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(181 - 200 of 226)

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Mutations in DEPDC5 cause familial focal epilepsy with variable foci
Silencing the Majority of Cerebellar Granule Cells Uncovers Their Essential Role in Motor Learning and Consolidation
The Mechanism of Functional Up-Regulation of P2X3 Receptors of Trigeminal Sensory Neurons in a Genetic Mouse Model of Familial Hemiplegic Migraine Type 1 (FHM-1)
Migraine is not associated with enhanced atherosclerosis
Effects of LPS on P2X3 receptors of trigeminal sensory neurons and macrophages from mice expressing the R192Q Cacna1a gene mutation of familial hemiplegic migraine-1
Epigenetic mechanisms in migraine: a promising avenue?
Limited regional cerebellar dysfunction induces focal dystonia in mice
TNF alpha Levels and Macrophages Expression Reflect an Inflammatory Potential of Trigeminal Ganglia in a Mouse Model of Familial Hemiplegic Migraine
Reduced Sleep and Low Adenosinergic Sensitivity in Cacna1a R192Q Mutant Mice
Presynaptic Ca(v)2.1 calcium channels carrying familial hemiplegic migraine mutation R192Q allow faster recovery from synaptic depression in mouse calyx of Held
Metabolic profiling of mouse cerebrospinal fluid by sheathless CE-MS
PRRT2 MUTATION CAUSES BENIGN FAMILIAL INFANTILE CONVULSIONS
Functional crosstalk in culture between macrophages and trigeminal sensory neurons of a mouse genetic model of migraine
Cerebellar Ataxia by Enhanced Ca(V)2.1 Currents Is Alleviated by Ca2+-Dependent K+-Channel Activators in Cacna1a(S218L) Mutant Mice
De novo mutations in ATP1A3 cause alternating hemiplegia of childhood
Genetic HLA Associations in Complex Regional Pain Syndrome With and Without Dystonia
Imaging mass spectrometry to visualize biomolecule distributions in mouse brain tissue following hemispheric cortical spreading depression
Genome-wide association analysis identifies susceptibility loci for migraine without aura
Crosstalk between the purinergic system and known algogenic mediators in mouse trigeminal ganglia: implications for basic mechanisms of migraine pain
Purkinje Cell-Specific Ablation of Ca(V)2.1 Channels is Sufficient to Cause Cerebellar Ataxia in Mice

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