Dataset Information

Role of ?-adrenergic signaling in masseter muscle.

ABSTRACT: In skeletal muscle, the major isoform of ?-adrenergic receptor (?-AR) is ?2-AR and the minor isoform is ?1-AR, which is opposite to the situation in cardiac muscle. Despite extensive studies in cardiac muscle, the physiological roles of the ?-AR subtypes in skeletal muscle are not fully understood. Therefore, in this work, we compared the effects of chronic ?1- or ?2-AR activation with a specific ?1-AR agonist, dobutamine (DOB), or a specific ?2-AR agonist, clenbuterol (CB), on masseter and cardiac muscles in mice. In cardiac muscle, chronic ?1-AR stimulation induced cardiac hypertrophy, fibrosis and myocyte apoptosis, whereas chronic ?2-AR stimulation induced cardiac hypertrophy without histological abnormalities. In masseter muscle, however, chronic ?1-AR stimulation did not induce muscle hypertrophy, but did induce fibrosis and apoptosis concomitantly with increased levels of p44/42 MAPK (ERK1/2) (Thr-202/Tyr-204), calmodulin kinase II (Thr-286) and mammalian target of rapamycin (mTOR) (Ser-2481) phosphorylation. On the other hand, chronic ?2-AR stimulation in masseter muscle induced muscle hypertrophy without histological abnormalities, as in the case of cardiac muscle, concomitantly with phosphorylation of Akt (Ser-473) and mTOR (Ser-2448) and increased expression of microtubule-associated protein light chain 3-II, an autophagosome marker. These results suggest that the ?1-AR pathway is deleterious and the ?2-AR is protective in masseter muscle. These data should be helpful in developing pharmacological approaches for the treatment of skeletal muscle wasting and weakness.

SUBMITTER: Ito A

PROVIDER: S-EPMC6464212 | biostudies-literature | 2019

REPOSITORIES: biostudies-literature

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Role of β-adrenergic signaling in masseter muscle.

Ito Aiko A Ohnuki Yoshiki Y Suita Kenji K Ishikawa Misao M Mototani Yasumasa Y Shiozawa Kouichi K Kawamura Naoya N Yagisawa Yuka Y Nariyama Megumi M Umeki Daisuke D Nakamura Yoshiki Y Okumura Satoshi S

PloS one 20190415 4

In skeletal muscle, the major isoform of β-adrenergic receptor (β-AR) is β2-AR and the minor isoform is β1-AR, which is opposite to the situation in cardiac muscle. Despite extensive studies in cardiac muscle, the physiological roles of the β-AR subtypes in skeletal muscle are not fully understood. Therefore, in this work, we compared the effects of chronic β1- or β2-AR activation with a specific β1-AR agonist, dobutamine (DOB), or a specific β2-AR agonist, clenbuterol (CB), on masseter and card ...[more]

PMID: 30986276

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Project description:BACKGROUND: The phenotype of large diameter sensory afferent neurons changes in several models of neuropathic pain. We asked if similar changes also occur in "functional" pain syndromes. METHODOLOGY/PRINCIPAL FINDINGS: Acidic saline (AS, pH 4.0) injections into the masseter muscle were used to induce persistent myalgia. Controls received saline at pH 7.2. Nocifensive responses of Experimental rats to applications of Von Frey Filaments to the masseters were above control levels 1-38 days post-injection. This effect was bilateral. Expression of c-Fos in the Trigeminal Mesencephalic Nucleus (NVmes), which contains the somata of masseter muscle spindle afferents (MSA), was above baseline levels 1 and 4 days after AS. The resting membrane potentials of neurons exposed to AS (n = 167) were hyperpolarized when compared to their control counterparts (n = 141), as were their thresholds for firing, high frequency membrane oscillations (HFMO), bursting, inward and outward rectification. The amplitude of HFMO was increased and spontaneous ectopic firing occurred in 10% of acid-exposed neurons, but never in Controls. These changes appeared within the same time frame as the observed nocifensive behaviour. Ectopic action potentials can travel centrally, but also antidromically to the peripheral terminals of MSA where they could cause neurotransmitter release and activation of adjacent fibre terminals. Using immunohistochemistry, we confirmed that annulospiral endings of masseter MSA express the glutamate vesicular transporter VGLUT1, indicating that they can release glutamate. Many capsules also contained fine fibers that were labelled by markers associated with nociceptors (calcitonin gene-related peptide, Substance P, P2X3 receptors and TRPV1 receptors) and that expressed the metabotropic glutamate receptor, mGluR5. Antagonists of glutamatergic receptors given together with the 2(nd) injection of AS prevented the hypersensitivity observed bilaterally but were ineffective if given contralaterally. CONCLUSIONS/SIGNIFICANCE: Low pH leads to changes in several electrical properties of MSA, including initiation of ectopic action potentials which could propagate centrally but could also invade the peripheral endings causing glutamate release and activation of nearby nociceptors within the spindle capsule. This peripheral drive could contribute both to the transition to, and maintenance of, persistent muscle pain as seen in some "functional" pain syndromes.

Dataset Information

Role of ?-adrenergic signaling in masseter muscle.

Publications

Role of β-adrenergic signaling in masseter muscle.

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