Ca V2.1 voltage activated calcium channels and synaptic transmission in familial hemiplegic migraine pathogenesis

Studies on the genetic forms of epilepsy, chronic pain, and migraine caused by mutations in ion channels have given crucial insights into the molecular mechanisms, pathogenesis, and therapeutic approaches to complex neurological disorders. In this review we focus on the role of mutated Ca V2.1 (i.e....

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Autores principales:	Uchitel, Osvaldo Daniel, Di Guilmi, Mariano Nicolas
Publicado:	2012
Materias:	Ca V2.1 (P/Q-type) Ca 2+ channels Cortical spreading depression Familial hemiplegic migraine R192Q and S218L knock in mice Synaptic transmission calcium channel calcium channel P type calcium channel Q type sodium channel Nav1.1 unclassified drug voltage activated calcium channel Cav2.1 voltage gated calcium channel calcium channel N type voltage dependent calcium channel (P Q type) voltage-dependent calcium channel (P-Q type) article brain cell cell function disease activity enzyme activation experimental model familial hemiplegic migraine gain of function mutation gene mutation human hyperpolarization migraine with aura nerve cell excitability nerve cell plasticity neurotransmission neurotransmitter release nonhuman pathogenesis protein expression protein function regulatory mechanism spreading cortical depression synapse synaptic transmission transgenic mouse animal brain cortex genetics mouse mutation pathology pathophysiology review Animals Calcium Channels, N-Type Cerebral Cortex Cortical Spreading Depression Humans Mice Mice, Transgenic Migraine with Aura Mutation Synaptic Transmission
Acceso en línea:	https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_09284257_v106_n1-2_p12_Uchitel http://hdl.handle.net/20.500.12110/paper_09284257_v106_n1-2_p12_Uchitel
Aporte de:	Biblioteca Digital - Facultad de Ciencias Exactas y Naturales (UBA) de Universidad de Buenos Aires

id	paper:paper_09284257_v106_n1-2_p12_Uchitel
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spelling	paper:paper_09284257_v106_n1-2_p12_Uchitel2023-06-08T15:52:13Z Ca V2.1 voltage activated calcium channels and synaptic transmission in familial hemiplegic migraine pathogenesis Uchitel, Osvaldo Daniel Di Guilmi, Mariano Nicolas Ca V2.1 (P/Q-type) Ca 2+ channels Cortical spreading depression Familial hemiplegic migraine R192Q and S218L knock in mice Synaptic transmission calcium channel calcium channel P type calcium channel Q type sodium channel Nav1.1 unclassified drug voltage activated calcium channel Cav2.1 voltage gated calcium channel calcium channel N type voltage dependent calcium channel (P Q type) voltage-dependent calcium channel (P-Q type) article brain cell cell function disease activity enzyme activation experimental model familial hemiplegic migraine gain of function mutation gene mutation human hyperpolarization migraine with aura nerve cell excitability nerve cell plasticity neurotransmission neurotransmitter release nonhuman pathogenesis protein expression protein function regulatory mechanism spreading cortical depression synapse synaptic transmission transgenic mouse animal brain cortex genetics migraine with aura mouse mutation pathology pathophysiology review Animals Calcium Channels, N-Type Cerebral Cortex Cortical Spreading Depression Humans Mice Mice, Transgenic Migraine with Aura Mutation Synaptic Transmission Studies on the genetic forms of epilepsy, chronic pain, and migraine caused by mutations in ion channels have given crucial insights into the molecular mechanisms, pathogenesis, and therapeutic approaches to complex neurological disorders. In this review we focus on the role of mutated Ca V2.1 (i.e., P/Q-type) voltage-activated Ca 2+ channels, and on the ultimate consequences that mutations causing familial hemiplegic migraine type-1 (FHM1) have in neurotransmitter release. Transgenic mice harboring the human pathogenic FHM1 mutation R192Q or S218L (KI) have been used as models to study neurotransmission at several central and peripheral synapses. FHM1 KI mice are a powerful tool to explore presynaptic regulation associated with expression of Ca V2.1 channels. Mutated Ca V2.1 channels activate at more hyperpolarizing potentials and lead to a gain-of-function in synaptic transmission. This gain-of-function might underlie alterations in the excitatory/ inhibitory balance of synaptic transmission, favoring a persistent state of hyperexcitability in cortical neurons that would increase the susceptibility for cortical spreading depression (CSD), a mechanism believed to initiate the attacks of migraine with aura. © 2011 Elsevier Ltd. Fil:Uchitel, O.D. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. Fil:Di Guilmi, M.N. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. 2012 https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_09284257_v106_n1-2_p12_Uchitel http://hdl.handle.net/20.500.12110/paper_09284257_v106_n1-2_p12_Uchitel
institution	Universidad de Buenos Aires
institution_str	I-28
repository_str	R-134
collection	Biblioteca Digital - Facultad de Ciencias Exactas y Naturales (UBA)
topic	Ca V2.1 (P/Q-type) Ca 2+ channels Cortical spreading depression Familial hemiplegic migraine R192Q and S218L knock in mice Synaptic transmission calcium channel calcium channel P type calcium channel Q type sodium channel Nav1.1 unclassified drug voltage activated calcium channel Cav2.1 voltage gated calcium channel calcium channel N type voltage dependent calcium channel (P Q type) voltage-dependent calcium channel (P-Q type) article brain cell cell function disease activity enzyme activation experimental model familial hemiplegic migraine gain of function mutation gene mutation human hyperpolarization migraine with aura nerve cell excitability nerve cell plasticity neurotransmission neurotransmitter release nonhuman pathogenesis protein expression protein function regulatory mechanism spreading cortical depression synapse synaptic transmission transgenic mouse animal brain cortex genetics migraine with aura mouse mutation pathology pathophysiology review Animals Calcium Channels, N-Type Cerebral Cortex Cortical Spreading Depression Humans Mice Mice, Transgenic Migraine with Aura Mutation Synaptic Transmission
spellingShingle	Ca V2.1 (P/Q-type) Ca 2+ channels Cortical spreading depression Familial hemiplegic migraine R192Q and S218L knock in mice Synaptic transmission calcium channel calcium channel P type calcium channel Q type sodium channel Nav1.1 unclassified drug voltage activated calcium channel Cav2.1 voltage gated calcium channel calcium channel N type voltage dependent calcium channel (P Q type) voltage-dependent calcium channel (P-Q type) article brain cell cell function disease activity enzyme activation experimental model familial hemiplegic migraine gain of function mutation gene mutation human hyperpolarization migraine with aura nerve cell excitability nerve cell plasticity neurotransmission neurotransmitter release nonhuman pathogenesis protein expression protein function regulatory mechanism spreading cortical depression synapse synaptic transmission transgenic mouse animal brain cortex genetics migraine with aura mouse mutation pathology pathophysiology review Animals Calcium Channels, N-Type Cerebral Cortex Cortical Spreading Depression Humans Mice Mice, Transgenic Migraine with Aura Mutation Synaptic Transmission Uchitel, Osvaldo Daniel Di Guilmi, Mariano Nicolas Ca V2.1 voltage activated calcium channels and synaptic transmission in familial hemiplegic migraine pathogenesis
topic_facet	Ca V2.1 (P/Q-type) Ca 2+ channels Cortical spreading depression Familial hemiplegic migraine R192Q and S218L knock in mice Synaptic transmission calcium channel calcium channel P type calcium channel Q type sodium channel Nav1.1 unclassified drug voltage activated calcium channel Cav2.1 voltage gated calcium channel calcium channel N type voltage dependent calcium channel (P Q type) voltage-dependent calcium channel (P-Q type) article brain cell cell function disease activity enzyme activation experimental model familial hemiplegic migraine gain of function mutation gene mutation human hyperpolarization migraine with aura nerve cell excitability nerve cell plasticity neurotransmission neurotransmitter release nonhuman pathogenesis protein expression protein function regulatory mechanism spreading cortical depression synapse synaptic transmission transgenic mouse animal brain cortex genetics migraine with aura mouse mutation pathology pathophysiology review Animals Calcium Channels, N-Type Cerebral Cortex Cortical Spreading Depression Humans Mice Mice, Transgenic Migraine with Aura Mutation Synaptic Transmission
description	Studies on the genetic forms of epilepsy, chronic pain, and migraine caused by mutations in ion channels have given crucial insights into the molecular mechanisms, pathogenesis, and therapeutic approaches to complex neurological disorders. In this review we focus on the role of mutated Ca V2.1 (i.e., P/Q-type) voltage-activated Ca 2+ channels, and on the ultimate consequences that mutations causing familial hemiplegic migraine type-1 (FHM1) have in neurotransmitter release. Transgenic mice harboring the human pathogenic FHM1 mutation R192Q or S218L (KI) have been used as models to study neurotransmission at several central and peripheral synapses. FHM1 KI mice are a powerful tool to explore presynaptic regulation associated with expression of Ca V2.1 channels. Mutated Ca V2.1 channels activate at more hyperpolarizing potentials and lead to a gain-of-function in synaptic transmission. This gain-of-function might underlie alterations in the excitatory/ inhibitory balance of synaptic transmission, favoring a persistent state of hyperexcitability in cortical neurons that would increase the susceptibility for cortical spreading depression (CSD), a mechanism believed to initiate the attacks of migraine with aura. © 2011 Elsevier Ltd.
author	Uchitel, Osvaldo Daniel Di Guilmi, Mariano Nicolas
author_facet	Uchitel, Osvaldo Daniel Di Guilmi, Mariano Nicolas
author_sort	Uchitel, Osvaldo Daniel
title	Ca V2.1 voltage activated calcium channels and synaptic transmission in familial hemiplegic migraine pathogenesis
title_short	Ca V2.1 voltage activated calcium channels and synaptic transmission in familial hemiplegic migraine pathogenesis
title_full	Ca V2.1 voltage activated calcium channels and synaptic transmission in familial hemiplegic migraine pathogenesis
title_fullStr	Ca V2.1 voltage activated calcium channels and synaptic transmission in familial hemiplegic migraine pathogenesis
title_full_unstemmed	Ca V2.1 voltage activated calcium channels and synaptic transmission in familial hemiplegic migraine pathogenesis
title_sort	ca v2.1 voltage activated calcium channels and synaptic transmission in familial hemiplegic migraine pathogenesis
publishDate	2012
url	https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_09284257_v106_n1-2_p12_Uchitel http://hdl.handle.net/20.500.12110/paper_09284257_v106_n1-2_p12_Uchitel
work_keys_str_mv	AT uchitelosvaldodaniel cav21voltageactivatedcalciumchannelsandsynaptictransmissioninfamilialhemiplegicmigrainepathogenesis AT diguilmimarianonicolas cav21voltageactivatedcalciumchannelsandsynaptictransmissioninfamilialhemiplegicmigrainepathogenesis
_version_	1768546123647025152

Ca V2.1 voltage activated calcium channels and synaptic transmission in familial hemiplegic migraine pathogenesis

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