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The aim of this study was to elucidate the mechanisms responsible for the effects of innervation on the maturation of excitation-contraction coupling apparatus in human skeletal muscle. For this purpose, we compared the establishment of the excitation-contraction coupling mechanism in myotubes differentiated in four different experimental paradigms: 1) aneurally cultured, 2) cocultured with fetal rat spinal cord explants, 3) aneurally cultured in medium conditioned by cocultures, and 4) aneurally cultured in medium supplemented with purified recombinant chick neural agrin. [Ca.sup.2+] imaging indicated that coculturing human muscle cells with rat spinal cord explants increased the fraction of cells showing a functional excitation-contraction coupling mechanism. The effect of spinal cord explants was mimicked by treatment with medium conditioned by cocultures or by addition of 1 nM of recombinant neural agrin to the medium. The treatment with neural agrin increased the number of human muscle cells in which functional ryanodine receptors (RyRs) and dihydropyridine-sensitive L-type [Ca.sup.2+] channels were detectable. Our data are consistent with the hypothesis that agrin, released from neurons, controls the maturation of the excitation-contraction coupling mechanism and that this effect is due to modulation of both RyRs and L-type [Ca.sup.2+] channels. Thus, a novel role for neural agrin in skeletal muscle maturation is proposed. neurotrophic factor; calcium homeostasis; differentiation; skeletal muscle

The release of glutamate by hippocampal neurons by a calcium dependent mechanism is independent of the formation and maturation of synaptic contacts. The exocytic-endocytic recycling of synaptic vesicles is Ca2+ dependent. In the development stages, the omega-agatoxin IVA- and omega-conotoxin GVIA control the secretion of neurotransmitter, glutamate. A change in the subtype of calcium channels is directed by the neuronal differentiation and synaptic contacts maturation.

A study of nerve cell model shows that the calcium ion (Ca2+) waves interact with the plasma membrane and contributes to the overall excitability and differential processing of inputs and electrochemical computations in nerve cell. Ca2+ waves run bidirectionally in PC12 cells and are differentiated by treatment with NGF depending on the stimulus along the thin neurites and the distribution along the InsP3 Ca2+ stores.

Emerging evidence highlights the several roles that meninges play in relevant brain functions as they are a protective membrane for the brain, produce and release several trophic factors important for neural cell migration and survival, control cerebrospinal fluid dynamics, and embrace numerous immune interactions affecting neural parenchymal functions. Furthermore, different groups have identified subsets of neural progenitors residing in the meninges during development and in the adulthood in different mammalian species, including humans. Interestingly, these immature neural cells are able to migrate from the meninges to the neural parenchyma and differentiate into functional cortical neurons or oligodendrocytes. Immature neural cells residing in the meninges promptly react to brain disease. Injury-induced expansion and migration of meningeal neural progenitors have been observed following experimental demyelination, traumatic spinal cord and brain injury, amygdala lesion, stroke, and progressive ataxia. In this review, we summarize data on the function of meninges as stem cell niche and on the presence of immature neural cells in the meninges, and discuss their roles in brain health and disease. Furthermore, we consider the potential exploitation of meningeal neural progenitors for the regenerative medicine to treat neurological disorders. [ABSTRACT FROM AUTHOR]