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Mariana Casas - One of the best experts on this subject based on the ideXlab platform.

  • cav1 1 controls atp release to elicit gene expression in adult Muscle Fibers 1164 12
    The FASEB Journal, 2014
    Co-Authors: Gonzalo Jorquera, Denisse Valladares, Bruno Allard, Vincent Jacquemond, Enrique Jaimovich, Mariana Casas
    Abstract:

    In adult Muscle Fibers, Cav1.1 acts as voltage sensor for both excitation-contraction coupling and the activation of a signaling cascade that regulates gene expression. We have shown that ATP is released through pannexin-1 channels after electrical stimulation at 20 Hz, having a key role in the induction of transcriptional changes related to fast-to-Slow Muscle Fiber phenotype transition. Myotubes lacking the Cav1.1α1 subunit displayed almost no ATP release after electrical stimulation. ATP release and gene transcription was also altered in adult Muscle Fibers knock-down for Cav1.1α1. In dystrophic Fibers, there was also an increase in basal ATP release, but a default in the stimulation-dependent increase in ATP release and transcription activation observed in control Fibers. This can be interpreted as uncoupling between electrical stimulation and ATP release in dystrophic Muscles. All these data suggest that Cav1.1 controls ATP release trough Pannexin-1 channels, activating it after low stimulation frequ...

  • Cav1.1 controls frequency-dependent events regulating adult skeletal Muscle plasticity.
    Journal of Cell Science, 2013
    Co-Authors: Gonzalo Jorquera, Vincent Jacquemond, Enrique Jaimovich, Francisco Altamirano, Ariel Contreras-ferrat, Gonzalo Almarza, Sonja Buvinic, Mariana Casas
    Abstract:

    An important pending question in neuromuscular biology is how skeletal Muscle cells decipher the stimulation pattern coming from motoneurons to define their phenotype as Slow or fast twitch Muscle Fibers. We have previously shown that voltage-gated L-type calcium channel (Cav1.1) acts as a voltage sensor for activation of inositol (1,4,5)-trisphosphate [Ins(1,4,5)P₃]-dependent Ca(2+) signals that regulates gene expression. ATP released by Muscle cells after electrical stimulation through pannexin-1 channels plays a key role in this process. We show now that stimulation frequency determines both ATP release and Ins(1,4,5)P₃ production in adult skeletal Muscle and that Cav1.1 and pannexin-1 colocalize in the transverse tubules. Both ATP release and increased Ins(1,4,5)P₃ was seen in flexor digitorum brevis Fibers stimulated with 270 pulses at 20 Hz, but not at 90 Hz. 20 Hz stimulation induced transcriptional changes related to fast-to-Slow Muscle Fiber phenotype transition that required ATP release. Addition of 30 µM ATP to Fibers induced the same transcriptional changes observed after 20 Hz stimulation. Myotubes lacking the Cav1.1-α1 subunit released almost no ATP after electrical stimulation, showing that Cav1.1 has a central role in this process. In adult Muscle Fibers, ATP release and the transcriptional changes produced by 20 Hz stimulation were blocked by both the Cav1.1 antagonist nifedipine (25 µM) and by the Cav1.1 agonist (-)S-BayK 8644 (10 µM). We propose a new role for Cav1.1, independent of its calcium channel activity, in the activation of signaling pathways allowing Muscle Fibers to decipher the frequency of electrical stimulation and to activate specific transcriptional programs that define their phenotype.

  • cav1 1 controls atp release in adult Muscle Fibers
    Biophysical Journal, 2013
    Co-Authors: Gonzalo Jorquera, Bruno Allard, Vincent Jacquemond, Enrique Jaimovich, C Gentil, Mariana Casas
    Abstract:

    In adult Muscle Fibers, Cav1.1 acts as voltage sensor for both excitation-contraction coupling and the activation of a signaling cascade that regulates gene expression. We have shown that ATP is released trough pannexin-1 channels after electrical stimulation at 20 Hz, having a key role in the induction of transcriptional changes related to fast-to-Slow Muscle Fiber phenotype transition. Myotubes lacking the Cav1.1-α1 subunit displayed almost no ATP release after electrical stimulation. The same was observed in adult Fibers treated with the Cav1.1 antagonist nifedipine (25µM), showing that Cav1.1 has a central role controlling ATP release.We examined the activation of this signaling cascade in Muscle Fibers where a knock-down of the α1s subunit of Cav1.1 was obtained by a U7-exon skipping strategy using adenovirus-associated viral vectors (AAV-U7delα1s).Four months after AAV-U7delα1s injection we observed a significant reduction of Cav1.1 protein as well as atrophy and fibrosis of the treated Muscles. Indo-1 Ca2+ transients and Ca2+ current in voltage-clamped Fibers isolated from FDB treated Muscles showed that the peak Ca2+ transient elicited by short depolarizing pulses was reduced by 35% whereas the maximal conductance of the Ca2+ channels was reduced by 30%. We also found increased basal ATP release with spontaneous release events. AAV-U7delα1s treated Fibers showed higher mRNA levels of the Slow isoform of Troponin I and lower mRNA levels of the fast isoform of Troponin I compared with non-treated Muscles. The transcriptional changes observed in these two genes after electrical stimulation were absent in AAV-U7delα1s treated Fibers.These results suggest that Cav1.1 controls ATP release trough Pannexin-1 channels, activating it after low stimulation frequencies and blocking ATP release during resting. The loss of this control perturbs the normal transcriptional response to electrical activity of adult Muscle Fibers.ACT1111, FONDECYT 1110467, FONDAP 15010006

Gonzalo Jorquera - One of the best experts on this subject based on the ideXlab platform.

  • cav1 1 controls atp release to elicit gene expression in adult Muscle Fibers 1164 12
    The FASEB Journal, 2014
    Co-Authors: Gonzalo Jorquera, Denisse Valladares, Bruno Allard, Vincent Jacquemond, Enrique Jaimovich, Mariana Casas
    Abstract:

    In adult Muscle Fibers, Cav1.1 acts as voltage sensor for both excitation-contraction coupling and the activation of a signaling cascade that regulates gene expression. We have shown that ATP is released through pannexin-1 channels after electrical stimulation at 20 Hz, having a key role in the induction of transcriptional changes related to fast-to-Slow Muscle Fiber phenotype transition. Myotubes lacking the Cav1.1α1 subunit displayed almost no ATP release after electrical stimulation. ATP release and gene transcription was also altered in adult Muscle Fibers knock-down for Cav1.1α1. In dystrophic Fibers, there was also an increase in basal ATP release, but a default in the stimulation-dependent increase in ATP release and transcription activation observed in control Fibers. This can be interpreted as uncoupling between electrical stimulation and ATP release in dystrophic Muscles. All these data suggest that Cav1.1 controls ATP release trough Pannexin-1 channels, activating it after low stimulation frequ...

  • Cav1.1 controls frequency-dependent events regulating adult skeletal Muscle plasticity.
    Journal of Cell Science, 2013
    Co-Authors: Gonzalo Jorquera, Vincent Jacquemond, Enrique Jaimovich, Francisco Altamirano, Ariel Contreras-ferrat, Gonzalo Almarza, Sonja Buvinic, Mariana Casas
    Abstract:

    An important pending question in neuromuscular biology is how skeletal Muscle cells decipher the stimulation pattern coming from motoneurons to define their phenotype as Slow or fast twitch Muscle Fibers. We have previously shown that voltage-gated L-type calcium channel (Cav1.1) acts as a voltage sensor for activation of inositol (1,4,5)-trisphosphate [Ins(1,4,5)P₃]-dependent Ca(2+) signals that regulates gene expression. ATP released by Muscle cells after electrical stimulation through pannexin-1 channels plays a key role in this process. We show now that stimulation frequency determines both ATP release and Ins(1,4,5)P₃ production in adult skeletal Muscle and that Cav1.1 and pannexin-1 colocalize in the transverse tubules. Both ATP release and increased Ins(1,4,5)P₃ was seen in flexor digitorum brevis Fibers stimulated with 270 pulses at 20 Hz, but not at 90 Hz. 20 Hz stimulation induced transcriptional changes related to fast-to-Slow Muscle Fiber phenotype transition that required ATP release. Addition of 30 µM ATP to Fibers induced the same transcriptional changes observed after 20 Hz stimulation. Myotubes lacking the Cav1.1-α1 subunit released almost no ATP after electrical stimulation, showing that Cav1.1 has a central role in this process. In adult Muscle Fibers, ATP release and the transcriptional changes produced by 20 Hz stimulation were blocked by both the Cav1.1 antagonist nifedipine (25 µM) and by the Cav1.1 agonist (-)S-BayK 8644 (10 µM). We propose a new role for Cav1.1, independent of its calcium channel activity, in the activation of signaling pathways allowing Muscle Fibers to decipher the frequency of electrical stimulation and to activate specific transcriptional programs that define their phenotype.

  • cav1 1 controls atp release in adult Muscle Fibers
    Biophysical Journal, 2013
    Co-Authors: Gonzalo Jorquera, Bruno Allard, Vincent Jacquemond, Enrique Jaimovich, C Gentil, Mariana Casas
    Abstract:

    In adult Muscle Fibers, Cav1.1 acts as voltage sensor for both excitation-contraction coupling and the activation of a signaling cascade that regulates gene expression. We have shown that ATP is released trough pannexin-1 channels after electrical stimulation at 20 Hz, having a key role in the induction of transcriptional changes related to fast-to-Slow Muscle Fiber phenotype transition. Myotubes lacking the Cav1.1-α1 subunit displayed almost no ATP release after electrical stimulation. The same was observed in adult Fibers treated with the Cav1.1 antagonist nifedipine (25µM), showing that Cav1.1 has a central role controlling ATP release.We examined the activation of this signaling cascade in Muscle Fibers where a knock-down of the α1s subunit of Cav1.1 was obtained by a U7-exon skipping strategy using adenovirus-associated viral vectors (AAV-U7delα1s).Four months after AAV-U7delα1s injection we observed a significant reduction of Cav1.1 protein as well as atrophy and fibrosis of the treated Muscles. Indo-1 Ca2+ transients and Ca2+ current in voltage-clamped Fibers isolated from FDB treated Muscles showed that the peak Ca2+ transient elicited by short depolarizing pulses was reduced by 35% whereas the maximal conductance of the Ca2+ channels was reduced by 30%. We also found increased basal ATP release with spontaneous release events. AAV-U7delα1s treated Fibers showed higher mRNA levels of the Slow isoform of Troponin I and lower mRNA levels of the fast isoform of Troponin I compared with non-treated Muscles. The transcriptional changes observed in these two genes after electrical stimulation were absent in AAV-U7delα1s treated Fibers.These results suggest that Cav1.1 controls ATP release trough Pannexin-1 channels, activating it after low stimulation frequencies and blocking ATP release during resting. The loss of this control perturbs the normal transcriptional response to electrical activity of adult Muscle Fibers.ACT1111, FONDECYT 1110467, FONDAP 15010006

Vincent Jacquemond - One of the best experts on this subject based on the ideXlab platform.

  • cav1 1 controls atp release to elicit gene expression in adult Muscle Fibers 1164 12
    The FASEB Journal, 2014
    Co-Authors: Gonzalo Jorquera, Denisse Valladares, Bruno Allard, Vincent Jacquemond, Enrique Jaimovich, Mariana Casas
    Abstract:

    In adult Muscle Fibers, Cav1.1 acts as voltage sensor for both excitation-contraction coupling and the activation of a signaling cascade that regulates gene expression. We have shown that ATP is released through pannexin-1 channels after electrical stimulation at 20 Hz, having a key role in the induction of transcriptional changes related to fast-to-Slow Muscle Fiber phenotype transition. Myotubes lacking the Cav1.1α1 subunit displayed almost no ATP release after electrical stimulation. ATP release and gene transcription was also altered in adult Muscle Fibers knock-down for Cav1.1α1. In dystrophic Fibers, there was also an increase in basal ATP release, but a default in the stimulation-dependent increase in ATP release and transcription activation observed in control Fibers. This can be interpreted as uncoupling between electrical stimulation and ATP release in dystrophic Muscles. All these data suggest that Cav1.1 controls ATP release trough Pannexin-1 channels, activating it after low stimulation frequ...

  • Cav1.1 controls frequency-dependent events regulating adult skeletal Muscle plasticity.
    Journal of Cell Science, 2013
    Co-Authors: Gonzalo Jorquera, Vincent Jacquemond, Enrique Jaimovich, Francisco Altamirano, Ariel Contreras-ferrat, Gonzalo Almarza, Sonja Buvinic, Mariana Casas
    Abstract:

    An important pending question in neuromuscular biology is how skeletal Muscle cells decipher the stimulation pattern coming from motoneurons to define their phenotype as Slow or fast twitch Muscle Fibers. We have previously shown that voltage-gated L-type calcium channel (Cav1.1) acts as a voltage sensor for activation of inositol (1,4,5)-trisphosphate [Ins(1,4,5)P₃]-dependent Ca(2+) signals that regulates gene expression. ATP released by Muscle cells after electrical stimulation through pannexin-1 channels plays a key role in this process. We show now that stimulation frequency determines both ATP release and Ins(1,4,5)P₃ production in adult skeletal Muscle and that Cav1.1 and pannexin-1 colocalize in the transverse tubules. Both ATP release and increased Ins(1,4,5)P₃ was seen in flexor digitorum brevis Fibers stimulated with 270 pulses at 20 Hz, but not at 90 Hz. 20 Hz stimulation induced transcriptional changes related to fast-to-Slow Muscle Fiber phenotype transition that required ATP release. Addition of 30 µM ATP to Fibers induced the same transcriptional changes observed after 20 Hz stimulation. Myotubes lacking the Cav1.1-α1 subunit released almost no ATP after electrical stimulation, showing that Cav1.1 has a central role in this process. In adult Muscle Fibers, ATP release and the transcriptional changes produced by 20 Hz stimulation were blocked by both the Cav1.1 antagonist nifedipine (25 µM) and by the Cav1.1 agonist (-)S-BayK 8644 (10 µM). We propose a new role for Cav1.1, independent of its calcium channel activity, in the activation of signaling pathways allowing Muscle Fibers to decipher the frequency of electrical stimulation and to activate specific transcriptional programs that define their phenotype.

  • cav1 1 controls atp release in adult Muscle Fibers
    Biophysical Journal, 2013
    Co-Authors: Gonzalo Jorquera, Bruno Allard, Vincent Jacquemond, Enrique Jaimovich, C Gentil, Mariana Casas
    Abstract:

    In adult Muscle Fibers, Cav1.1 acts as voltage sensor for both excitation-contraction coupling and the activation of a signaling cascade that regulates gene expression. We have shown that ATP is released trough pannexin-1 channels after electrical stimulation at 20 Hz, having a key role in the induction of transcriptional changes related to fast-to-Slow Muscle Fiber phenotype transition. Myotubes lacking the Cav1.1-α1 subunit displayed almost no ATP release after electrical stimulation. The same was observed in adult Fibers treated with the Cav1.1 antagonist nifedipine (25µM), showing that Cav1.1 has a central role controlling ATP release.We examined the activation of this signaling cascade in Muscle Fibers where a knock-down of the α1s subunit of Cav1.1 was obtained by a U7-exon skipping strategy using adenovirus-associated viral vectors (AAV-U7delα1s).Four months after AAV-U7delα1s injection we observed a significant reduction of Cav1.1 protein as well as atrophy and fibrosis of the treated Muscles. Indo-1 Ca2+ transients and Ca2+ current in voltage-clamped Fibers isolated from FDB treated Muscles showed that the peak Ca2+ transient elicited by short depolarizing pulses was reduced by 35% whereas the maximal conductance of the Ca2+ channels was reduced by 30%. We also found increased basal ATP release with spontaneous release events. AAV-U7delα1s treated Fibers showed higher mRNA levels of the Slow isoform of Troponin I and lower mRNA levels of the fast isoform of Troponin I compared with non-treated Muscles. The transcriptional changes observed in these two genes after electrical stimulation were absent in AAV-U7delα1s treated Fibers.These results suggest that Cav1.1 controls ATP release trough Pannexin-1 channels, activating it after low stimulation frequencies and blocking ATP release during resting. The loss of this control perturbs the normal transcriptional response to electrical activity of adult Muscle Fibers.ACT1111, FONDECYT 1110467, FONDAP 15010006

Enrique Jaimovich - One of the best experts on this subject based on the ideXlab platform.

  • cav1 1 controls atp release to elicit gene expression in adult Muscle Fibers 1164 12
    The FASEB Journal, 2014
    Co-Authors: Gonzalo Jorquera, Denisse Valladares, Bruno Allard, Vincent Jacquemond, Enrique Jaimovich, Mariana Casas
    Abstract:

    In adult Muscle Fibers, Cav1.1 acts as voltage sensor for both excitation-contraction coupling and the activation of a signaling cascade that regulates gene expression. We have shown that ATP is released through pannexin-1 channels after electrical stimulation at 20 Hz, having a key role in the induction of transcriptional changes related to fast-to-Slow Muscle Fiber phenotype transition. Myotubes lacking the Cav1.1α1 subunit displayed almost no ATP release after electrical stimulation. ATP release and gene transcription was also altered in adult Muscle Fibers knock-down for Cav1.1α1. In dystrophic Fibers, there was also an increase in basal ATP release, but a default in the stimulation-dependent increase in ATP release and transcription activation observed in control Fibers. This can be interpreted as uncoupling between electrical stimulation and ATP release in dystrophic Muscles. All these data suggest that Cav1.1 controls ATP release trough Pannexin-1 channels, activating it after low stimulation frequ...

  • Cav1.1 controls frequency-dependent events regulating adult skeletal Muscle plasticity.
    Journal of Cell Science, 2013
    Co-Authors: Gonzalo Jorquera, Vincent Jacquemond, Enrique Jaimovich, Francisco Altamirano, Ariel Contreras-ferrat, Gonzalo Almarza, Sonja Buvinic, Mariana Casas
    Abstract:

    An important pending question in neuromuscular biology is how skeletal Muscle cells decipher the stimulation pattern coming from motoneurons to define their phenotype as Slow or fast twitch Muscle Fibers. We have previously shown that voltage-gated L-type calcium channel (Cav1.1) acts as a voltage sensor for activation of inositol (1,4,5)-trisphosphate [Ins(1,4,5)P₃]-dependent Ca(2+) signals that regulates gene expression. ATP released by Muscle cells after electrical stimulation through pannexin-1 channels plays a key role in this process. We show now that stimulation frequency determines both ATP release and Ins(1,4,5)P₃ production in adult skeletal Muscle and that Cav1.1 and pannexin-1 colocalize in the transverse tubules. Both ATP release and increased Ins(1,4,5)P₃ was seen in flexor digitorum brevis Fibers stimulated with 270 pulses at 20 Hz, but not at 90 Hz. 20 Hz stimulation induced transcriptional changes related to fast-to-Slow Muscle Fiber phenotype transition that required ATP release. Addition of 30 µM ATP to Fibers induced the same transcriptional changes observed after 20 Hz stimulation. Myotubes lacking the Cav1.1-α1 subunit released almost no ATP after electrical stimulation, showing that Cav1.1 has a central role in this process. In adult Muscle Fibers, ATP release and the transcriptional changes produced by 20 Hz stimulation were blocked by both the Cav1.1 antagonist nifedipine (25 µM) and by the Cav1.1 agonist (-)S-BayK 8644 (10 µM). We propose a new role for Cav1.1, independent of its calcium channel activity, in the activation of signaling pathways allowing Muscle Fibers to decipher the frequency of electrical stimulation and to activate specific transcriptional programs that define their phenotype.

  • cav1 1 controls atp release in adult Muscle Fibers
    Biophysical Journal, 2013
    Co-Authors: Gonzalo Jorquera, Bruno Allard, Vincent Jacquemond, Enrique Jaimovich, C Gentil, Mariana Casas
    Abstract:

    In adult Muscle Fibers, Cav1.1 acts as voltage sensor for both excitation-contraction coupling and the activation of a signaling cascade that regulates gene expression. We have shown that ATP is released trough pannexin-1 channels after electrical stimulation at 20 Hz, having a key role in the induction of transcriptional changes related to fast-to-Slow Muscle Fiber phenotype transition. Myotubes lacking the Cav1.1-α1 subunit displayed almost no ATP release after electrical stimulation. The same was observed in adult Fibers treated with the Cav1.1 antagonist nifedipine (25µM), showing that Cav1.1 has a central role controlling ATP release.We examined the activation of this signaling cascade in Muscle Fibers where a knock-down of the α1s subunit of Cav1.1 was obtained by a U7-exon skipping strategy using adenovirus-associated viral vectors (AAV-U7delα1s).Four months after AAV-U7delα1s injection we observed a significant reduction of Cav1.1 protein as well as atrophy and fibrosis of the treated Muscles. Indo-1 Ca2+ transients and Ca2+ current in voltage-clamped Fibers isolated from FDB treated Muscles showed that the peak Ca2+ transient elicited by short depolarizing pulses was reduced by 35% whereas the maximal conductance of the Ca2+ channels was reduced by 30%. We also found increased basal ATP release with spontaneous release events. AAV-U7delα1s treated Fibers showed higher mRNA levels of the Slow isoform of Troponin I and lower mRNA levels of the fast isoform of Troponin I compared with non-treated Muscles. The transcriptional changes observed in these two genes after electrical stimulation were absent in AAV-U7delα1s treated Fibers.These results suggest that Cav1.1 controls ATP release trough Pannexin-1 channels, activating it after low stimulation frequencies and blocking ATP release during resting. The loss of this control perturbs the normal transcriptional response to electrical activity of adult Muscle Fibers.ACT1111, FONDECYT 1110467, FONDAP 15010006

Bruno Allard - One of the best experts on this subject based on the ideXlab platform.

  • cav1 1 controls atp release to elicit gene expression in adult Muscle Fibers 1164 12
    The FASEB Journal, 2014
    Co-Authors: Gonzalo Jorquera, Denisse Valladares, Bruno Allard, Vincent Jacquemond, Enrique Jaimovich, Mariana Casas
    Abstract:

    In adult Muscle Fibers, Cav1.1 acts as voltage sensor for both excitation-contraction coupling and the activation of a signaling cascade that regulates gene expression. We have shown that ATP is released through pannexin-1 channels after electrical stimulation at 20 Hz, having a key role in the induction of transcriptional changes related to fast-to-Slow Muscle Fiber phenotype transition. Myotubes lacking the Cav1.1α1 subunit displayed almost no ATP release after electrical stimulation. ATP release and gene transcription was also altered in adult Muscle Fibers knock-down for Cav1.1α1. In dystrophic Fibers, there was also an increase in basal ATP release, but a default in the stimulation-dependent increase in ATP release and transcription activation observed in control Fibers. This can be interpreted as uncoupling between electrical stimulation and ATP release in dystrophic Muscles. All these data suggest that Cav1.1 controls ATP release trough Pannexin-1 channels, activating it after low stimulation frequ...

  • cav1 1 controls atp release in adult Muscle Fibers
    Biophysical Journal, 2013
    Co-Authors: Gonzalo Jorquera, Bruno Allard, Vincent Jacquemond, Enrique Jaimovich, C Gentil, Mariana Casas
    Abstract:

    In adult Muscle Fibers, Cav1.1 acts as voltage sensor for both excitation-contraction coupling and the activation of a signaling cascade that regulates gene expression. We have shown that ATP is released trough pannexin-1 channels after electrical stimulation at 20 Hz, having a key role in the induction of transcriptional changes related to fast-to-Slow Muscle Fiber phenotype transition. Myotubes lacking the Cav1.1-α1 subunit displayed almost no ATP release after electrical stimulation. The same was observed in adult Fibers treated with the Cav1.1 antagonist nifedipine (25µM), showing that Cav1.1 has a central role controlling ATP release.We examined the activation of this signaling cascade in Muscle Fibers where a knock-down of the α1s subunit of Cav1.1 was obtained by a U7-exon skipping strategy using adenovirus-associated viral vectors (AAV-U7delα1s).Four months after AAV-U7delα1s injection we observed a significant reduction of Cav1.1 protein as well as atrophy and fibrosis of the treated Muscles. Indo-1 Ca2+ transients and Ca2+ current in voltage-clamped Fibers isolated from FDB treated Muscles showed that the peak Ca2+ transient elicited by short depolarizing pulses was reduced by 35% whereas the maximal conductance of the Ca2+ channels was reduced by 30%. We also found increased basal ATP release with spontaneous release events. AAV-U7delα1s treated Fibers showed higher mRNA levels of the Slow isoform of Troponin I and lower mRNA levels of the fast isoform of Troponin I compared with non-treated Muscles. The transcriptional changes observed in these two genes after electrical stimulation were absent in AAV-U7delα1s treated Fibers.These results suggest that Cav1.1 controls ATP release trough Pannexin-1 channels, activating it after low stimulation frequencies and blocking ATP release during resting. The loss of this control perturbs the normal transcriptional response to electrical activity of adult Muscle Fibers.ACT1111, FONDECYT 1110467, FONDAP 15010006