title: Barnacle muscle: Ca2+, activation and mechanics.
abstract: In this review, aspects of the ways in which Ca2+ is transported and regulated within muscle cells have been considered, with particular reference to crustacean muscle fibres. The large size of these fibres permits easy access to the internal environment of the cell, allowing it to be altered by microinjection or microperfusion. At rest, Ca2+ is not in equilibrium across the cell membrane, it enters the cell down a steep electrochemical gradient. The free [Ca2+] at rest is maintained at a value close to 200 nM by a combination of internal buffering systems, mainly the SR, mitochondria, and the fixed and diffusible Ca(2+)-binding proteins, as well as by an energy-dependent extrusion system operating across the external cell membrane. This system relies upon the inward movement of Na+ down its own electrochemical gradient to provide the energy for the extrusion of Ca2+ ions. As a result of electrical excitation, voltage-sensitive channels for Ca2+ are activated and permit Ca2+ to enter the cell more rapidly than at rest. It has been possible to determine both the amount of Ca2+ entering by this step, and what part this externally derived Ca2+ plays in the development of force as well as in the free Ca2+ change. The latter can be determined directly by Ca(2+)-sensitive indicators introduced into the cell sarcoplasm. A combination of techniques, allowing both the total and free Ca2+ changes to be assessed during electrical excitation, has provided valuable information as to how muscle cells buffer their Ca2+ in order to regulate the extent of the change in the free Ca2+ concentration. The data indicate that the entering Ca2+ can only make a small direct contribution to the force developed by the cell. The implication here is that the major source of Ca2+ for contraction must be derived from the internal Ca2+ storage sites within the SR system, a view reinforced by caged Ca2+ methods. The ability to measure the free Ca2+ concentration changes within a single cell during activation has also provided the opportunity to analyse, in detail, the likely relations between free Ca2+ and the process of force development in muscle. The fact that the free Ca2+ change precedes the development of force implies that there are delays in the mechanism, either at the site of Ca2+ attachment on the myofibril, or at some later stage in the process of force development that were not previously anticipated.(ABSTRACT TRUNCATED AT 400 WORDS)
authors.affiliation: University Laboratory of Physiology, Oxford, England, UK.
authors.forename: C C
authors.initials: CC
authors.lastname: Ashley
authors.forename: P J
authors.initials: PJ
authors.lastname: Griffiths
authors.forename: T J
authors.initials: TJ
authors.lastname: Lea
authors.forename: I P
authors.initials: IP
authors.lastname: Mulligan
authors.forename: R E
authors.initials: RE
authors.lastname: Palmer
authors.forename: S J
authors.initials: SJ
authors.lastname: Simnett
mesh_terms: D000818:Animals; D002118:Calcium / Q000378:metabolism*; D009119:Muscle Contraction / Q000502:physiology*; D009132:Muscles / Q000378:metabolism*; D001468:Thoracica / Q000378:metabolism / Q000502:physiology*
chemical_list: D002118:Calcium