External calcium dependence of extensor digitorum longus muscle contractility during bupivacaine-induced regeneration

Abstract

The effect of the intramuscular injection of bupivacaine hydrochloride on selected morphological characteristics and contractile properties of adult rat extensor digitorum longus muscle was studied. Recovery of normal fiber size was already present 30 days after bupivacaine injection and at 90 days after injection, values of the normalized twitch tension (mN/mg of tissue) and of the fatigue index approached those measured in control muscle, whereas the normalized tetanic tension remained 57% of control. At 7–30 days postinjection, twitch force was decreased by reducing [Ca2+]0 (substituted by Mg2+) or adding Co2+ (5 mmol/L−1). By contrast, potentiation of the twitch was recorded in the presence of Cd2+ (2 mmol/L−1). Glycerol treatment only reduced, but did not eliminate, twitches developed by muscles 7 days after injection. Present results emphasize the importance of the recovery process in the loss of the susceptibility of the contractile responses to extracellular calcium in bupivacaine‐injected muscles. These data may be of interest in the evaluation of functional aspects of muscles in which injections of viral vector or autologous myoblasts have been performed. © 1996 John Wiley & Sons, Inc.

External Ca2+‐dependent excitation–contraction coupling in a population of ageing mouse skeletal muscle fibres

“…If ageing causes a subunit switch from α1 S to α1 C similar to regenerating skeletal muscle (Pereon et al 1997 a ), DHPR–RyR coupling would become cardiac‐like (dependent upon influx of external Ca 2+ ions) similar to regenerating skeletal muscle (Louboutin et al 1995, 1996; Pereon et al 1997 b ). In this case, the absence of external Ca 2+ would prevent Ca 2+ influx through the α1 C to trigger CICR from the RyR1.…”

“…This splice variant has been found in adult human skeletal muscle at levels at or below 10% of total DHPR transcripts. However, in myotubes regenerating from human satellite cells – a condition known to induce Ca 2+ ‐dependent EC coupling (Louboutin et al 1995, 1996; Pereon et al 1997 a ) – this 19 amino acid deletion transcript has been found to make up more than 66% of total DHPR transcript (K. Jurkat‐Rott and F. Lehmann‐Horn, personal communication). The functional significance of this splice variant and its expression level in ageing muscle have not yet been examined.…”

“…Ca 2+ ‐dependent EC coupling in developing muscle could also be due to transient expression of RyR3 (Flucher et al 1999; Chun et al 2003) or RyR1 splice variants (Futatsugi et al 1995) or a combination of all these different isoforms, together allowing the RyR to be responsive to Ca 2+ influx through the DHPR at normal cytoplasmic Mg 2+ concentrations. Regenerating skeletal muscle, which goes through many stages similar to developing skeletal muscle, is at least partially dependent on external Ca 2+ for effective EC coupling and contraction (Louboutin et al 1995, 1996; Pereon et al 1997 a ). This is also presumably due to the transient expression of α1 C during the regeneration period (Pereon et al 1997 a ).…”

Effects of aging on thyroarytenoid muscle regeneration

“…BPVC is a myotoxic agent that induces acute muscle fiber degeneration, presumably by binding to sarcolemma and affecting Ca ++ uptake 16, 43, 44. The muscle injury caused by BPVC is transient and followed by rapid, near‐complete recovery of the muscle tissue 45, 46. The satellite cell population, basal lamina, peripheral nerves and blood supply are preserved, all of which are essential for successful muscle regeneration 43, 44, 47.…”

Pannexin 1 channels in skeletal muscles

“…In the latter, Ca 2+ uptake depends on the activation of purinergic ionotropic P2X 4 receptors (Sandonà et al, 2005), which are highly expressed in this type of muscle. For fast twitch muscles, the potentiation response is independent of the extracellular Ca 2+ concentration (Louboutin et al, 1996), but requires extracellular ATP. Accordingly, extracellular ATPases inhibit the potentiation response (Sandonà et al, 2005) and, together with the absence of P2X receptors, have led to suggest that the potentiation response in these muscles is mediated by activation of metabotropic P2 receptors as P2Y 1 receptors (Riquelme et al, 2013).…”