Receptor

Insulin enhances acid-sensing ion channel currents in rat primary sensory neurons

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