|1.||van den Maagdenberg, Arn M J M: 28 articles (05/2015 - 03/2004)|
|2.||Ferrari, Michel D: 21 articles (05/2015 - 03/2004)|
|3.||Pietrobon, Daniela: 13 articles (01/2015 - 10/2002)|
|4.||Frants, Rune R: 8 articles (03/2014 - 03/2004)|
|5.||Tottene, Angelita: 7 articles (01/2015 - 10/2002)|
|6.||Uchitel, Osvaldo D: 7 articles (01/2015 - 09/2008)|
|7.||Broos, Ludo A M: 7 articles (03/2014 - 03/2004)|
|8.||Mori, Yasuo: 6 articles (09/2015 - 11/2004)|
|9.||Mizusawa, Hidehiro: 6 articles (09/2015 - 08/2008)|
|10.||Ishikawa, Kinya: 6 articles (09/2015 - 08/2008)|
|1.||Brain Injuries (Brain Injury)
01/28/2016 - "These findings demonstrate that the mutant Cav2.1 channel exerts a protective effect against cryogenic brain injury in rolling Nagoya mice. "
01/28/2016 - "To examine the relationship between Cav2.1 channel function and brain injury, we induced cryogenic brain damage in homozygous rolling Nagoya (rol/rol), control wild-type (+/+), ω-agatoxin IVA-pretreated +/+ (ω-aga +/+), and ω-agatoxin IVA-post-treated +/+ (ω-aga-post-treated +/+) mice. "
01/28/2016 - "Analysis of the protective effects of a neuronal Cav2.1 calcium channel in brain injury."
|2.||Migraine with Aura (Familial Hemiplegic Migraine)
05/01/2015 - "This study investigated plasma metabolic changes in transgenic mice that harbor a gene mutation in voltage-gated CaV2.1 Ca(2+) channels previously identified in patients with familial hemiplegic migraine, a subtype of migraine with auras. "
03/01/2009 - "In the present study, we systematically compare the biophysical effects of three type-1 familial hemiplegic migraine (FHM-1) mutations in two predominant splice variants of the neuronal Ca(V)2.1 P/Q-type channel. "
10/01/2002 - "Insights into the pathogenesis of migraine with aura may be gained from a study of human Ca(V)2.1 channels containing mutations linked to familial hemiplegic migraine (FHM). "
02/25/2015 - "To explain cognitive and memory difficulties observed in some familial hemiplegic migraine (FHM) patients, we examined hippocampal neurotransmission and plasticity in knock-in mice expressing the FHM type 1 (FHM1) R192Q gain-of function mutation in the CACNA1A gene that encodes the α1A subunit of neuronal CaV2.1 channels. "
01/01/2015 - "Familial hemiplegic migraine type 1 (FHM1) is caused by gain-of-function mutations in CaV2.1 (P/Q-type) Ca(2+) channels. "
07/01/2010 - "Studies in mice revealed that LTCCs indirectly also contribute to neurological symptoms in Ca2+ channelopathies affecting non-LTCCs, such as Cav2.1 alpha1 in tottering mice. "
10/01/2004 - "However, studies in mice revealed that LTCC dysfunction also contributes to neurological symptoms in Ca2+ channelopathies affecting non-LTCCs, such as Ca(v)2.1 alpha1 in tottering mice. "
07/01/2010 - "For each channelopathy, the review describes the disease phenotype as well as the functional consequences of the disease-causing mutations on recombinant human CaV2.1 channels and, in the case of FHM1 and SCA6, on neuronal CaV2.1 channels expressed at the endogenous physiological level in knockin mouse models. "
07/01/2010 - "CaV2.1 channelopathies."
06/01/2005 - "These data indicate that Ca(V)2.1 channels have a dominant and efficient specific role in initiating fast synaptic transmission at central excitatory synapses in vivo, and suggest that the Ca(V)2.1 channelopathies are primarily synaptic diseases. "
07/01/2013 - "This review, first, briefly summarizes current understanding of the pathophysiological mechanisms that are believed to underlie migraine headache, migraine aura and the onset of a migraine attack, and briefly describes the localization and function of neuronal Ca(V)2.1 channels in the brain regions that have been implicated in migraine pathogenesis. "
01/01/2013 - "Recent data show that transgenic mice expressing familial hemiplegic migraine (FHM) type 1 mutations in voltage-gated Ca2+ channels (Cav2.1) develop mutation-specific aura-like signs after a cortical SD similar to patients with the respective mutation. "
03/04/2004 - "These include increased Ca(v)2.1 current density in cerebellar neurons, enhanced neurotransmission at the neuromuscular junction, and, in the intact animal, a reduced threshold and increased velocity of cortical spreading depression (CSD; the likely mechanism for the migraine aura). "
05/21/2014 - "Specific missense mutations in the CACNA1A gene, which encodes a subunit of voltage-gated CaV2.1 channels, are associated with familial hemiplegic migraine type 1 (FHM1), a rare monogenic subtype of common migraine with aura. "
04/13/2011 - "Familial hemiplegic migraine type 1, a monogenic migraine variant with aura, is linked to gain-of-function mutations in the CACNA1A gene encoding Ca(V)2.1 channels. "
|5.||Migraine Disorders (Migraine)
09/01/2014 - "Mechanism underlying unaltered cortical inhibitory synaptic transmission in contrast with enhanced excitatory transmission in CaV2.1 knockin migraine mice."
03/01/2014 - "Transgenic knock-in (KI) migraine mouse models were generated that carried either the FHM1 R192Q or the S218L mutation and were shown to exhibit increased CaV2.1 channel activity. "
11/22/2013 - "The E1015K variant in the synprint region of the CaV2.1 channel alters channel function and is associated with different migraine phenotypes."
07/01/2013 - "Then, the review describes and discusses i) the functional consequences of FHM1 mutations on the biophysical properties of recombinant human Ca(V)2.1 channels and native Ca(V)2.1 channels in neurons of knockin mouse models carrying the mild R192Q or severe S218L mutations in the orthologous gene, and ii) the functional consequences of these mutations on neurophysiological processes in the cerebral cortex and trigeminovascular system thought to be involved in the pathophysiology of migraine, and the insights into migraine mechanisms obtained from the functional analysis of these processes in FHM1 knockin mice. "
01/01/2010 - "High cortical spreading depression susceptibility and migraine-associated symptoms in Ca(v)2.1 S218L mice."
|1.||Calcium Channels (Calcium Channel)
|2.||Q-Type Calcium Channels (Q-Type Calcium Channel)
|4.||Neurotransmitter Agents (Neurotransmitter)
|5.||Prostaglandins B (PGB)
|6.||Adenosine Triphosphatases (ATPase)
|8.||Episodic ataxia with nystagmus
|10.||GTP-Binding Proteins (G-Protein)