ATP decreases mechanical sensitivity of muscle thin-fiber afferents in rats

Matsuda, Teru; Kubo, Asako; Taguchi, Toru; Mizumura, Kazue

doi:10.1016/j.neures.2015.04.001

Cited by 5 publications

(5 citation statements)

References 28 publications

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“…Consistent with previous studies (Matsuda et al 2015;Hotta et al 2019), we confirmed that I.M. administration of the control solution did not affect mechanical responsiveness.…”

Section: Muscle-nerve Preparationsupporting

confidence: 92%

“…, ; Matsuda et al . ). These two characteristics form the rationale for assessing group IV muscle afferent responsiveness in the present study.…”

Section: Methodsmentioning

confidence: 97%

“…Although group IV afferent fibres are generally more metabolically-sensitive and group III fibres more mechanically-sensitive Jankowski et al 2013), group IV fibres are polymodal in nature with many similarly responding to mechanical stimuli (Kumazawa & Mizumura, 1977). Moreover, group IV fibres are plentiful and more easily identified in the preparation utilized (Taguchi et al 2005;Hotta et al 2015Hotta et al , 2019Matsuda et al 2015). These two characteristics form the rationale for assessing group IV muscle afferent responsiveness in the present study.…”

Section: Figure 1 Local Application Of Control Solution Did Not Chanmentioning

confidence: 94%

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Insulin potentiates the response to mechanical stimuli in small dorsal root ganglion neurons and thin fibre muscle afferents in vitro

Hotta

Katanosaka

Mizumura

et al. 2019

The Journal of Physiology

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Key points Insulin is known to activate the sympathetic nervous system centrally. A mechanical stimulus to tissues activates the sympathetic nervous system via thin fibre afferents. Evidence suggests that insulin modulates putative mechanosensitive channels in the dorsal root ganglion neurons of these afferents. In the present study, we report the novel finding that insulin augments the mechanical responsiveness of thin fibre afferents not only at dorsal root ganglion, but also at muscle tissue levels. Our data suggest that sympathoexcitation is mediated via the insulin‐induced mechanical sensitization peripherally. The present study proposes a novel physiological role of insulin in the regulation of mechanical sensitivity in somatosensory thin fibre afferents. Abstract Insulin activates the sympathetic nervous system, although the mechanism underlying insulin‐induced sympathoexcitation remains to be determined. A mechanical stimulus to tissues such as skin and/or skeletal muscle, no matter whether the stimulation is noxious or not, activates the sympathetic nervous system via thin fibre afferents. Evidence suggests that insulin modulates putative mechanosensitive channels in the dorsal root ganglion (DRG) neurons of these afferents. Accordingly, we investigated whether insulin augments whole‐cell current responses to mechanical stimuli in small DRG neurons of normal healthy mice. We performed whole‐cell patch clamp recordings using cultured DRG neurons and observed mechanically‐activated (MA) currents induced by mechanical stimuli applied to the cell surface. Local application of vehicle solution did not change MA currents or mechanical threshold in cultured DRG neurons. Insulin (500 mU mL−1) significantly augmented the amplitude of MA currents (P < 0.05) and decreased the mechanical threshold (P < 0.05). Importantly, pretreatment with the insulin receptor antagonist, GSK1838705, significantly suppressed the insulin‐induced potentiation of the mechanical response. We further examined the impact of insulin on thin fibre muscle afferent activity in response to mechanical stimuli in normal healthy rats in vitro. Using a muscle–nerve preparation, we recorded single group IV fibre activity to a ramp‐shaped mechanical stimulation. Insulin significantly decreased mechanical threshold (P < 0.05), although it did not significantly increase the response magnitude to the mechanical stimulus. In conclusion, these data suggest that insulin augments the mechanical responsiveness of small DRG neurons and potentially sensitizes group IV afferents to mechanical stimuli at the muscle tissue level, possibly contributing to insulin‐induced sympathoexcitation.

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“…Consistent with previous studies (Matsuda et al 2015;Hotta et al 2019), we confirmed that I.M. administration of the control solution did not affect mechanical responsiveness.…”

Section: Muscle-nerve Preparationsupporting

confidence: 92%

“…, ; Matsuda et al . ). These two characteristics form the rationale for assessing group IV muscle afferent responsiveness in the present study.…”

Section: Methodsmentioning

confidence: 97%

Section: Figure 1 Local Application Of Control Solution Did Not Chanmentioning

confidence: 94%

See 1 more Smart Citation

Insulin potentiates the response to mechanical stimuli in small dorsal root ganglion neurons and thin fibre muscle afferents in vitro

Hotta

Katanosaka

Mizumura

et al. 2019

The Journal of Physiology

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“…An earlier study demonstrated that almost 70% of group IV afferents are activated by local mechanical stimulation to the muscle (Bernardi & Neto, 1979). In addition, practically speaking, group IV fibres are more easily accessible and numerous compared to group III fibres (Hotta et al., 2015; Hotta, Kubo et al., 2019; Matsuda et al., 2015; Taguchi et al., 2005). For example, given a total of 1480 afferents from a previous study, there were ∼144 group Ia, 72 group Ib, 155 group II, 110 group III, and ∼1300 group IV units (Mitchell & Schmidt, 1983).…”

Section: Discussionmentioning

confidence: 99%

Antagonism of TRPV4 channels partially reduces mechanotransduction in rat skeletal muscle afferents

Fukazawa

Hori

Hotta

et al. 2023

The Journal of Physiology

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“…Upon cell damage and inflammation [18] high extracellular levels of ATP may induce purinergic signaling [19] and contribute to muscle pain [6, 20, 21]. In the rat ATP at concentrations present in muscle cells activated the majority of unmyelinated nociceptive and non-nociceptive afferent fibres [22] but high concentrations of ATP may decrease mechanical sensitivity of thin muscle afferents [23]. …”

Section: Introductionmentioning

confidence: 99%

ATP-sensitive muscle afferents activate spinal trigeminal neurons with meningeal afferent input in rat – pathophysiological implications for tension-type headache

et al. 2016

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BackgroundTension-type headache and other primary headaches may be triggered or aggravated by disorders of pericranial muscles, which is possibly due to convergent or collateral afferent input from meningeal and muscular receptive areas. In rodent models high extracellular concentrations of ATP caused muscle nociception and central sensitization of second order neurons. In a rat model of meningeal nociception we asked if spinal trigeminal activity induced by ATP can be modulated by local anaesthesia of distinct muscles.MethodsOngoing activity was recorded from spinal trigeminal neurons with afferent input from the cranial dura mater, the temporal muscle and neck muscles. The stable ATP analogue α,β-methylene adenosine 5′-triphosphate (α,β-meATP, 10 mM) was injected into the ipsilateral temporal muscle, 30 min later followed by injection of local anaesthetics (lidocaine, 2 %) into the ipsilateral neck muscles and/or the temporal muscle.ResultsInjection of α,β-meATP into the temporal muscle caused progressive increase in ongoing activity of most of the spinal trigeminal neurons within 30 min. Injection of lidocaine into the neck muscles and/or the temporal muscle reduced this activation to previous levels within 10 min.ConclusionsDistinct spinal trigeminal neurons processing meningeal nociceptive information are under the control of convergent afferent input from several pericranial muscles. Blockade of at least one of these inputs can normalize central trigeminal activity. This may explain why therapeutic manipulations of head muscles can be beneficial in primary headaches.

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ATP decreases mechanical sensitivity of muscle thin-fiber afferents in rats

Cited by 5 publications

References 28 publications

Insulin potentiates the response to mechanical stimuli in small dorsal root ganglion neurons and thin fibre muscle afferents in vitro

Insulin potentiates the response to mechanical stimuli in small dorsal root ganglion neurons and thin fibre muscle afferents in vitro

Antagonism of TRPV4 channels partially reduces mechanotransduction in rat skeletal muscle afferents

ATP-sensitive muscle afferents activate spinal trigeminal neurons with meningeal afferent input in rat – pathophysiological implications for tension-type headache

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