Effects of aging on sarcoplasmic reticulum function and contraction duration in skeletal muscles of the rat

Narayanan, Njanoor; Jones, Douglas L.; Xu, A.; Yu, Jingcheng

doi:10.1152/ajpcell.1996.271.4.c1032

Cited by 77 publications

(70 citation statements)

References 29 publications

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“…Here we find that GH chronic treatment ameliorates the contractile function in aged skeletal muscle fibres by shifting the rheobase towards more positive values, typical of adults. This effect may be related to the GHinduced production of muscle insulin-like growth factor-1 (IGF-1), which in turn normalises intracellular Ca 2+ level by the restoration of the expression, turnover and activity of proteins involved in the contractile machinery (Narayanan et al, 1996;Renganathan et al, 1997;Ferrington et al, 1998;Wang et al, 1999). We also confirm the efficacy of longterm GH administration in the restoration of gCl and gK (De Luca et al, 1997).…”

Section: S Pierno Et Alsupporting

confidence: 67%

Growth hormone secretagogues modulate the electrical and contractile properties of rat skeletal muscle through a ghrelin‐specific receptor

Pierno

Desaphy

et al. 2003

British J Pharmacology

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1 Growth hormone secretagogues (GHS) exhibit potent growth hormone (GH)-releasing activity through the activation of a pituitary receptor. Here, we consider the possibility that GHS can target a specific receptor in rat skeletal muscle and have a role in the control of muscle function. 2 By means of the intracellular microelectrode technique, we found that in vitro application of hexarelin and L-163,255 dose dependently reduced resting chloride (gCl) and potassium (gK) conductances in rat skeletal muscle. These effects were prevented by the GHS-receptor antagonist [DLys-3]-GHRP-6, and by either phospholipase C or protein kinase C (PKC) inhibitors. Ghrelin, a natural ligand of GHS receptors, also induced a reduction of muscle gCl and gK, which was antagonised by [D-Lys-3]-GHRP-6. 3 Both GHS shifted the mechanical threshold for the contraction of muscle fibres towards more negative voltages. Accordingly, by means of FURA-2 fluorescent measurements, we demonstrated that L-163,255 induced a resting [Ca 2+ ] i increase, which was reversible and not blocked by nifedipine or removal of external Ca 2+ . 4 Ageing is a condition characterised by a deficit of GH secretion, which in turn modifies the electrical and contractile properties of skeletal muscle. In contrast to GH, chronic treatment of aged rats with hexarelin or L-163,255 failed to restore the electrical and contractile muscle properties. Moreover, the two GHS applied in vitro were able to antagonise the beneficial effect on gCl and gK obtained through chronic treatment of aged animals with GH. 5 Thus, skeletal muscle expresses a specific GHS receptor able to decrease gCl and gK through a PKC-mediated intracellular pathway. This peripheral action may account for the lack of restoration of skeletal muscle function in long-term GHS-treated aged animals.

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Section: S Pierno Et Alsupporting

confidence: 67%

Growth hormone secretagogues modulate the electrical and contractile properties of rat skeletal muscle through a ghrelin‐specific receptor

Pierno

Desaphy

et al. 2003

British J Pharmacology

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“…Shin, et al demonstrated that in skeletal muscle CSQ is also involved in retrograde regulation of RyR function and store-operated Ca 2+ entry (SOCE) (Shin et al, 2003). Additional evidence is available that CSQ function is altered during muscle aging (Narayanan et al, 1996;Margreth et al, 1999). Thus, changes in the SR luminal Ca 2+ buffering capacity, or modification of the RyR release machinery from the luminal side, certainly plays an important role in the retrograde regulation of Ca 2+ signaling in striated muscle Brochet et al, 2005).…”

Section: Differential Properties Of Ca 2+ Sparks In Cardiac and Skelementioning

confidence: 99%

Altered Ca2+ sparks in aging skeletal and cardiac muscle

Weisleder

2008

Ageing Research Reviews

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Ca 2+ sparks are the fundamental units that comprise Ca 2+ -induced Ca 2+ release (CICR) in striated muscle cells. In cardiac muscle, spontaneous Ca 2+ sparks underlie the rhythmic CICR activity during heart contraction. In skeletal muscle, Ca 2+ sparks remain quiescent during the resting state and are activated in a plastic fashion to accommodate various levels of stress. With aging, the plastic Ca 2+ spark signal becomes static in skeletal muscle, whereas loss of CICR control leads to leaky Ca 2+ spark activity in aged cardiomyocytes. Ca 2+ spark responses reflect the integrated function of the intracellular Ca 2+ regulatory machinery centered around the triad or dyad junctional complexes of striated muscles, which harbor the principal molecular players of excitation-contraction coupling. This review highlights the contribution of age-related modification of the Ca 2+ release machinery and the effect of membrane structure and membrane cross-talk on the altered Ca 2+ spark signaling during aging of striated muscles.

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“…For example, a loss in the rate of calcium uptake activity (30-50%) in SR enriched vesicles has been observed that correlates with the extent (40%) of increase in relaxation times (147,(149)(150)(151)(152)(153).…”

Section: Aging In Skeletal Musclementioning

confidence: 99%

“…The few studies that have addressed possible alterations in expression levels of both RyR and DHPRs in senescent skeletal muscle report no age-related changes in receptor density based on either antibody detection by Western blots or binding of radioactive ligand, i.e., ryanodine or the dihydropyridine, PN-200-110 (143,146,147). However, another study suggested a preferential loss of DHPR density that resulted in an overall loss of DHPR: RyR coupling (148).…”

Section: Aging In Skeletal Musclementioning

confidence: 99%