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Article ; Online: Peripheral transient receptor potential vanilloid type 4 hypersensitivity contributes to chronic sickle cell disease pain.

Ehlers, Vanessa L / Sadler, Katelyn E / Stucky, Cheryl L

2023 Volume 164, Issue 8, Page(s) 1874–1886

Abstract: Abstract: Debilitating pain affects the lives of patients with sickle cell disease (SCD). Current pain treatment for patients with SCD fail to completely resolve acute or chronic SCD pain. Previous research indicates that the cation channel transient ... ...

Abstract	Abstract: Debilitating pain affects the lives of patients with sickle cell disease (SCD). Current pain treatment for patients with SCD fail to completely resolve acute or chronic SCD pain. Previous research indicates that the cation channel transient receptor potential vanilloid type 4 (TRPV4) mediates peripheral hypersensitivity in various inflammatory and neuropathic pain conditions that may share similar pathophysiology with SCD, but this channel's role in chronic SCD pain remains unknown. Thus, the current experiments examined whether TRPV4 regulates hyperalgesia in transgenic mouse models of SCD. Acute blockade of TRPV4 alleviated evoked behavioral hypersensitivity to punctate, but not dynamic, mechanical stimuli in mice with SCD. TRPV4 blockade also reduced the mechanical sensitivity of small, but not large, dorsal root ganglia neurons from mice with SCD. Furthermore, keratinocytes from mice with SCD showed sensitized TRPV4-dependent calcium responses. These results shed new light on the role of TRPV4 in SCD chronic pain and are the first to suggest a role for epidermal keratinocytes in the heightened sensitivity observed in SCD.
MeSH term(s)	Animals ; Mice ; Anemia, Sickle Cell/complications ; Anemia, Sickle Cell/metabolism ; Antineoplastic Agents/therapeutic use ; Chronic Pain ; Hyperalgesia/drug therapy ; Mice, Transgenic ; TRPV Cation Channels/genetics ; TRPV Cation Channels/metabolism
Chemical Substances	Antineoplastic Agents ; TRPV Cation Channels ; Trpv4 protein, mouse
Language	English
Publishing date	2023-03-10
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	193153-2
ISSN	1872-6623 ; 0304-3959
ISSN (online)	1872-6623
ISSN	0304-3959
DOI	10.1097/j.pain.0000000000002889
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Article ; Online: Cutaneous pain in disorders affecting peripheral nerves.

Stucky, Cheryl L / Mikesell, Alexander R

Neuroscience letters

2021 Volume 765, Page(s) 136233

Abstract: Our ability to quickly detect and respond to harmful environmental stimuli is vital for our safety and survival. This inherent acute pain detection is a "gift" because it both protects our body from harm and allows healing of damaged tissues [1]. Damage ... ...

Abstract	Our ability to quickly detect and respond to harmful environmental stimuli is vital for our safety and survival. This inherent acute pain detection is a "gift" because it both protects our body from harm and allows healing of damaged tissues [1]. Damage to tissues from trauma or disease can result in distorted or amplified nociceptor signaling and sensitization of the spinal cord and brain (Central Nervous System; CNS) pathways to normal input from light touch mechanoreceptors. Together, these processes can result in nagging to unbearable chronic pain and extreme sensitivity to light skin touch (allodynia). Unlike acute protective pain, chronic pain and allodynia serve no useful purpose and can severely reduce the quality of life of an affected person. Chronic pain can arise from impairment to peripheral neurons, a phenomenon called "peripheral neuropathic pain." Peripheral neuropathic pain can be caused by many insults that directly affect peripheral sensory neurons, including mechanical trauma, metabolic imbalance (e.g., diabetes), autoimmune diseases, chemotherapeutic agents, viral infections (e.g., shingles). These insults cause "acquired" neuropathies such as small-fiber neuropathies, diabetic neuropathy, chemotherapy-induced peripheral neuropathy, and post herpetic neuralgia. Peripheral neuropathic pain can also be caused by genetic factors and result in hereditary neuropathies that include Charcot-Marie-Tooth disease, rare channelopathies and Fabry disease. Many acquired and hereditary neuropathies affect the skin, our largest organ and protector of nearly our entire body. Here we review how cutaneous nociception (pain perceived from the skin) is altered following diseases that affect peripheral nerves that innervate the skin. We provide an overview of how noxious stimuli are detected and encoded by molecular transducers on subtypes of cutaneous afferent endings and conveyed to the CNS. Next, we discuss several acquired and hereditary diseases and disorders that cause painful or insensate (lack of sensation) cutaneous peripheral neuropathies, the symptoms and percepts patients experience, and how cutaneous afferents and other peripheral cell types are altered in function in these disorders. We highlight exciting new research areas that implicate non-neuronal skin cells, particularly keratinocytes, in cutaneous nociception and peripheral neuropathies. Finally, we conclude with ideas for innovative new directions, areas of unmet need, and potential opportunities for novel cutaneous therapeutics that may avoid CNS side effects, as well as ideas for improved translation of mechanisms identified in preclinical models to patients.
MeSH term(s)	Animals ; Cell Communication ; Disease Models, Animal ; Humans ; Keratinocytes/metabolism ; Nociception ; Nociceptors/metabolism ; Pain/etiology ; Pain/pathology ; Peripheral Nerves/pathology ; Peripheral Nervous System Diseases/complications ; Peripheral Nervous System Diseases/pathology ; Schwann Cells/metabolism ; Skin/innervation
Language	English
Publishing date	2021-10-01
Publishing country	Ireland
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	194929-9
ISSN	1872-7972 ; 0304-3940
ISSN (online)	1872-7972
ISSN	0304-3940
DOI	10.1016/j.neulet.2021.136233
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Article ; Online: Use the force, fluke: Ligand-independent gating of Schistosoma mansoni ion channel TRPM

Chulkov, Evgeny G / Isaeva, Elena / Stucky, Cheryl L / Marchant, Jonathan S

International journal for parasitology

2023 Volume 53, Issue 8, Page(s) 427–434

Abstract: The parasitic flatworm ion channel, ... ...

Abstract	The parasitic flatworm ion channel, TRPM
MeSH term(s)	Schistosoma mansoni ; TRPM Cation Channels/metabolism ; Helminth Proteins/metabolism ; Humans ; Animals ; Pressure ; Adenosine Diphosphate Ribose/metabolism
Chemical Substances	TRPM Cation Channels ; Helminth Proteins ; Adenosine Diphosphate Ribose (20762-30-5)
Language	English
Publishing date	2023-01-04
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	120518-3
ISSN	1879-0135 ; 0020-7519
ISSN (online)	1879-0135
ISSN	0020-7519
DOI	10.1016/j.ijpara.2022.11.004
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Zs.A 789: Show issues

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Article ; Online: Fabry disease pain: patient and preclinical parallels.

Burand, Anthony J / Stucky, Cheryl L

Pain

2020 Volume 162, Issue 5, Page(s) 1305–1321

Abstract: Abstract: Severe neuropathic pain is a hallmark of Fabry disease, a genetic disorder caused by a deficiency in lysosomal α-galactosidase A. Pain experienced by these patients significantly impacts their quality of life and ability to perform everyday ... ...

Abstract	Abstract: Severe neuropathic pain is a hallmark of Fabry disease, a genetic disorder caused by a deficiency in lysosomal α-galactosidase A. Pain experienced by these patients significantly impacts their quality of life and ability to perform everyday tasks. Patients with Fabry disease suffer from peripheral neuropathy, sensory abnormalities, acute pain crises, and lifelong ongoing pain. Although treatment of pain through medication and enzyme replacement therapy exists, pain persists in many of these patients. Some has been learned in the past decades regarding clinical manifestations of pain in Fabry disease and the pathological effects of α-galactosidase A insufficiency in neurons. Still, it is unclear how pain and sensory abnormalities arise in patients with Fabry disease and how these can be targeted with therapeutics. Our knowledge is limited in part due to the lack of adequate preclinical models to study the disease. This review will detail the types of pain, sensory abnormalities, influence of demographics on pain, and current strategies to treat pain experienced by patients with Fabry disease. In addition, we discuss the current knowledge of Fabry pain pathogenesis and which aspects of the disease preclinical models accurately recapitulate. Understanding the commonalities and divergences between humans and preclinical models can be used to further interrogate mechanisms causing the pain and sensory abnormalities as well as advance development of the next generation of therapeutics to treat pain in patients with Fabry disease.
MeSH term(s)	Fabry Disease/complications ; Humans ; Neuralgia/etiology ; Neurons ; Quality of Life ; alpha-Galactosidase/genetics ; alpha-Galactosidase/therapeutic use
Chemical Substances	alpha-Galactosidase (EC 3.2.1.22)
Language	English
Publishing date	2020-12-01
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	193153-2
ISSN	1872-6623 ; 0304-3959
ISSN (online)	1872-6623
ISSN	0304-3959
DOI	10.1097/j.pain.0000000000002152
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Article ; Online: HomeCageScan analysis reveals ongoing pain in Fabry rats.

Burand, Anthony J / Waltz, Tyler B / Manis, Anna D / Hodges, Matthew R / Stucky, Cheryl L

Neurobiology of pain (Cambridge, Mass.)

2023 Volume 13, Page(s) 100113

Abstract: HomeCageScan (HCS) is an automated behavioral scoring system that can be used to classify and quantify rodent behaviors in the home cage. Although HCS has been used for a number of inducible models of severe pain, little has been done to test this system ...

Abstract	HomeCageScan (HCS) is an automated behavioral scoring system that can be used to classify and quantify rodent behaviors in the home cage. Although HCS has been used for a number of inducible models of severe pain, little has been done to test this system in clinically relevant genetic disease models associated with chronic pain such as Fabry disease. Rats with Fabry disease exhibit mechanical hypersensitivity, however, it is unclear if these rodents also exhibit ongoing non-evoked pain. Therefore, we analyzed HCS data from male and female rats with Fabry disease. Using hierarchical clustering and principal component analysis, we found both sex and genotype differences in several home cage behaviors. Additionally, we used hierarchical clustering to derive behavioral clusters in an unbiased manner. Analysis of these behavioral clusters showed that primarily female Fabry animals moved less, spent less time caring for themselves (e.g., less time spent grooming and drinking), explored less, and slept more; changes that are similar to lifestyle changes observed in patients with long lasting chronic pain. We also show that sniffing, one of the exploratory behaviors that is depressed in Fabry animals, can be partly restored with the analgesic gabapentin, suggesting that depressed sniffing may reflect ongoing pain. Therefore, this approach to HCS data analysis can be used to assess drug efficacy in Fabry disease and potentially other genetic and inducible rodent models associated with persistent pain.
Language	English
Publishing date	2023-01-05
Publishing country	United States
Document type	Journal Article
ISSN	2452-073X
ISSN (online)	2452-073X
DOI	10.1016/j.ynpai.2022.100113
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Article: A Mouse Model of Postoperative Pain.

Cowie, Ashley M / Stucky, Cheryl L

Bio-protocol

2019 Volume 9, Issue 2

Abstract: Postoperative pain is highly debilitating and hinders recovery. Opioids are the main pain medication used for acute postoperative pain. Given the devastating opioid addiction and overdose epidemic across the US, non-opioid pain therapeutics are ... ...

Abstract	Postoperative pain is highly debilitating and hinders recovery. Opioids are the main pain medication used for acute postoperative pain. Given the devastating opioid addiction and overdose epidemic across the US, non-opioid pain therapeutics are desperately needed. In order to develop novel, non-opioid therapies for the treatment of postoperative pain and identify the mechanisms underlying this pain, rodent models of incisional pain have been established. The protocol herein describes in detail how to create a mouse model of postoperative pain that was adapted from established protocols. This model of postoperative pain is frequently-used, highly reproducible, and results in peripheral and central nervous system alterations.
Language	English
Publishing date	2019-03-12
Publishing country	United States
Document type	Journal Article
ZDB-ID	2833269-6
ISSN	2331-8325
ISSN	2331-8325
DOI	10.21769/BioProtoc.3140
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Article ; Online: Innovations and advances in modelling and measuring pain in animals.

Sadler, Katelyn E / Mogil, Jeffrey S / Stucky, Cheryl L

Nature reviews. Neuroscience

2021 Volume 23, Issue 2, Page(s) 70–85

Abstract: Best practices in preclinical algesiometry (pain behaviour testing) have shifted over the past decade as a result of technological advancements, the continued dearth of translational progress and the emphasis that funding institutions and journals have ... ...

Abstract	Best practices in preclinical algesiometry (pain behaviour testing) have shifted over the past decade as a result of technological advancements, the continued dearth of translational progress and the emphasis that funding institutions and journals have placed on rigour and reproducibility. Here we describe the changing trends in research methods by analysing the methods reported in preclinical pain publications from the past 40 years, with a focus on the last 5 years. We also discuss how the status quo may be hampering translational success. This discussion is centred on four fundamental decisions that apply to every pain behaviour experiment: choice of subject (model organism), choice of assay (pain-inducing injury), laboratory environment and choice of outcome measures. Finally, we discuss how human tissues, which are increasingly accessible, can be used to validate the translatability of targets and mechanisms identified in animal pain models.
MeSH term(s)	Animal Testing Alternatives ; Animals ; Disease Models, Animal ; Humans ; Models, Animal ; Pain/diagnosis ; Pain Measurement/methods ; Pain Measurement/trends
Language	English
Publishing date	2021-11-26
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2034150-7
ISSN	1471-0048 ; 1471-0048 ; 1471-003X
ISSN (online)	1471-0048
ISSN	1471-0048 ; 1471-003X
DOI	10.1038/s41583-021-00536-7
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Zs.A 5473: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MG 47: Show issues

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Article ; Online: Blocking COX-2 for sickle cell pain relief.

Sadler, Katelyn E / Stucky, Cheryl L

Blood

2019 Volume 133, Issue 18, Page(s) 1924–1925

MeSH term(s)	Anemia, Sickle Cell ; Animals ; Cyclooxygenase 2 ; Dinoprostone ; Glycerol ; Hyperalgesia ; Mice ; Nociceptors ; Pain
Chemical Substances	Cyclooxygenase 2 (EC 1.14.99.1) ; Dinoprostone (K7Q1JQR04M) ; Glycerol (PDC6A3C0OX)
Language	English
Publishing date	2019-04-26
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Comment
ZDB-ID	80069-7
ISSN	1528-0020 ; 0006-4971
ISSN (online)	1528-0020
ISSN	0006-4971
DOI	10.1182/blood-2019-03-900944
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Article ; Online: Neuronal transient receptor potential (TRP) channels and noxious sensory detection in sickle cell disease.

Sadler, Katelyn E / Stucky, Cheryl L

Neuroscience letters

2018 Volume 694, Page(s) 184–191

Abstract: Pain is the leading cause for hospitalization in patients with sickle cell disease (SCD). While the characteristics of SCD pain can vary widely between patients and between phases of the disease (e.g. vasoocclusive crisis pain vs. chronic pain), similar ... ...

Abstract	Pain is the leading cause for hospitalization in patients with sickle cell disease (SCD). While the characteristics of SCD pain can vary widely between patients and between phases of the disease (e.g. vasoocclusive crisis pain vs. chronic pain), similar neuronal mechanisms likely underlie the various aspects of nociceptive processing. In the peripheral nervous system, small unmyelinated C fibers and lightly-myelinated Aδ fibers detect and transmit noxious stimuli. Both classes of neurons express members of the transient receptor potential (TRP) family, a group of ligand gated ion-channels that are activated by thermal, chemical, and mechanical stimuli. Promiscuous TRP channel family members are activated by a wide range of stimuli, many of which are dysregulated in patients with SCD and transgenic SCD mouse models. In 2011, our lab published the first report of TRP channel contributions to rodent SCD pain. Since that time, additional basic and clinical research efforts have investigated the genetic and biochemical status of TRP channels in SCD, placing particular focus on TRPV1. This review will discuss these advances and highlight the clinical SCD presentations that have not yet been studied, but which may be mediated by TRP channel activity.
MeSH term(s)	Anemia, Sickle Cell/complications ; Anemia, Sickle Cell/physiopathology ; Animals ; Humans ; Hyperalgesia/complications ; Nociception/physiology ; Pain/complications ; Pain/physiopathology ; TRPA1 Cation Channel/physiology ; TRPM Cation Channels/physiology ; TRPV Cation Channels/physiology ; Transient Receptor Potential Channels/physiology
Chemical Substances	TRPA1 Cation Channel ; TRPA1 protein, human ; TRPM Cation Channels ; TRPM8 protein, human ; TRPV Cation Channels ; TRPV1 protein, human ; Transient Receptor Potential Channels
Language	English
Publishing date	2018-11-30
Publishing country	Ireland
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	194929-9
ISSN	1872-7972 ; 0304-3940
ISSN (online)	1872-7972
ISSN	0304-3940
DOI	10.1016/j.neulet.2018.11.056
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Article ; Online: Keratinocytes contribute to normal cold and heat sensation.

Sadler, Katelyn E / Moehring, Francie / Stucky, Cheryl L

eLife

2020 Volume 9

Abstract: Keratinocytes are the most abundant cell type in the epidermis, the most superficial layer of skin. Historically, epidermal-innervating sensory neurons were thought to be the exclusive detectors and transmitters of environmental stimuli. However, recent ... ...

Abstract	Keratinocytes are the most abundant cell type in the epidermis, the most superficial layer of skin. Historically, epidermal-innervating sensory neurons were thought to be the exclusive detectors and transmitters of environmental stimuli. However, recent work from our lab (Moehring et al., 2018) and others (Baumbauer et al., 2015) has demonstrated that keratinocytes are also critical for normal mechanotransduction and mechanically-evoked behavioral responses in mice. Here, we asked whether keratinocyte activity is also required for normal cold and heat sensation. Using calcium imaging, we determined that keratinocyte cold activity is conserved across mammalian species and requires the release of intracellular calcium through one or more unknown cold-sensitive proteins. Both epidermal cell optogenetic inhibition and interruption of ATP-P2X4 signaling reduced reflexive behavioral responses to cold and heat stimuli. Based on these data and our previous findings, keratinocyte purinergic signaling is a modality-conserved amplification system that is required for normal somatosensation in vivo.
MeSH term(s)	Animals ; Calcium/metabolism ; Cells, Cultured ; Cold Temperature ; Female ; Hot Temperature ; Humans ; Keratin-14/antagonists & inhibitors ; Keratin-14/metabolism ; Keratinocytes/physiology ; Male ; Mice ; Mice, Transgenic ; Rats ; Rats, Sprague-Dawley ; Receptors, Purinergic/metabolism ; Sciuridae ; Sensory Receptor Cells/metabolism ; Signal Transduction ; Species Specificity ; Thermosensing/physiology
Chemical Substances	Keratin-14 ; Receptors, Purinergic ; Calcium (SY7Q814VUP)
Language	English
Publishing date	2020-07-30
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2687154-3
ISSN	2050-084X ; 2050-084X
ISSN (online)	2050-084X
ISSN	2050-084X
DOI	10.7554/eLife.58625
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