PubMed · 11779748
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M Corr, N J Zvaifler. 2002. Mesenchymal precursor cells.. https://doi.org/10.1136/ard.61.1.3
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Most vertebrate muscles are composed of a mixture of fiber types. However, studies of muscle mechanics have concentrated on homogeneous bundles of fibers. Hindlimb muscles of the tiger salamander, Ambystoma tigrinum, present an excellent system to explore the consequences of fiber heterogeneity. Isometric twitches and work loops were obtained in vitro from two muscles, the m. iliotibialis pars posterior (heterogeneous, containing types I, IIa and IIb fibers) and the m. iliofibularis (nearly homogeneous for type IIa fibers). Maximal isometric twitch and tetanic stresses in m. iliotibialis posterior were significantly greater than in iliofibularis. Work loops were obtained over a range of frequencies (0.5-3.0 Hz) and strains (2-6% muscle length) that encompassed the observed ranges in vivo. Work per cycle from the homogeneous iliofibularis declined from 1.5-3.0 Hz, while that from the heterogeneous m. iliotibialis posterior increased from 0.5 Hz to 2.5 Hz and declined at 3.0 Hz. Power output from the iliofibularis rose with frequency to at least 3 Hz; power from the iliotibialis posterior rose with frequency to 2.5 Hz and declined thereafter. Mass-specific work per cycle and power output were higher in iliofibularis than iliotibialis posterior over most frequencies and strains tested.
In response to retinal disease and injury, the axon terminals of rod photoreceptors demonstrate dramatic structural plasticity, including axonal retraction, neurite extension, and the development of presynaptic varicosities. Cone cell terminals, however, are relatively inactive. Similar events are observed in primary cultures of salamander photoreceptors. To investigate the mechanisms underlying these disparate presynaptic responses, antagonists to voltage-gated L-type and cGMP-gated channels, known to be present on rod and cone cell terminals, respectively, were used to block calcium influx during critical periods of plasticity in vitro. In rod cells, L-type channel antagonists nicardipine and verapamil inhibited not only the outgrowth of processes and the formation of varicosities, but also the synthesis of vesicle proteins, SV2 and synaptophysin. In contrast, the synthesis of opsin in rod cells was unaffected. In cone cells, L-type channel antagonists caused only modest changes. However, cobalt bromide, which blocks all calcium channels, and l-cis-diltiazem, a potent antagonist of cGMP-gated channels, significantly inhibited varicosity formation and synthesis of SV2 in cone cells. Moreover, the cGMP-gated channel agonist 8-bromo-cGMP caused a significant increase in varicosity formation by cone but not rod cells. Thus voltage-gated L-type channels in rod cells and cGMP-gated channels in cone cells are the primary calcium channels required for structural plasticity and the accompanying upregulation of synaptic vesicle synthesis. The differing responses of rod and cone terminals to injury and disease may be determined by these differences in the regulation of Ca2+ influx.
Changes in fluorescence were measured with an argon ion laser from the outer segments of isolated salamander rods containing the Ca(2+)-sensitive fluorescent dye fluo-5F. When the outer segments were exposed to a 0Ca(2+)/0Na(+) solution designed to minimise surface membrane Ca(2+) fluxes, exposure to intense light from the laser evoked a slow increase in fluorescence, reflecting a light-induced rise in outer segment [Ca(2+)](i). The time course of this slow fluorescence rise could be fitted with the sum of two asymptotic exponential functions of approximately equal amplitude, having time constants of approximately 200 ms and 5.7 s. When rods were exposed to saturating background light to reduce outer segment [Ca(2+)](i) before laser illumination, the relative amplitude of the two exponentials was altered so as to reduce the contribution from the one with the shorter time constant. Examination of the initial time course of fluorescence when recording at high temporal resolution revealed a further rapid rise with a time constant of 1-2 ms, which could be observed even from rods in Ringer solution. This initial rapid rise could be abolished by pre-exposing the rod to bleaching illumination, whether the bleach was given in Ringer solution or in 0Ca(2+)/0Na(+) solution. It would therefore appear that the rapid rise in fluorescence is generated in some way by the bleaching of the photopigment. Unlike the slower components of fluorescence increase, the rapid initial rise was virtually unaffected in waveform or amplitude when rods were pre-exposed in Ringer solution to light which was bright enough to suppress completely the circulating current but which bleached a negligible fraction of the photopigment. Furthermore, pre-incubation with the AM ester of the Ca(2+) chelator BAPTA, although completely abolishing the slower components of fluorescence increase, had virtually no effect on the rapid rise. These results indicate that the rapid component, though triggered by rhodopsin bleaching, does not reflect an increase in outer segment [Ca(2+)](i). Neither the rapid nor the slower components of fluorescence increase were affected by exposure of the outer segment to 10 microM of the membrane-permeant compound N,N,N',N'-tetrakis(2-pyridyl-methyl)ethylenediamine (TPEN), which chelates heavy metals such as Zn(2+), or 100 microM 2-aminoethoxydiphenylborate (2-APB), a membrane-permeant blocker of IP(3) receptors. These results appear to exclude a role for changes in heavy metal concentration or Ca(2+) release via IP(3) receptors in the light-induced increases in dye fluorescence. Estimates of absolute Ca(2+) concentration and of rod buffering capacity suggest that the slower components of fluorescence increase represent the release of around 10-50 micromoles Ca(2+) per litre cytoplasmic volume from bound or sequestered stores after bleaching.