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Article ; Online: Selective PDE4B and PDE4D inhibitors produce distinct behavioral responses to ethanol and GABAergic drugs in mice.

Blednov, Yuri A / Da Costa, Adriana / Mason, Sonia / Mayfield, Jody / Messing, Robert O

2023 Volume 231, Page(s) 109508

Abstract: Apremilast is a phosphodiesterase (PDE) type 4 inhibitor that is nonselective at subtypes PDE4A-D. It modulates ethanol and GABAergic responses via protein kinase A (PKA) phosphorylation of specific ... ...

Abstract	Apremilast is a phosphodiesterase (PDE) type 4 inhibitor that is nonselective at subtypes PDE4A-D. It modulates ethanol and GABAergic responses via protein kinase A (PKA) phosphorylation of specific GABA
MeSH term(s)	Mice ; Male ; Female ; Animals ; Ethanol ; Propofol ; Mice, Inbred C57BL ; Cyclic Nucleotide Phosphodiesterases, Type 4/metabolism ; Hypnotics and Sedatives/pharmacology ; Phosphodiesterase 4 Inhibitors/pharmacology ; Ataxia ; Diazepam/pharmacology
Chemical Substances	Ethanol (3K9958V90M) ; D159687 ; apremilast (UP7QBP99PN) ; Propofol (YI7VU623SF) ; PDE4B inhibitor A33 ; Cyclic Nucleotide Phosphodiesterases, Type 4 (EC 3.1.4.17) ; Hypnotics and Sedatives ; Phosphodiesterase 4 Inhibitors ; Diazepam (Q3JTX2Q7TU) ; PDE4B protein, mouse (EC 3.1.4.17)
Language	English
Publishing date	2023-03-18
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	218272-5
ISSN	1873-7064 ; 0028-3908
ISSN (online)	1873-7064
ISSN	0028-3908
DOI	10.1016/j.neuropharm.2023.109508
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Article ; Online: Knockdown of Tlr3 in dorsal striatum reduces ethanol consumption and acute functional tolerance in male mice.

Dilly, Geoffrey A / Blednov, Yuri A / Warden, Anna S / Ezerskiy, Lubov / Fleischer, Caleb / Plotkin, Jesse D / Patil, Shruti / Osterndorff-Kahanek, Elizabeth A / Mayfield, Jody / Mayfield, R Dayne / Homanics, Gregg E / Messing, Robert O

Brain, behavior, and immunity

2024 Volume 118, Page(s) 437–448

Abstract: Systemic activation of toll-like receptor 3 (TLR3) signaling using poly(I:C), a TLR3 agonist, drives ethanol consumption in several rodent models, while global knockout of Tlr3 reduces drinking in C57BL/6J male mice. To determine if brain TLR3 pathways ... ...

Abstract	Systemic activation of toll-like receptor 3 (TLR3) signaling using poly(I:C), a TLR3 agonist, drives ethanol consumption in several rodent models, while global knockout of Tlr3 reduces drinking in C57BL/6J male mice. To determine if brain TLR3 pathways are involved in drinking behavior, we used CRISPR/Cas9 genome editing to generate a Tlr3 floxed (Tlr3
MeSH term(s)	Mice ; Male ; Animals ; Toll-Like Receptor 3/metabolism ; Mice, Inbred C57BL ; Ethanol/pharmacology ; Signal Transduction ; Alcohol Drinking/metabolism ; Poly I-C/pharmacology
Chemical Substances	Toll-Like Receptor 3 ; Ethanol (3K9958V90M) ; Poly I-C (O84C90HH2L)
Language	English
Publishing date	2024-03-16
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	639219-2
ISSN	1090-2139 ; 0889-1591
ISSN (online)	1090-2139
ISSN	0889-1591
DOI	10.1016/j.bbi.2024.03.021
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Article ; Online: Apremilast-induced increases in acute ethanol intoxication and decreases in ethanol drinking in mice involve PKA phosphorylation of GABA

Blednov, Yuri A / Da Costa, Adriana / Mason, Sonia / Mayfield, Jody / Moss, Stephen J / Messing, Robert O

Neuropharmacology

2022 Volume 220, Page(s) 109255

Abstract: We previously showed that apremilast, an FDA-approved PDE4 inhibitor, selectively alters behavioral responses to ethanol and certain GABAergic drugs in a PKA-dependent manner in C57BL6/J mice. Here, we investigated if PKA phosphorylation of β3 ... ...

Abstract	We previously showed that apremilast, an FDA-approved PDE4 inhibitor, selectively alters behavioral responses to ethanol and certain GABAergic drugs in a PKA-dependent manner in C57BL6/J mice. Here, we investigated if PKA phosphorylation of β3 GABA
MeSH term(s)	Alcohol Drinking/drug therapy ; Alcoholic Intoxication ; Alcoholism ; Animals ; Ataxia ; Diazepam ; Ethanol/pharmacology ; Female ; Hypnotics and Sedatives ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Phosphodiesterase 4 Inhibitors/pharmacology ; Phosphorylation ; Propofol ; Receptors, GABA-A/metabolism ; Thalidomide/analogs & derivatives ; gamma-Aminobutyric Acid
Chemical Substances	Hypnotics and Sedatives ; Phosphodiesterase 4 Inhibitors ; Receptors, GABA-A ; Ethanol (3K9958V90M) ; Thalidomide (4Z8R6ORS6L) ; gamma-Aminobutyric Acid (56-12-2) ; Diazepam (Q3JTX2Q7TU) ; apremilast (UP7QBP99PN) ; Propofol (YI7VU623SF)
Language	English
Publishing date	2022-09-21
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	218272-5
ISSN	1873-7064 ; 0028-3908
ISSN (online)	1873-7064
ISSN	0028-3908
DOI	10.1016/j.neuropharm.2022.109255
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Article ; Online: Deletion of Tlr3 reduces acute tolerance to alcohol and alcohol consumption in the intermittent access procedure in male mice.

Blednov, Yuri A / Da Costa, Adriana / Mayfield, Jody / Harris, R Adron / Messing, Robert O

Addiction biology

2020 Volume 26, Issue 2, Page(s) e12932

Abstract: Pharmacological studies implicate toll-like receptor 3 (TLR3) signaling in alcohol drinking. We examined the role of TLR3 in behavioral responses to alcohol and GABAergic drugs by studying ... ...

Abstract	Pharmacological studies implicate toll-like receptor 3 (TLR3) signaling in alcohol drinking. We examined the role of TLR3 in behavioral responses to alcohol and GABAergic drugs by studying Tlr3
MeSH term(s)	Animals ; Diazepam/pharmacology ; Drug Tolerance/genetics ; Ethanol/pharmacology ; Isoxazoles/pharmacology ; Male ; Mice ; Mice, Knockout ; Myeloid Differentiation Factor 88/genetics ; Sex Factors ; Substance Withdrawal Syndrome ; Toll-Like Receptor 3/genetics ; gamma-Aminobutyric Acid/drug effects
Chemical Substances	Isoxazoles ; Myeloid Differentiation Factor 88 ; Toll-Like Receptor 3 ; Ethanol (3K9958V90M) ; gamma-Aminobutyric Acid (56-12-2) ; gaboxadol (K1M5RVL18S) ; Diazepam (Q3JTX2Q7TU)
Language	English
Publishing date	2020-06-30
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	1324314-7
ISSN	1369-1600 ; 1355-6215
ISSN (online)	1369-1600
ISSN	1355-6215
DOI	10.1111/adb.12932
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Article ; Online: Glial gene networks associated with alcohol dependence.

Erickson, Emma K / Blednov, Yuri A / Harris, R Adron / Mayfield, R Dayne

Scientific reports

2019 Volume 9, Issue 1, Page(s) 10949

Abstract: Chronic alcohol abuse alters the molecular structure and function of brain cells. Recent work suggests adaptations made by glial cells, such as astrocytes and microglia, regulate physiological and behavioral changes associated with addiction. Defining ... ...

Abstract	Chronic alcohol abuse alters the molecular structure and function of brain cells. Recent work suggests adaptations made by glial cells, such as astrocytes and microglia, regulate physiological and behavioral changes associated with addiction. Defining how alcohol dependence alters the transcriptome of different cell types is critical for developing the mechanistic hypotheses necessary for a nuanced understanding of cellular signaling in the alcohol-dependent brain. We performed RNA-sequencing on total homogenate and glial cell populations isolated from mouse prefrontal cortex (PFC) following chronic intermittent ethanol vapor exposure (CIE). Compared with total homogenate, we observed unique and robust gene expression changes in astrocytes and microglia in response to CIE. Gene co-expression network analysis revealed biological pathways and hub genes associated with CIE in astrocytes and microglia that may regulate alcohol-dependent phenotypes. Astrocyte identity and synaptic calcium signaling genes were enriched in alcohol-associated astrocyte networks, while TGF-β signaling and inflammatory response genes were disrupted by CIE treatment in microglia gene networks. Genes related to innate immune signaling, specifically interferon pathways, were consistently up-regulated across CIE-exposed astrocytes, microglia, and total homogenate PFC tissue. This study illuminates the cell-specific effects of chronic alcohol exposure and provides novel molecular targets for studying alcohol dependence.
MeSH term(s)	Alcoholism/genetics ; Animals ; Astrocytes/metabolism ; Astrocytes/pathology ; Ethanol/metabolism ; Gene Regulatory Networks ; Male ; Mice ; Mice, Inbred C57BL ; Microglia/metabolism ; Microglia/pathology ; Prefrontal Cortex/metabolism ; Prefrontal Cortex/pathology ; RNA-Seq ; Transcriptome
Chemical Substances	Ethanol (3K9958V90M)
Language	English
Publishing date	2019-07-29
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-019-47454-4
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Article ; Online: Effects of Pharmacologically Targeting Neuroimmune Pathways on Alcohol Drinking in Mice Selectively Bred to Drink to Intoxication.

Ozburn, Angela R / Metten, Pamela / Potretzke, Sheena / Townsley, Kayla G / Blednov, Yuri A / Crabbe, John C

Alcoholism, clinical and experimental research

2020 Volume 44, Issue 2, Page(s) 553–566

Abstract: Background: Rodent models of high alcohol drinking offer opportunities to better understand factors for alcohol use disorders (AUD) and test potential treatments. Selective breeding was carried out to create 2 unique High Drinking in the Dark (HDID-1, ... ...

Abstract	Background: Rodent models of high alcohol drinking offer opportunities to better understand factors for alcohol use disorders (AUD) and test potential treatments. Selective breeding was carried out to create 2 unique High Drinking in the Dark (HDID-1, HDID-2) mouse lines that represent models of genetic risk for binge-like drinking. A number of studies have indicated that neuroimmune genes are important for regulation of alcohol drinking. We tested whether compounds shown to reduce drinking in other models also reduce alcohol intake in these unique genetic lines. Methods: We report tests of gabapentin, tesaglitazar, fenofibrate, caffeic acid phenethyl ester (CAPE), ibrutinib, and rolipram. Although these compounds have different mechanisms of action, they have all been shown to reduce inflammatory responses. We evaluated effects of these compounds on alcohol intake. In order to facilitate comparison with previously published findings for some compounds, we employed similar schedules that were previously used for that compound. Results: Gabapentin increased ethanol (EtOH) binge-like alcohol drinking in female HDID-1 and HS/NPT mice. Tesaglitazar and fenofibrate did not alter 2-bottle choice (2BC) drinking in male HDID-1 or HS/NPT mice. However, tesaglitazar had no effect on DID EtOH intake but reduced blood alcohol levels (BAL), and fenofibrate increased DID intake with no effects on BAL. CAPE had no effect on EtOH intake. Ibrutinib reduced intake in female HDID-1 in initial testing, but did not reduce intake in a second week of testing. Rolipram reduced DID intake and BALs in male and female HDID-1, HDID-2, and HS/NPT mice. Conclusions: A number of compounds shown to reduce EtOH drinking in other models, and genotypes are not effective in HDID mice or their genetically heterogeneous founders, HS/NPT. The most promising compound was the PDE4 inhibitor, rolipram. These results highlight the importance of assessing generalizability when rigorously testing compounds for therapeutic development.
MeSH term(s)	Alcohol Drinking/drug therapy ; Alcohol Drinking/genetics ; Alcohol Drinking/immunology ; Alcoholic Intoxication/drug therapy ; Alcoholic Intoxication/genetics ; Alcoholic Intoxication/immunology ; Alkanesulfonates/administration & dosage ; Animals ; Binge Drinking/drug therapy ; Binge Drinking/genetics ; Binge Drinking/immunology ; Dose-Response Relationship, Drug ; Drug Delivery Systems/methods ; Female ; Fenofibrate/administration & dosage ; Gabapentin/administration & dosage ; Male ; Mice ; Mice, Inbred Strains ; Mice, Transgenic ; Neuroimmunomodulation/drug effects ; Neuroimmunomodulation/immunology ; Phenylpropionates/administration & dosage ; Rolipram/administration & dosage ; Signal Transduction/drug effects ; Signal Transduction/physiology
Chemical Substances	Alkanesulfonates ; Phenylpropionates ; tesaglitazar (6734037O3L) ; Gabapentin (6CW7F3G59X) ; Rolipram (K676NL63N7) ; Fenofibrate (U202363UOS)
Language	English
Publishing date	2020-01-13
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	428999-7
ISSN	1530-0277 ; 0145-6008
ISSN (online)	1530-0277
ISSN	0145-6008
DOI	10.1111/acer.14269
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Article: CNS cell-type localization and LPS response of TLR signaling pathways.

McCarthy, Gizelle M / Bridges, Courtney R / Blednov, Yuri A / Harris, R Adron

F1000Research

2017 Volume 6, Page(s) 1144

Abstract: Background: ...

Abstract	Background:
Language	English
Publishing date	2017-07-19
Publishing country	England
Document type	Journal Article
ZDB-ID	2699932-8
ISSN	2046-1402
ISSN	2046-1402
DOI	10.12688/f1000research.12036.1
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Article ; Online: Behavioral and Genetic Evidence for GIRK Channels in the CNS: Role in Physiology, Pathophysiology, and Drug Addiction.

Mayfield, Jody / Blednov, Yuri A / Harris, R Adron

International review of neurobiology

2015 Volume 123, Page(s) 279–313

Abstract: G protein-coupled inwardly rectifying potassium (GIRK) channels are widely expressed throughout the brain and mediate the inhibitory effects of many neurotransmitters. As a result, these channels are important for normal CNS function and have also been ... ...

Abstract	G protein-coupled inwardly rectifying potassium (GIRK) channels are widely expressed throughout the brain and mediate the inhibitory effects of many neurotransmitters. As a result, these channels are important for normal CNS function and have also been implicated in Down syndrome, Parkinson's disease, psychiatric disorders, epilepsy, and drug addiction. Knockout mouse models have provided extensive insight into the significance of GIRK channels under these conditions. This review examines the behavioral and genetic evidence from animal models and genetic association studies in humans linking GIRK channels with CNS disorders. We further explore the possibility that subunit-selective modulators and other advanced research tools will be instrumental in establishing the role of individual GIRK subunits in drug addiction and other relevant CNS diseases and in potentially advancing treatment options for these disorders.
MeSH term(s)	Animals ; Brain/metabolism ; G Protein-Coupled Inwardly-Rectifying Potassium Channels/genetics ; G Protein-Coupled Inwardly-Rectifying Potassium Channels/metabolism ; Humans ; Mice ; Mice, Knockout ; Substance-Related Disorders/genetics ; Substance-Related Disorders/metabolism
Chemical Substances	G Protein-Coupled Inwardly-Rectifying Potassium Channels
Language	English
Publishing date	2015
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	209876-3
ISSN	2162-5514 ; 0074-7742
ISSN (online)	2162-5514
ISSN	0074-7742
DOI	10.1016/bs.irn.2015.05.016
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Article ; Online: Effects of Tacrolimus and Other Immune Targeting Compounds on Binge-Like Ethanol Drinking in High Drinking in the Dark Mice.

Grigsby, Kolter B / Savarese, Antonia M / Metten, Pamela / Mason, Barbara J / Blednov, Yuri A / Crabbe, John C / Ozburn, Angela R

Neuroscience insights

2020 Volume 15, Page(s) 2633105520975412

Abstract: High Drinking in the Dark (HDID-1) mice represent a unique genetic risk model of binge-like drinking and a novel means of screening potential pharmacotherapies to treat alcohol use disorders (AUDs). We tested the effects of tacrolimus (0, 0.5, 1, and 2 ... ...

Abstract	High Drinking in the Dark (HDID-1) mice represent a unique genetic risk model of binge-like drinking and a novel means of screening potential pharmacotherapies to treat alcohol use disorders (AUDs). We tested the effects of tacrolimus (0, 0.5, 1, and 2 mg/kg), sirolimus (0, 5, 10, and 20 mg/kg), palmitoylethanolamide (PEA; 0, 75, 150, and 225 mg/kg), and secukinumab (0, 5, 20, and 60 mg/kg) on binge-like ethanol intake (2-day, "Drinking in the Dark" [DID]) and blood alcohol levels (BALs) in HDID-1 mice. Tacrolimus reduced ethanol intake and BALs. Tacrolimus had no effect on water intake, but reduced saccharin intake. There was no effect of sirolimus, PEA, or secukinumab on ethanol intake or BALs. These results compare and contrast with previous work addressing these compounds or their targeted mechanisms of action on ethanol drinking, highlighting the importance of screening a wide range of models and genotypes to inform the role of neuroimmune signaling in AUDs.
Language	English
Publishing date	2020-11-25
Publishing country	United States
Document type	Journal Article
ISSN	2633-1055
ISSN (online)	2633-1055
DOI	10.1177/2633105520975412
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Article ; Online: Inbred Substrain Differences Influence Neuroimmune Response and Drinking Behavior.

Warden, Anna S / DaCosta, Adriana / Mason, Sonia / Blednov, Yuri A / Mayfield, Roy Dayne / Harris, Robert Adron

Alcoholism, clinical and experimental research

2020 Volume 44, Issue 9, Page(s) 1760–1768

Abstract: Background: The inbred mouse strain C57BL/6 is widely used in both models of addiction and immunological disease. However, there are pronounced phenotypic differences in ethanol (EtOH) consumption and innate immune response between C57BL/6 substrains. ... ...

Abstract	Background: The inbred mouse strain C57BL/6 is widely used in both models of addiction and immunological disease. However, there are pronounced phenotypic differences in ethanol (EtOH) consumption and innate immune response between C57BL/6 substrains. The focus of this study was to examine the effects of substrain on innate immune response and neuroimmune-induced escalation of voluntary EtOH consumption. The main goal was to identify whether substrain differences in immune response can account for differences in EtOH behavior. Methods: We compared acute innate immune response with a viral dsRNA mimic, polyinosinic:polycytidylic acid (poly(I:C)), in brain using qRT-PCR in both C57BL/6N and C57BL/6J mice. Next, we used a neuroimmune model of escalation using poly(I:C) to compare drinking behavior between substrains. Finally, we compared brain neuroimmune response with both EtOH and repeated poly(I:C) in both substrains as a way to account for differences in EtOH behavior. Results: We found that C57BL/6 substrains have differing immune response and drinking behaviors. C57BL/6N mice have a shorter but more robust inflammatory response to acute poly(I:C). In contrast, C57BL/6J mice have a smaller but longer-lasting acute immune response to poly(I:C). In our neuroimmune-induced escalation model, C57BL/6J mice but not C57BL/6N mice escalate EtOH intake after poly(I:C). Finally, only C57BL/6J mice show enhanced proinflammatory transcript abundance after poly(I:C) and EtOH, suggesting that longer-lasting immune responses are critical to neuroimmune drinking phenotypes. Conclusions: Altogether, this work has elucidated additional influences that substrain has on both innate immune response and drinking phenotypes. Our observations highlight the importance of considering and reporting the source and background used for production of transgenic and knockout mice. These data provide further evidence that genetic background must be carefully considered when investigating the role of neuroimmune signaling in EtOH abuse.
MeSH term(s)	Alcohol Drinking/genetics ; Alcohol Drinking/immunology ; Alcohol Drinking/physiopathology ; Animals ; Behavior, Animal ; Central Nervous System Depressants/administration & dosage ; Ethanol/administration & dosage ; Immunity, Innate/genetics ; Immunity, Innate/immunology ; Interferon Inducers/pharmacology ; Mice ; Mice, Inbred C57BL ; Mice, Inbred Strains ; Mice, Knockout ; Mice, Transgenic ; Models, Animal ; Neuroimmunomodulation/genetics ; Neuroimmunomodulation/immunology ; Poly I-C/pharmacology
Chemical Substances	Central Nervous System Depressants ; Interferon Inducers ; Ethanol (3K9958V90M) ; Poly I-C (O84C90HH2L)
Language	English
Publishing date	2020-08-02
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	428999-7
ISSN	1530-0277 ; 0145-6008
ISSN (online)	1530-0277
ISSN	0145-6008
DOI	10.1111/acer.14410
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