Zobrazeno 1 - 10
of 16
pro vyhledávání: '"R Oliver Goral"'
Autor:
Matthias Lübbert, R Oliver Goral, Rachel Satterfield, Travis Putzke, Arn MJM van den Maagdenberg, Naomi Kamasawa, Samuel M Young Jr
Publikováno v:
eLife, Vol 6 (2017)
In central nervous system (CNS) synapses, action potential-evoked neurotransmitter release is principally mediated by CaV2.1 calcium channels (CaV2.1) and is highly dependent on the physical distance between CaV2.1 and synaptic vesicles (coupling). A
Externí odkaz:
https://doaj.org/article/58c989c989ce4ecf8e238d592ea303b8
Autor:
R. Oliver Goral, Kathryn M. Harper, Briana J. Bernstein, Sydney A. Fry, Patricia W. Lamb, Sheryl S. Moy, Jesse D. Cushman, Jerrel L. Yakel
Publikováno v:
Frontiers in Behavioral Neuroscience, Vol 16 (2022)
Introduction: Altered signaling or function of acetylcholine (ACh) has been reported in various neurological diseases, including Alzheimer’s disease, Tourette syndrome, epilepsy among others. Many neurons that release ACh also co-transmit the neuro
Externí odkaz:
https://doaj.org/article/37d07ecc33924efab4a32cc003faff10
Autor:
Wei Dong, Tamara Radulovic, R. Oliver Goral, Connon Thomas, Monica Suarez Montesinos, Debbie Guerrero-Given, Akari Hagiwara, Travis Putzke, Yamato Hida, Manabu Abe, Kenji Sakimura, Naomi Kamasawa, Toshihisa Ohtsuka, Samuel M. Young, Jr.
Publikováno v:
Cell Reports, Vol 24, Iss 2, Pp 284-293.e6 (2018)
Summary: In the presynaptic terminal, the magnitude and location of Ca2+ entry through voltage-gated Ca2+ channels (VGCCs) regulate the efficacy of neurotransmitter release. However, how presynaptic active zone proteins control mammalian VGCC levels
Externí odkaz:
https://doaj.org/article/d0af342b3d8e4174a4c8048e4caa6636
Autor:
Priyadharishini Veeraraghavan, Matthias Lübbert, Toshihisa Ohtsuka, Tamara Radulovic, Samuel M. Young, Debbie Guerrero-Given, R. Oliver Goral, Naomi Kamasawa, Mónica S. Montesinos, Connon I. Thomas, Wei Dong, Kevin M Goff
Publikováno v:
J Physiol
Key points CAST/ELKS are positive regulators of presynaptic growth and are suppressors of active zone expansion at the developing mouse calyx of Held. CAST/ELKS regulate all three CaV 2 subtype channel levels in the presynaptic terminal and not just
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::9cbbaf6640fc0519ff90914aad47530e
https://doi.org/10.1113/jp279736
https://doi.org/10.1113/jp279736
Autor:
Matthias, Lübbert, R Oliver, Goral, Christian, Keine, Connon, Thomas, Debbie, Guerrero-Given, Travis, Putzke, Rachel, Satterfield, Naomi, Kamasawa, Samuel M, Young
Publikováno v:
Neuron. 101(2)
The abundance of presynaptic Ca(V)2 voltage-gated Ca(2+) channels (Ca(V)2) at mammalian active zones (AZs) regulates the efficacy of synaptic transmission. It is proposed that presynaptic Ca(V)2 levels are saturated in AZs due to a finite number of s
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=pmid________::c9f267fc976904c102d37709cf0d49b8
https://pubmed.ncbi.nlm.nih.gov/30545599
https://pubmed.ncbi.nlm.nih.gov/30545599
Autor:
R. Oliver Goral, Samuel M. Young, Naomi Kamasawa, Matthias Lübbert, Travis Putzke, Arn M. J. M. van den Maagdenberg, Rachel Satterfield
Publikováno v:
eLife
eLife, Vol 6 (2017)
eLife, 6
eLife, Vol 6 (2017)
eLife, 6
In central nervous system (CNS) synapses, action potential-evoked neurotransmitter release is principally mediated by CaV2.1 calcium channels (CaV2.1) and is highly dependent on the physical distance between CaV2.1 and synaptic vesicles (coupling). A
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::4aa886e7f0833fe65e380c8f6bade034
http://europepmc.org/articles/PMC5548488
http://europepmc.org/articles/PMC5548488
Autor:
Travis Putzke, Matthias Lübbert, R. Oliver Goral, Connon I. Thomas, Samuel M. Young, Debbie Guerrero-Given, Naomi Kamasawa, Christian Keine, Rachel Satterfield
Publikováno v:
Neuron. 101:260-273.e6
The abundance of presynaptic CaV2 voltage-gated Ca2+ channels (CaV2) at mammalian active zones (AZs) regulates the efficacy of synaptic transmission. It is proposed that presynaptic CaV2 levels are saturated in AZs due to a finite number of slots tha
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_________::0cefd33dfe53a6332bb7ab7bd23b4cef
https://doi.org/10.1016/j.neuron.2018.11.028
https://doi.org/10.1016/j.neuron.2018.11.028
Autor:
Mónica S. Montesinos, Kenji Sakimura, Akari Hagiwara, R. Oliver Goral, Yamato Hida, Samuel M. Young, Debbie Guerrero-Given, Connon I. Thomas, Travis Putzke, Tamara Radulovic, Toshihisa Ohtsuka, Naomi Kamasawa, Wei Dong, Manabu Abe
Publikováno v:
Cell reports
Cell Reports, Vol 24, Iss 2, Pp 284-293.e6 (2018)
Cell Reports, Vol 24, Iss 2, Pp 284-293.e6 (2018)
SUMMARY In the presynaptic terminal, the magnitude and location of Ca2+ entry through voltage-gated Ca2+ channels (VGCCs) regulate the efficacy of neurotransmitter release. However, how presynaptic active zone proteins control mammalian VGCC levels a
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::cd8f7e0c68e6a9aca3fc4dc46a9e3c82
https://doi.org/10.1016/j.celrep.2018.06.024
https://doi.org/10.1016/j.celrep.2018.06.024
Publikováno v:
Pflugers Archiv : European journal of physiology. 467(12)
SCN11A encodes the voltage-gated sodium channel NaV1.9, which deviates most strongly from the other eight NaV channels expressed in mammals. It is characterized by resistance to the prototypic NaV channel blocker tetrodotoxin and exhibits slow activa
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::b5a657bcd24bf1fd896e17938bbd4edf
https://pubmed.ncbi.nlm.nih.gov/25916202
https://pubmed.ncbi.nlm.nih.gov/25916202
Autor:
Andrea Hanson-Kahn, Janine Altmüller, Peter Nürnberg, Ingo Kurth, Istvan Katona, Miya Frick, Stefan H. Heinemann, Jonathan A. Bernstein, Ping Gong, R. Oliver Goral, Enrico Leipold, Martin Voigt, Joachim Weis, Christian A. Hübner
Publikováno v:
Nature Communications
Nature Communications 6, 10049 (2015). doi:10.1038/ncomms10049
Nature Communications 6, 10049 (2015). doi:10.1038/ncomms10049
Gain-of-function mutations in the human SCN11A-encoded voltage-gated Na+ channel NaV1.9 cause severe pain disorders ranging from neuropathic pain to congenital pain insensitivity. However, the entire spectrum of the NaV1.9 diseases has yet to be defi
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::07e4413bd44be0e6615788d580b3b1e4
