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Migraine Disorders: HELP
Articles by Andrew F. Russo
Based on 16 articles published since 2010
(Why 16 articles?)
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Between 2010 and 2020, Andrew F. Russo wrote the following 16 articles about Migraine Disorders.
 
+ Citations + Abstracts
1 Editorial Migraine meets membrane trafficking. 2014

Russo, Andrew F. ·Molecular Physiology and Biophysics, University of Iowa, USA andrew-russo@uiowa.edu. ·Cephalalgia · Pubmed #24711607.

ABSTRACT: -- No abstract --

2 Review Behavioral and cognitive animal models in headache research. 2019

Vuralli, Doga / Wattiez, Anne-Sophie / Russo, Andrew F / Bolay, Hayrunnisa. ·Department of Neurology and Algology, Gazi University Faculty of Medicine, Besevler, 06510, Ankara, Turkey. · Neuropsychiatry Center, Gazi University, Besevler, 06510, Ankara, Turkey. · Department of Molecular Physiology and Biophysics, University of Iowa, Iowa City, IA, USA. · Center for the Prevention and Treatment of Visual Loss, Iowa VA Health Care System, Iowa City, IA, USA. · Department of Neurology, University of Iowa, Iowa City, IA, USA. · Department of Neurology and Algology, Gazi University Faculty of Medicine, Besevler, 06510, Ankara, Turkey. hbolay@gazi.edu.tr. · Neuropsychiatry Center, Gazi University, Besevler, 06510, Ankara, Turkey. hbolay@gazi.edu.tr. ·J Headache Pain · Pubmed #30704400.

ABSTRACT: Animal models have provided a growing body of information about the pathophysiology of headaches and novel therapeutic targets. In recent years, experiments in awake animals have gained attention as more relevant headache models. Pain can be assessed in animals using behavioral alterations, which includes sensory-discriminative, affective-emotional and cognitive aspects. Spontaneous behavioral alterations such as increased grooming, freezing, eye blinking, wet dog shake and head shake and decreased locomotion, rearing, food or water consumption observed during pain episodes are oftentimes easy to translate into clinical outcomes, but are giving little information about the localization and modality of the pain. Evoked pain response such as tactile and thermal hypersensitivity measures are less translatable but gives more insight into mechanisms of action. Mechanical allodynia is usually assessed with von Frey monofilaments and dynamic aesthesiometer, and thermal allodynia can be evaluated with acetone evaporation test and Hargreaves' test in animal models. Anxiety and depression are the most frequent comorbid diseases in headache disorders. Anxiety-like behaviors are evaluated with the open-field, elevated plus-maze or light/dark box tests. Interpretation of the latter test is challenging in migraine models, as presence of photophobia or photosensitivity can also be measured in light/dark boxes. Depressive behavior is assessed with the forced-swim or tail suspension tests. The majority of headache patients complain of cognitive symptoms and migraine is associated with poor cognitive performance in clinic-based studies. Cluster headache and tension type headache patients also exhibit a reversible cognitive dysfunction during the headache attacks. However, only a limited number of animal studies have investigated cognitive aspects of headache disorders, which remains a relatively unexplored aspect of these pathologies. Thus, the headache field has an excellent and growing selection of model systems that are likely to yield exciting advances in the future.

3 Review CGRP in Animal Models of Migraine. 2019

Wattiez, Anne-Sophie / Wang, Mengya / Russo, Andrew F. ·Department of Molecular Physiology and Biophysics, University of Iowa, Iowa City, IA, USA. · Center for the Prevention and Treatment of Visual Loss, Iowa VA Health Care System, Iowa City, IA, USA. · Department of Pharmacology, University of Iowa, Iowa City, IA, USA. · Department of Molecular Physiology and Biophysics, University of Iowa, Iowa City, IA, USA. andrew-russo@uiowa.edu. · Center for the Prevention and Treatment of Visual Loss, Iowa VA Health Care System, Iowa City, IA, USA. andrew-russo@uiowa.edu. · Department of Pharmacology, University of Iowa, Iowa City, IA, USA. andrew-russo@uiowa.edu. ·Handb Exp Pharmacol · Pubmed #30689086.

ABSTRACT: With the approval of calcitonin gene-related peptide (CGRP) and CGRP receptor monoclonal antibodies by the Federal Drug Administration, a new era in the treatment of migraine patients is beginning. However, there are still many unknowns in terms of CGRP mechanisms of action that need to be elucidated to allow new advances in migraine therapies. CGRP has been studied both clinically and preclinically since its discovery. Here we review some of the preclinical data regarding CGRP in animal models of migraine.

4 Review CGRP as a neuropeptide in migraine: lessons from mice. 2015

Russo, Andrew F. ·Department of Molecular Physiology and Biophysics, University of Iowa, Iowa City, IA, 52242, USA. · Department of Neurology, University of Iowa, Iowa City, IA, 52242, USA. · Veterans Affairs Medical Center, Iowa City, IA, 52246, USA. ·Br J Clin Pharmacol · Pubmed #26032833.

ABSTRACT: Migraine is a neurological disorder that is far more than just a bad headache. A hallmark of migraine is altered sensory perception. A likely contributor to this altered perception is the neuropeptide calcitonin gene-related peptide (CGRP). Over the past decade, CGRP has become firmly established as a key player in migraine. Although the mechanisms and sites of action by which CGRP might trigger migraine remain speculative, recent advances with mouse models provide some hints. This brief review focuses on how CGRP might act as both a central and peripheral neuromodulator to contribute to the migraine-like symptom of light aversive behaviour in mice.

5 Review Calcitonin gene-related peptide (CGRP): a new target for migraine. 2015

Russo, Andrew F. ·Departments of 1Molecular Physiology and Biophysics and. ·Annu Rev Pharmacol Toxicol · Pubmed #25340934.

ABSTRACT: Migraine is a neurological disorder that manifests as a debilitating headache associated with altered sensory perception. The neuropeptide calcitonin gene-related peptide (CGRP) is now firmly established as a key player in migraine. Clinical trials carried out during the past decade have proved that CGRP receptor antagonists are effective for treating migraine, and antibodies to the receptor and CGRP are currently under investigation. Despite this progress in the clinical arena, the mechanisms by which CGRP triggers migraine remain uncertain. This review discusses mechanisms whereby CGRP enhances sensitivity to sensory input at multiple levels in both the periphery and central nervous system. Future studies on epistatic and epigenetic regulators of CGRP actions are expected to shed further light on CGRP actions in migraine. In conclusion, targeting CGRP represents an approachable therapeutic strategy for migraine.

6 Review CGRP and migraine: could PACAP play a role too? 2013

Kaiser, Eric A / Russo, Andrew F. ·Department of Molecular Physiology and Biophysics, University of Iowa, Iowa City, IA 52242, United States. ·Neuropeptides · Pubmed #24210136.

ABSTRACT: Migraine is a debilitating neurological disorder that affects about 12% of the population. In the past decade, the role of the neuropeptide calcitonin gene-related peptide (CGRP) in migraine has been firmly established by clinical studies. CGRP administration can trigger migraines, and CGRP receptor antagonists ameliorate migraine. In this review, we will describe multifunctional activities of CGRP that could potentially contribute to migraine. These include roles in light aversion, neurogenic inflammation, peripheral and central sensitization of nociceptive pathways, cortical spreading depression, and regulation of nitric oxide production. Yet clearly there will be many other contributing genes that could act in concert with CGRP. One candidate is pituitary adenylate cyclase-activating peptide (PACAP), which shares some of the same actions as CGRP, including the ability to induce migraine in migraineurs and light aversive behavior in rodents. Interestingly, both CGRP and PACAP act on receptors that share an accessory subunit called receptor activity modifying protein-1 (RAMP1). Thus, comparisons between the actions of these two migraine-inducing neuropeptides, CGRP and PACAP, may provide new insights into migraine pathophysiology.

7 Review Calcitonin gene-related peptide in migraine: intersection of peripheral inflammation and central modulation. 2011

Raddant, Ann C / Russo, Andrew F. ·Department of Molecular Physiology and Biophysics, University of Iowa, Iowa City, IA 52242, USA. ·Expert Rev Mol Med · Pubmed #22123247.

ABSTRACT: Over the past two decades, a convergence of basic and clinical evidence has established the neuropeptide calcitonin-gene-related peptide (CGRP) as a key player in migraine. Although CGRP is a recognised neuromodulator of nociception, its mechanism of action in migraine remains elusive. In this review, we present evidence that led us to propose that CGRP is well poised to enhance neurotransmission in migraine by both peripheral and central mechanisms. In the periphery, it is thought that local release of CGRP from the nerve endings of meningeal nociceptors following their initial activation by cortical spreading depression is critical for the induction of vasodilation, plasma protein extravasation, neurogenic inflammation and the consequential sensitisation of meningeal nociceptors. Mechanistically, we propose that CGRP release can give rise to a positive-feedback loop involved in localised increased synthesis and release of CGRP from neurons and a CGRP-like peptide called procalcitonin from trigeminal ganglion glia. Within the brain, the wide distribution of CGRP and CGRP receptors provides numerous possible targets for CGRP to act as a neuromodulator.

8 Article Calcitonin gene-related peptide (CGRP): Role in migraine pathophysiology and therapeutic targeting. 2020

Wattiez, Anne-Sophie / Sowers, Levi P / Russo, Andrew F. ·Department of Physiology and Biophysics, University of Iowa, Iowa City, IA, USA. · VA Center for the Prevention and Treatment of Visual Loss, VA Medical Center, Iowa City, IA, USA. · Department of Neurology, University of Iowa, Iowa City, IA, USA. ·Expert Opin Ther Targets · Pubmed #32003253.

ABSTRACT:

9 Article CGRP-based Migraine Therapeutics: How Might They Work, Why So Safe, and What Next? 2019

Russo, Andrew F. ·Department of Molecular Physiology and Biophysics, University of Iowa, Iowa City, IA, 52242. · Department of Neurology, University of Iowa, Iowa City, IA, 52242. · Department of Center for the Prevention and Treatment of Visual Loss; Iowa VA Health Care System, Iowa City, IA, 52246. ·ACS Pharmacol Transl Sci · Pubmed #31559394.

ABSTRACT: Migraine is a debilitating neurological condition that involves the neuropeptide calcitonin gene-related peptide (CGRP). An exciting development is the recent FDA approval of the first in an emerging class of CGRP-targeted drugs designed to prevent migraine. Yet despite this efficacy, there are some fundamental unanswered questions, such as

10 Article Increased receptor activity-modifying protein 1 in the nervous system is sufficient to protect against autonomic dysregulation and hypertension. 2019

Sabharwal, Rasna / Mason, Bianca N / Kuburas, Adisa / Abboud, Francois M / Russo, Andrew F / Chapleau, Mark W. ·1 Department of Internal Medicine, University of Iowa, Iowa City, IA, USA. · 2 Molecular and Cell Biology Program, University of Iowa, Iowa City, IA, USA. · 3 Department of Molecular Physiology and Biophysics, University of Iowa, Iowa City, IA, USA. · 4 Department of Neurology, Carver College of Medicine, University of Iowa, Iowa City, IA, USA. · 5 Veterans Affairs Medical Center, Iowa City, IA, USA. ·J Cereb Blood Flow Metab · Pubmed #29297736.

ABSTRACT: Calcitonin gene-related peptide (CGRP) can cause migraines, yet it is also a potent vasodilator that protects against hypertension. Given the emerging role of CGRP-targeted antibodies for migraine prevention, an important question is whether the protective actions of CGRP are mediated by vascular or neural CGRP receptors. To address this, we have characterized the cardiovascular phenotype of transgenic nestin/hRAMP1 mice that have selective elevation of a CGRP receptor subunit in the nervous system, human receptor activity-modifying protein 1 (hRAMP1). Nestin/hRAMP1 mice had relatively little hRAMP1 RNA in blood vessels and intravenous injection of CGRP caused a similar blood pressure decrease in transgenic and control mice. At baseline, nestin/hRAMP1 mice exhibited similar mean arterial pressure, heart rate, baroreflex sensitivity, and sympathetic vasomotor tone as control mice. We previously reported that expression of hRAMP1 in all tissues favorably improved autonomic regulation and attenuated hypertension induced by angiotensin II (Ang II). Similarly, in nestin/hRAMP1 mice, hypertension caused by Ang II or phenylephrine was greatly attenuated, and associated autonomic dysregulation and increased sympathetic vasomotor tone were diminished or abolished. We conclude that increased expression of neuronal CGRP receptors is sufficient to induce a protective change in cardiovascular autonomic regulation with implications for migraine therapy.

11 Article Induction of calcitonin gene-related peptide expression in rats by cortical spreading depression. 2019

Wang, Yan / Tye, Anne E / Zhao, Junli / Ma, Dongqing / Raddant, Ann C / Bu, Fan / Spector, Benjamin L / Winslow, Nolan K / Wang, Minyan / Russo, Andrew F. ·1 Centre for Neuroscience and. · 3 Department of Biological Sciences, Xi'an Jiaotong-Liverpool University (XJTLU), SIP, Suzhou 215123, China. · 2 Neuroscience Program, Departments of. · 4 Molecular Physiology and Biophysics, and. · 5 Neurology, University of Iowa, Iowa City, IA 52242, USA. · 6 Veterans Affairs Medical Center, Iowa City, IA 52246, USA. ·Cephalalgia · Pubmed #27919019.

ABSTRACT: OBJECTIVE: The neuropeptide calcitonin gene-related peptide (CGRP) has now been established as a key player in migraine. However, the mechanisms underlying the reported elevation of CGRP in the serum and cerebrospinal fluid of some migraineurs are not known. A candidate mechanism is cortical spreading depression (CSD), which is associated with migraine with aura and traumatic brain injury. The aim of this study was to investigate whether CGRP gene expression may be induced by experimental CSD in the rat cerebral cortex. METHODS: CSD was induced by topical application of KCl and monitored using electrophysiological methods. Quantitative PCR and ELISA were used to measure CGRP mRNA and peptide levels in discrete ipsilateral and contralateral cortical regions of the rat brain 24 hours following CSD events and compared with sham treatments. RESULTS: The data show that multiple, but not single, CSD events significantly increase CGRP mRNA levels at 24 hours post-CSD in the ipsilateral rat cerebral cortex. Increased CGRP was observed in the ipsilateral frontal, motor, somatosensory, and visual cortices, but not the cingulate cortex, or contralateral cortices. CSD also induced CGRP peptide expression in the ipsilateral, but not contralateral, cortex. CONCLUSIONS: Repeated CSD provides a mechanism for prolonged elevation of CGRP in the cerebral cortex, which may contribute to migraine and post-traumatic headache.

12 Article Vascular Contributions to Migraine: Time to Revisit? 2018

Mason, Bianca N / Russo, Andrew F. ·Department of Molecular Physiology and Biophysics, University of Iowa, Iowa City, IA, United States. · Department of Neurology, University of Iowa, Iowa City, IA, United States. · Center for the Prevention and Treatment of Visual Loss, Iowa VA Health Care System, Iowa City, IA, United States. ·Front Cell Neurosci · Pubmed #30127722.

ABSTRACT: Migraine is one of the most prevalent and disabling neurovascular disorders worldwide. However, despite the increase in awareness and research, the understanding of migraine pathophysiology and treatment options remain limited. For centuries, migraine was considered to be a vascular disorder. In fact, the throbbing, pulsating quality of the headache is thought to be caused by mechanical changes in vessels. Moreover, the most successful migraine treatments act on the vasculature and induction of migraine can be accomplished with vasoactive agents. However, over the past 20 years, the emphasis has shifted to the neural imbalances associated with migraine, and vascular changes have generally been viewed as an epiphenomenon that is neither sufficient nor necessary to induce migraine. With the clinical success of peripherally-acting antibodies that target calcitonin gene-related peptide (CGRP) and its receptor for preventing migraine, this neurocentric view warrants a critical re-evaluation. This review will highlight the likely importance of the vasculature in migraine.

13 Article CGRP receptor antagonist activity of olcegepant depends on the signalling pathway measured. 2018

Walker, Christopher S / Raddant, Ann C / Woolley, Michael J / Russo, Andrew F / Hay, Debbie L. ·1 School of Biological Sciences, University of Auckland, Auckland, New Zealand. · 2 Centre for Brain Research, University of Auckland, Auckland, New Zealand. · 3 Department of Molecular Physiology and Biophysics, University of Iowa, Iowa City, IA, USA. · 4 Institute of Clinical Studies, University of Birmingham, Edgbaston, Birmingham, UK. · 5 Department of Neurology, University of Iowa; Veterans Affairs Medical Center, Iowa City, IA, USA. ·Cephalalgia · Pubmed #28165287.

ABSTRACT: Background Calcitonin gene-related peptide (CGRP) is a neuropeptide that acts in the trigeminovascular system and is believed to play an important role in migraine. CGRP activates two receptors that are both present in the trigeminovascular system; the CGRP receptor and the amylin 1 (AMY

14 Article Induction of Migraine-Like Photophobic Behavior in Mice by Both Peripheral and Central CGRP Mechanisms. 2017

Mason, Bianca N / Kaiser, Eric A / Kuburas, Adisa / Loomis, Maria-Cristina M / Latham, John A / Garcia-Martinez, Leon F / Russo, Andrew F. ·Molecular and Cellular Biology Program. · Department of Molecular Physiology and Biophysics, and. · Alder Biopharmaceuticals, Bothell, Washington 98011. · Molecular and Cellular Biology Program, andrew-russo@uiowa.edu. · Department of Neurology, University of Iowa, Iowa City, Iowa 52242. · Veterans Affairs Medical Center, Iowa City, Iowa 52246, and. ·J Neurosci · Pubmed #28053042.

ABSTRACT: The neuropeptide calcitonin gene-related peptide (CGRP) is a key player in migraine. Although migraine can be treated using CGRP antagonists that act peripherally, the relevant sites of CGRP action remain unknown. To address the role of CGRP both within and outside the CNS, we used CGRP-induced light-aversive behavior in mice as a measure of migraine-associated photophobia. Peripheral (intraperitoneal) injection of CGRP resulted in light-aversive behavior in wild-type CD1 mice similar to aversion seen previously after central (intracerebroventricular) injection. The phenotype was also observed in C57BL/6J mice, although to a lesser degree and with more variability. After intraperitoneal CGRP, motility was decreased in the dark only, similar to motility changes after intracerebroventricular CGRP. In addition, as with intracerebroventricular CGRP, there was no general increase in anxiety as measured in an open-field assay after intraperitoneal CGRP. Importantly, two clinically effective migraine drugs, the 5-HT SIGNIFICANCE STATEMENT: The neuropeptide calcitonin gene-related peptide (CGRP) is a central player in migraine pathogenesis, yet its site(s) of action remains unknown. Some preclinical studies have pointed to central sites in the brain and brainstem. However, a peripheral site of action is indicated by the ability of intravenous CGRP to trigger migraine in humans and the efficacy of CGRP receptor antagonists that evidently do no penetrate the CNS in effective amounts. Resolving this issue is particularly important given recent clinical trials showing that anti-CGRP monoclonal antibodies can reduce and even prevent migraine attacks. In this study, we report that CGRP can act in both the brain and the periphery of the mouse to cause migraine-like photophobia by apparently distinct mechanisms.

15 Article Anti-CGRP antibodies block CGRP-induced diarrhea in mice. 2017

Kaiser, Eric A / Rea, Brandon J / Kuburas, Adisa / Kovacevich, Brian R / Garcia-Martinez, Leon F / Recober, Ana / Russo, Andrew F. ·Departments of Molecular Physiology and Biophysics, University of Iowa, Iowa City, IA 52242, United States. · Alder Biopharmaceuticals Inc., Bothell, WA 98011, United States. · Department of Neurology, University of Iowa, Iowa City, IA 52242, United States. · Departments of Molecular Physiology and Biophysics, University of Iowa, Iowa City, IA 52242, United States; Department of Neurology, University of Iowa, Iowa City, IA 52242, United States; Veterans Affairs Medical Center, Iowa City, IA 52246, United States. Electronic address: andrew-russo@uiowa.edu. ·Neuropeptides · Pubmed #27865545.

ABSTRACT: The multifunctional neuropeptide calcitonin gene-related peptide (CGRP) and its receptor are expressed throughout the gastrointestinal tract. Previous studies have shown that CGRP has roles in intestinal motility, water secretion, and inflammation. Furthermore, animal studies have demonstrated CGRP involvement in diarrhea secondary to C. difficile and food allergies. Diarrhea thus provides a convenient bioassay of CGRP activity in the GI system. In this proof of principle study, we report that prophylactic administration of an anti-CGRP antibody is able to block CGRP-induced diarrhea in mice. As a control, the CGRP-receptor antagonist olcegepant also attenuated the diarrhea response to CGRP. This preclinical study indicates that anti-CGRP antibodies may provide a new preventative therapy for gastrointestinal disorders involving CGRP.

16 Article Reactive oxygen species induce procalcitonin expression in trigeminal ganglia glia. 2014

Raddant, Ann C / Russo, Andrew F. ·Department of Molecular Physiology and Biophysics, University of Iowa, Iowa City, IA, USA. ·Headache · Pubmed #24512072.

ABSTRACT: OBJECTIVE: To examine calcitonin gene-related peptide (CGRP) gene expression under inflammatory conditions using trigeminal ganglia organ cultures as an experimental system. These cultures have increased proinflammatory signaling that may mimic neurogenic inflammation in the migraine state. BACKGROUND: The trigeminal nerve sends peripheral pain signals to the central nervous system during migraine. Understanding the dynamic processes that occur within the trigeminal nerve and ganglion may provide insights into events that contribute to migraine pain. A neuropeptide of particular interest is CGRP, which can be elevated and play a causal role in migraine. However, most studies have overlooked a second splice product of the Calca gene that encodes calcitonin (CT), a peptide hormone involved in calcium homeostasis. Importantly, a precursor form of CT called procalcitonin (proCT) can act as a partial agonist at the CGRP receptor and elevated proCT has recently been reported during migraine. METHODS: We used a trigeminal ganglion whole organ explant model, which has previously been demonstrated to induce pro-inflammatory agents in vitro. Quantitative polymerase chain reaction and immunohistochemistry were used to evaluate changes in messenger ribonucleic acid (mRNA) and protein levels of CGRP and proCT. RESULTS: Whole mouse trigeminal ganglia cultured for 24 hours showed a 10-fold increase in CT mRNA, with no change in CGRP mRNA. A similar effect was observed in ganglia from adult rats. ProCT immunoreactivity was localized in glial cells. Cutting the tissue blunted the increase in CT, suggesting that induction required the close environment of the intact ganglia. Consistent with this prediction, there were increased reactive oxygen species in the ganglia, and the elevated CT mRNA was reduced by antioxidant treatment. Surprisingly, reactive oxygen species were increased in neurons, not glia. CONCLUSIONS: These results demonstrate that reactive oxygen species can activate proCT expression from the CGRP gene in trigeminal glia by a paracrine regulatory mechanism. We propose that this glial recruitment pathway may occur following cortical spreading depression and neurogenic inflammation to increase CGRP nociceptive actions in migraine.