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1,406 results for “migraine”
FAAH inhibition in migraine pain
<p>This dataset comprises the findings obtained in the study aimed at investigating the relevance of fatty-acid amide hydrolase (FAAH) inhibition in the nitroglycerin (NTG) animal model of migraine, by testing the effects of the globally active FAAH inhibitor URB597. The attention was focused on mapping neuronal c-Fos protein expression, measurement of anandamide (AEA) and palmitoylethanolamide (PEA) levels in brain areas and in trigeminal ganglia, evaluation of pain-related trigeminal behavior and quantification of molecular mediators in rats that received URB597 (2 mg/kg i.p.) either before or after NTG administration (10 mg/kg, i.p.).</p> <ol> <li>Evaluation of c-Fos expression by immunohistochemistry: cell counts of individual brain nuclei were made from every sixth section throughout their rostrocaudal extent for each rat. The nuclei evaluated were identified with the rat brain atlas Paxinos and Watson 4th edition. Trigeminal nucleus caudalis (TNC): from bregma −14.08 mm (interaural −5.08 mm) until −17 mm (interaural −8 mm); nucleus tractus solitarii (NTS): from bregma −13.24 mm (interaural −4.24 mm) until −13.68 mm (interaural −4.68 mm); locus ceruleus (LC): from bregma −9.80 mm (interaural −0.80 mm) until −10.04 mm (interaural −1.04 mm); parabrachial nucleus (PAB): from bregma −8.80 mm (interaural 0.20 mm) until −9.80 mm (interaural −0.50 mm); periaqueductal gray (PAG): from bregma −7.80 mm (interaural 1.20 mm) until −8.80 mm (interaural 0.20 mm).</li> <li>Measurement of AEA and PEA levels: medulla, cervical spinal cord and trigeminal ganglia were homogenized in cold methanol (2 ml) containing AEA-d4 and PEA-d4 as internal standards. After extraction the lipids were measured using a Xevo TQ UPLC-MS/MS system equipped with a reversed-phase BEH C18 column (2.1 × 50 mm, 1.7 μm particle size) (Waters, Milford, USA).</li> <li>Pain-related behavior in the orofacial formalin test: the face rubbing was measured counting the seconds the animal spent grooming the injected area (upper lip, lateral to the nose) with the ipsilateral forepaw or hindpaw 0–6 min (Phase I) or 12–45 min (Phase II) after formalin injection (50 µl, s.c.). The observation time was divided into 15 blocks of 3 min each.</li> </ol> <p>mRNA expression levels: calcitonin gene-related peptide (CGRP), neuronal nitric oxide synthase (nNOS), interleukin-1β (IL-1β) and tumor necrosis factor-alpha (TNF-alpha) mRNA were evaluated in in medulla, cervical spinal cord and trigeminal ganglia; whereas, in dura mater were evaluated IL-1β and inducible NOS (iNOS). mRNA levels were measured by rt-PCR. All samples were assayed in triplicate and gene expression levels were calculated according to 2−∆∆Ct = 2− (∆Ct gene − ∆Ct housekeeping gene) formula by using Ct (cycle threshold) values.</p>
Modulation of glia activation by TRPA1 antagonism in a pre-clinical model of migraine
<p>This dataset comprises the findings obtained in the study aimed at investigating the relationship between TRPA1 channels and glia activation in the modulation of trigeminal hyperalgesia in preclinical models of migraine.</p> <p><strong><em>In vivo</em></strong> assessments performed in male Sprague-Dawley rats four hours after treatment with nitroglycerin (10mg/kg, i.p.) or its vehicle in the acute model, and 24h after the last treatment with nitroglycerin (5mg/kg, i.p.) or its vehicle in the chronic model (injections every other day over a 9-day period for a total of five injections):</p> <p>- evaluation of trigeminal hyperalgesia in the orofacial formalin test: the face rubbing was measured counting the seconds the animal spent grooming the injected area (upper lip, lateral to the nose) with the ipsilateral forepaw or hindpaw 0–3 min (Phase I) or 12–45 min (Phase II) after formalin injection (50 µl, s.c.). The observation time was divided into 15 blocks of 3 min each.</p> <p><strong><em>Ex vivo</em></strong> assessments performed on samples collected at the end of the behavioral test:</p> <p>- Microglia and astroglia activation was evaluated the trigeminal nucleus caudalis by means of immunofluorescence staining. Specifically, the medullary segment containing the trigeminal nucleus caudalis (between +1 and -5 mm from the obex) was removed and cut transversely at 30 µm thickness on a freezing sliding microtome. The anti-cluster of differentiation molecule 11b (anti-CD11b, 1:300) primary antibody (to detect microglia) or rabbit anti-glial fibrillary acidic protein (anti-GFAP, 1:500) primary antibody (to label astrocytes) were used. Cell count for microglia and astroglia was assessed by counting CD11b- or GFAP-positive cells, respectively, from a stack of 16 pictures (1μm-thick, 20x magnification) taken from four representative sections alongside the trigeminal nucleus caudalis. The total number of CD11b- and GFAP-positive cells of the four sections were summed and expressed per mm<sup>2</sup>. Glial activation state was rated on a scale ranging from score 0 to 3. The final activation state was calculated as the average of the scores assessed for each of the four representative sections of the trigeminal nucleus caudalis.</p> <p>- Satellite glial cells activation (anti-GFAP, 1:600), calcitonin gene-related peptide (CGRP) immunoreactivity (anti-CGRP, 1:500) and macrophage infiltration (anti-Iba1, 1:500) were evaluated in trigeminal ganglia using immunofluorescence staining. Specifically, trigeminal ganglia were removed and sectioned longitudinally at 20 µm thickness using a cryostat. In the trigeminal ganglia, the number of Iba1+ cells/area and the % of GFAP-encircled neurons and of CGRP+ neurons were assessed in whole TG sections acquired at 20X magnification.</p> <p>- Gene expression analysis: mRNA expression levels of (TNF-alpha), interleukin (IL) -1beta, IL-6, IL-10, inducible nitric oxide synthase (iNOS), GFAP, CD11b and CGRP in medulla oblongata and trigeminal ganglia. mRNA levels were measured by rt-PCR. All samples were assayed in triplicate and gene expression levels were calculated according to 2−∆∆Ct = 2− (∆Ct gene − ∆Ct housekeeping gene) formula by using Ct (cycle threshold) values.</p> <p><strong>Results </strong>- In nitroglycerin-treated rats, ADM_12 showed an anti-hyperalgesic effect in both the acute and chronic models. ADM_12 was able to counteract the acute and chronic nitroglycerin-induced changes in cytokines’ gene expression in both the areas of interest. In the acute nitroglycerin model, we reported a significant increase in microglial and astroglial activation in the trigeminalis nucleus caudalis area, which was abolished by ADM_12 treatment. In the chronic model, we detected an activation of satellite glial cells in the trigeminal ganglia in nitroglycerin-treated rats; this was inhibited by ADM_12. This latter also prevented the increase in CGRP gene expression levels in the trigeminal ganglia of nitroglycerin-treated animals.</p> <p> </p> <p> </p>
Antagonism of CGRP Receptor: Central and Peripheral Mechanisms and Mediators in an Animal Model of Chronic Migraine
<p>This dataset includes the findings obtained in the study aimed at investigating in more depth the interplay between the neuropeptide CGRP and the inflammatory mediators within the mechanisms of neuronal sensitization in an animal model of chronic migraine, using olcegepant as a pharmacological probe. Male Sprague-Dawley rats were exposed to nitroglycerin (NTG, 10 mg/kg, i.p.) or NTG vehicle and treated with the CGRP receptor antagonist olcegepant (1 or 2 mg/kg, i.p.) or vehicle (1 ml/kg, i.p.) 1h before the orofacial formalin test. Additionally, sets of rats received NTG (5 mg/kg, i.p.) or vehicle (equivalent volume) co-administered with olcegepant (2 mg/kg i.p.) or its vehicle every other day over a 9-day period. Twenty-four hours after the last injection of NTG (or vehicle), a first set of rats underwent the orofacial formalin test. In a second set, we evaluated the gene expression of CGRP and gene and protein expression of pro-inflammatory cytokines in specific areas involved in migraine pain. We also assessed the CGRP and cytokine levels in serum.</p> <p>The in vivo and ex vivo assessments were:</p> <p>1) Pain-related behavior in the orofacial formalin test: the face rubbing was measured counting the seconds the animal spent grooming the injected area (upper lip, lateral to the nose) with the ipsilateral forepaw or hindpaw 0–6 min (Phase I) or 12–45 min (Phase II) after formalin injection (50 µl, s.c.). The observation time was divided into 15 blocks of 3 min each.</p> <p>2) mRNA expression levels: CGRP, tumor necrosis factor-alpha (TNF-alpha), interleukin-1beta (IL-1beta), transient receptor potential ankyrin 1 (TRPA1) in cervical spinal cord (CSC), medulla-pons and trigeminal ganglia (TGs). mRNA levels were measured by rt-PCR. The same RNA was used for miRNAs (Mir-34a-5p, Mir-382-5p, Mir-155-5p) extraction in the same areas. All samples were assayed in triplicate and gene expression levels were calculated according to 2−∆∆Ct = 2− (∆Ct gene − ∆Ct housekeeping gene) formula by using Ct (cycle threshold) values.</p> <p>3) Pro-inflammatory cytokines in medulla-pons, CSC and TGs were evaluated using ELISA procedure. CGRP, TNF-alpha and IL-1beta serum levels were measured using commercial ELISA kits.</p> <p>Results in brief</p> <p>Olcegepant attenuated nitroglycerin-induced trigeminal hyperalgesia in the second phase of the orofacial formalin test. Interestingly, it also reduced gene expression and protein levels of CGRP, pro-inflammatory cytokines, inflammatory-associated miRNAs (miR-155-5p, miR-382-5p and miR-34a-5p) and TRPA1 channels in medulla-pons area, cervical spinal cord and trigeminal ganglia. Similarly, olcegepant reduced the NTG-induced increase of CGRP and inflammatory.</p>
Characterization of the biochemical and behavioral effects of cannabidiol: implications for migraine
<p>This dataset comprises the findings obtained in the study aimed at investigating the anti-migraine effects of cannabidiol (CBD) in the migraine rat models based by nitroglycerin (NTG) administration. We assayed CBD distribution (15 and 30mg/kg, i.p.) in plasma and in cranial areas related to migraine pain in male Sprague Dawley rats treated chronically (5 days). Successively, we tested CBD activity on the behavioral and biochemical effects induced in the acute and the chronic migraine animal models by NTG administration. In the acute migraine model, rats received CBD (15 mg or 30 mg/kg, i.p) 3 h after NTG (10 mg/kg i.p.) or vehicle injection. In the chronic migraine model, rats were treated with CBD and NTG every other day over nine days with the following doses: CBD 30 mg/kg i.p., NTG 10 mg/kg i.p. We evaluated behavioral parameters with the open field and the orofacial formalin tests. We explored the fatty acid amide hydrolase (FAAH) gene expression, cytokines mRNA and protein levels in selected brain areas and CGRP serum level. CBD levels in the meninges, trigeminal ganglia, cervical spinal cord, medulla pons, and plasma were higher 1 h after the last treatment than after 24 h, suggesting that CBD penetrates but does not accumulate in these tissues. In the acute model, CBD significantly reduced NTG-induced trigeminal hyperalgesia and CGRP and cytokine mRNA levels in peripheral and central sites. In the chronic model, CBD caused only a significant decrease in NTG-induced IL-6 protein levels in the medulla-pons, and trigeminal ganglion. It also reduced CGRP serum levels. In both experimental conditions, there was no modulation of anxiety, motor/exploratory behavior, or grooming.</p> <p>The in vivo and ex vivo assessments were:</p> <p>1) mRNA expression levels: CGRP, SP, interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-alpha) and FAAH in cervical spinal cord, medulla-pons and trigeminal ganglia. mRNA levels were measured by rt-PCR. All samples were assayed in triplicate and gene expression levels were calculated according to 2−∆∆Ct = 2− (∆Ct gene − ∆Ct housekeeping gene) formula by using Ct (cycle threshold) values.</p> <p>2) Central and peripheral CBD levels were quantified in rat brain tissue and plasma samples using a previously proven online solid phase extraction (SPE) high-performance liquid chromatography (HPLC) method coupled with tandem mass spectrometry (MS/MS).</p> <p>3) Cytokines and CGRP protein levels were measured using the ELISA kits. The samples' measured absorbance was compared to a standard curve using a microplate reader.</p> <p>4) Behavior Formalin test= the face rubbing was measured counting the seconds the animal spent grooming the injected area (seconds).</p> <p>5) open field test= distance (expressed in meters) travelled in the apparatus; time spent (expressed in seconds) in the center of the apparatus; number of rearing; time spent in grooming behavior (expressed in seconds).</p> <p>Results in brief</p> <p>These data show that CBD modulates migraine-related nociceptive transmission, likely via a complex signaling mechanism involving different pathways.</p>
Potentiation of endocannabinoids and other lipid amides prevents hyperalgesia and inflammation in a pre-clinical model of migraine
<p>This dataset comprises the findings obtained in the study aimed at investigating the anti-migraine effects of two URB597 analogs with improved solubility and bioavailability – ARN14633 ([4-fluoro-3-[3-(methylcarbamoyl)phenyl]phenyl] N-cyclohexylcarbamate) and ARN14280 ([3-(3-carbamoylphenyl)-4-(difluoromethoxy)phenyl] N-cyclohexylcarbamate), in the migraine rat model based by nitroglycerin (NTG) administration. Two compounds significantly attenuated the nocifensive behavior induced by NTG compared with original URB597 administered in the same conditions. Additionally, both inhibitors reverted the neurobiological changes induced by NTG in specific peripheral and central areas. Although the precise mechanism underlying these effects remains to be elucidated, our results support further investigational studies of FAAH blockade as a potential therapeutic strategy to treat migraine conditions.</p> <p>ARN14633 (1 mg/kg, i.p.), ARN14280 (3 mg/kg, i.p.) and URB597 (2mg/kg, i.p.) were administered to adult male Sprague-Dawley rats 3 hours after NTG injection. One hour after the administration of either compound, rats were subjected to the orofacial formalin test and compared. In addition, the anti-migraine effects of two URB597 analogs were evaluated by neuronal nitric oxide synthase, pain mediators peptides, pro-inflammatory cytokines gene expression and lipid amides levels in specific areas.</p> <p><strong>The in vivo and ex vivo assessments were:</strong></p> <p>1) mRNA expression levels: CGRP, SP, interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-alpha) and IL-1beta in cervical spinal cord, medulla-pons and trigeminal ganglia. mRNA levels were measured by rt-PCR. All samples were assayed in triplicate and gene expression levels were calculated according to 2−∆∆Ct = 2− (∆Ct gene − ∆Ct housekeeping gene) formula by using Ct (cycle threshold) values.</p> <p>2) Central and peripheral Endocannabinoids levels: Lipid amides levels were measured using a Xevo TQ UPLC-MS/MS system equipped with a reversed-phase BEH C18 column (2.1 × 50 mm, 1.7 μm particle size) (Waters, Milford, USA). The mobile phase consisted of 0.1% formic acid in water as solvent A and 0.1% formic acid in acetonitrile as solvent B. A linear gradient was used: 0.0–0.5 min 20% B; 0.5–2.5 min 20 to 100% B; and 2.5–3.0 min maintained at 100% B. The column was reconditioned to 20% B for 1 min. Analysis time was 4 min and the injection volume was 5 μL.</p> <p><strong>Results in brief</strong></p> <p>ARN14633 and ARN14280 attenuated NTG-induced nocifensive behavior compared with URB597. Additionally, the new FAAH inhibitors reduced transcription of genes encoding neuronal nitric oxide synthase, pain mediators peptides (calcitonin gene-related peptide, substance P) and pro-inflammatory cytokines (tumor necrosis factor-alpha, interleukin-1beta and 6) in the trigeminal ganglion, cervical spinal cord and medulla. Finally, both compounds strongly elevated levels of endocannabinoids and/or other FAAH substrates in cervical spinal cord and medulla, and, to a lesser extent, in the trigeminal ganglia.</p>
AMG 334 20160172 Pediatric Migraine PK Study.
ClinicalTrials.gov study NCT03499119. IPD Sharing: YES. Countries: 1. Publications: 1.
A Long-term Efficacy, Safety, and Tolerability Study of BOTOX® in Patients With Chronic Migraine
ClinicalTrials.gov study NCT01516892. IPD Sharing: Not stated. Countries: 3. Publications: 4.
Comparison of Therapeutic Effects of Greater Occipital Nerve Block, Topiramate, and Flunarizine on Episodic Migraine
ClinicalTrials.gov study NCT03712917. IPD Sharing: NO. Countries: 1. Publications: 2.
Efficacy, Safety, and Tolerability of Multiple Dosing Regimens of Oral Atogepant (AGN-241689) in Episodic Migraine Prevention
ClinicalTrials.gov study NCT02848326. IPD Sharing: Not stated. Countries: 1. Publications: 4.
Ascending Single Doses of Erenumab (AMG 334) in Healthy Adults and Migraine Patients
ClinicalTrials.gov study NCT01688739. IPD Sharing: Not stated. Countries: 1. Publications: 2.
Prospective Exploratory Study on rTMS for Migraine Under the Guidance of MEG
ClinicalTrials.gov study NCT06796725. IPD Sharing: UNDECIDED. Countries: 1. Publications: 2.
Investigation and Modulation of the Mu-Opioid Mechanisms in Migraine (in Vivo)
ClinicalTrials.gov study NCT02964741. IPD Sharing: NO. Countries: 1. Publications: 2.
Corticosteroids for Acute Migraine in the Emergency Department
ClinicalTrials.gov study NCT02847494. IPD Sharing: NO. Countries: 1. Publications: 1.
"Follow the Sutures". A New Procedure for Injection of Botulinum Toxin for Chronic Migraine
ClinicalTrials.gov study NCT03543254. IPD Sharing: NO. Countries: 1. Publications: 1.
A Randomized, Sham-controlled Study of gammaCore ® (nVNS) for Prevention of Episodic Migraine
ClinicalTrials.gov study NCT02378844. IPD Sharing: NO. Countries: 8. Publications: 1.
Safety and Efficacy of Nerivio™ for the Acute Treatment of Migraine in Adolescents
ClinicalTrials.gov study NCT04089761. IPD Sharing: NO. Countries: 1. Publications: 1.
Trial in Adult Subjects With Acute Migraines
ClinicalTrials.gov study NCT03461757. IPD Sharing: Not stated. Countries: 1. Publications: 4.
PArtial REbreathing for Migraine With Aura 1
ClinicalTrials.gov study NCT05546385. IPD Sharing: UNDECIDED. Countries: 2. Publications: 1.
Evaluation of Treatment Satisfaction and Preference for Sumavel DosePro in the Treatment of Migraine
ClinicalTrials.gov study NCT01016834. IPD Sharing: Not stated. Countries: 1. Publications: 2.
Rizatriptan for Episodic Dizziness in Vestibular Migraine
ClinicalTrials.gov study NCT02447991. IPD Sharing: Not stated. Countries: 1. Publications: 1.
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