A5072194111- Migraine and Headache Studies
- Neuroscience of respiration and sleep
- Neuroscience and Neuropharmacology Research
- Epilepsy research and treatment
- Biochemical effects in animals
- Neurological Complications and Syndromes
- Metabolism and Genetic Disorders
- Mitochondrial Function and Pathology
- Genetic Neurodegenerative Diseases
- Neural dynamics and brain function
- Cannabis and Cannabinoid Research
- Circadian rhythm and melatonin
- Ion channel regulation and function
- Nicotinic Acetylcholine Receptors Study
Leiden University Medical Center
2019-2025
Hacettepe University
2018-2021
Background The therapeutic use of cannabidiol (CBD) and Δ9-tetrahydrocannabinol (THC) to treat migraine has been understudied. Using three mouse models, we examined the impact CBD THC on migraine-relevant behaviors triggered by: 1) calcitonin gene-related peptide (CGRP), 2) sodium nitroprusside (SNP), 3) cortical spreading depolarization (CSD). Methods Both male female CD1 mice were treated with (100 mg/kg) or (1 alone in combinations (1, 30 100 prior injection CGRP SNP. assessed for light...
Abstract Here we show, for the first time, spontaneous cortical spreading depolarization (CSD) events – electrophysiological correlate of migraine aura in animals by using generated familial hemiplegic type 3 (FHM3) transgenic mouse model. The mutant mice express L263V‐mutated α 1 subunits voltage‐gated Na V 1.1 sodium channels ( Scn1a L263V ). CSDs consistently propagated from visual to motor cortex, recapitulating what has been shown patients with aura. This model may be valuable...
Dravet syndrome (DS) is an epileptic encephalopathy that still lacks biomarkers for epileptogenesis and its treatment. Dysfunction of NaV1.1 sodium channels, which are chiefly expressed in inhibitory interneurons, explains the phenotype. Understanding network effects these cellular deficits may help predict epileptogenesis. Here, we studied θ-γ coupling as a potential marker altered functioning DS mouse model. We found cortical was reduced both male female juvenile mice persisted only if...
Abstract Background Cortical spreading depolarization (CSD), the neurophysiological correlate of migraine aura, can activate trigeminal pain pathways, but neurobiological mechanisms and behavioural consequences remain unclear. Here we investigated effects optogenetically-induced CSDs on headache-related behaviour neuroinflammatory responses in transgenic mice carrying a familial hemiplegic type 1 (FHM1) mutation. Methods CSD events (3 total) were evoked minimally invasive manner by...
Early onset seizures are a hallmark of Dravet syndrome. Previous studies in rodent models have shown that the epileptic phenotype is caused by loss-of-function voltage-gated NaV 1.1 sodium channels, which chiefly expressed γ-aminobutyric acid (GABA)ergic neurons. Recently, possibly critical role has been attributed to hippocampus seizure phenotype, as local hippocampal ablation channels decreased threshold for hyperthermia-induced seizures. However, effect restricted cortical sites not...
Neuroinflammatory changes involving neuronal HMGB1 release and astrocytic NF-κB nuclear translocation occur following cortical spreading depolarization (CSD) in wildtype (WT) mice but it is unknown to what extent this occurs the migraine brain. We therefore investigated familial hemiplegic type 1 (FHM1) knock-in mice, which express an intrinsic hyperexcitability phenotype, of neuroinflammation without after CSD. CSD was evoked one hemisphere by pinprick (single CSD) or topical KCl...
The initial phase of neuronal death is not well characterized. Here, we show that expansion the nuclear membrane without losing its integrity along with peripheralization chromatin are immediate signs injury. Importantly, these changes can be identified commonly used stains and as markers poor perfusion-fixation. Although frozen sections widely used, no available to ensure observed were confounded by perfusion-induced hypoxia/ischemia. Moreover, HMGB1 was immediately released p53...