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Article: Sexual Differences in Addictions and Dual Disorders: Importance of Gender Perspective.

Benito, Ana / Rodríguez de Fonseca, Fernando / Haro, Gonzalo

2022 Volume 12, Issue 10

Abstract: Sex (the biological attributes of females and males) and gender (socially constructed roles, behaviours, and identities) both affect molecular and cellular processes, protective and vulnerability factors, social and relational life [ ... ]. ...

Abstract	Sex (the biological attributes of females and males) and gender (socially constructed roles, behaviours, and identities) both affect molecular and cellular processes, protective and vulnerability factors, social and relational life [...].
Language	English
Publishing date	2022-10-04
Publishing country	Switzerland
Document type	Editorial
ZDB-ID	2651993-8
ISSN	2076-3425
ISSN	2076-3425
DOI	10.3390/brainsci12101346
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Article ; Online: Oleoylethanolamide restores stress-induced prepulse inhibition deficits and modulates inflammatory signaling in a sex-dependent manner.

González-Portilla, Macarena / Montagud-Romero, Sandra / Rodríguez de Fonseca, Fernando / Rodríguez-Arias, Marta

Psychopharmacology

2023

Abstract: Rationale: Social stress contributes to the development of depressive and anxiety symptomatology and promotes pro-inflammatory signaling in the central nervous system. In this study, we explored the effects of a lipid messenger with anti-inflammatory ... ...

Abstract	Rationale: Social stress contributes to the development of depressive and anxiety symptomatology and promotes pro-inflammatory signaling in the central nervous system. In this study, we explored the effects of a lipid messenger with anti-inflammatory properties - oleoylethanolamide (OEA) - on the behavioral deficits caused by social stress in both male and female mice. Methods: Adult mice were assigned to an experimental group according to the stress condition (control or stress) and treatment (vehicle or OEA, 10 mg/kg, i.p.). Male mice in the stress condition underwent a protocol consisting of four social defeat (SD) encounters. In the case of female mice, we employed a procedure of vicarious SD. After the stress protocol resumed, anxiety, depressive-like behavior, social interaction, and prepulse inhibition (PPI) were assessed. In addition, we characterized the stress-induced inflammatory profile by measuring IL-6 and CX3CL1 levels in the striatum and hippocampus. Results: Our results showed that both SD and VSD induced behavioral alterations. We found that OEA treatment restored PPI deficits in socially defeated mice. Also, OEA affected differently stress-induced anxiety and depressive-like behavior in male and female mice. Biochemical analyses showed that both male and female stressed mice showed increased levels of IL-6 in the striatum compared to control mice. Similarly, VSD female mice exhibited increased striatal CX3CL1 levels. These neuroinflammation-associated signals were not affected by OEA treatment. Conclusions: In summary, our results confirm that SD and VSD induced behavioral deficits together with inflammatory signaling in the striatum and hippocampus. We observed that OEA treatment reverses stress-induced PPI alterations in male and female mice. These data suggest that OEA can exert a buffering effect on stress-related sensorimotor gating behavioral processing.
Language	English
Publishing date	2023-06-14
Publishing country	Germany
Document type	Journal Article
ZDB-ID	130601-7
ISSN	1432-2072 ; 0033-3158
ISSN (online)	1432-2072
ISSN	0033-3158
DOI	10.1007/s00213-023-06403-w
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Article ; Online: Alcohol binge drinking induces downregulation of blood-brain barrier proteins in the rat frontal cortex -but not in the hippocampus- that is not prevented by OEA pretreatment.

Rodríguez-González, Alicia / Moya, Marta / Rodríguez de Fonseca, Fernando / Gómez de Heras, Raquel / Orio, Laura

Advances in drug and alcohol research

2023 Volume 3, Page(s) 11091

Abstract: Alcohol binge drinking promotes neuroinflammation which could be partially mediated by the passage of ABD-induced peripheral inflammatory molecules to the brain parenchyma through the blood-brain barrier. The BBB is sealed by tight junction proteins, ... ...

Abstract	Alcohol binge drinking promotes neuroinflammation which could be partially mediated by the passage of ABD-induced peripheral inflammatory molecules to the brain parenchyma through the blood-brain barrier. The BBB is sealed by tight junction proteins, which regulate the access of substances to the brain. Whether ABD alters the BBB or not remains controversial. Here, we measured the expression of BBB proteins in frontal cortex and hippocampus after an ABD procedure that was previously shown to induce neuroinflammation in the FC, and checked neuroinflammation in the hippocampus. Oleoylethanolamide is known to inhibit ABD-induced neuroinflammation in rat FC but the mechanisms of action are not clear: whereas OEA protects against alcohol-induced breakdown of the TJ proteins in the gut barrier reducing peripheral inflammation, its effect in the TJ of the BBB remains unknown. Here, we studied whether OEA (5 mg/kg, before each gavage) prevented alcohol-induced BBB dysfunction by measuring the expression of zona-occludens, occludin, and laminin in FC and hippocampus. ABD animals showed reduced laminin and occludin levels in the FC, indicative of BBB dysfunction, which is concordant with previous findings showing ABD-induced neuroinflammation in this brain region. OEA did not prevent ABD-induced changes in the BBB proteins in the FC, suggesting that the OEA main mechanism of action to inhibit neuroinflammation in this brain region is not related to prevention of TJ proteins alteration in the BBB. In the hippocampus, this ABD protocol did not alter BBB protein levels and no markers of neuroinflammation were found elevated.
Language	English
Publishing date	2023-02-24
Publishing country	Switzerland
Document type	Journal Article
ISSN	2674-0001
ISSN (online)	2674-0001
DOI	10.3389/adar.2023.11091
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Article ; Online: Inhibition of Adult Neurogenesis in Male Mice after Repeated Exposure to Paracetamol Overdose.

Suárez, Juan / de Ceglia, Marialuisa / Rodríguez-Pozo, Miguel / Vargas, Antonio / Santos, Ignacio / Melgar-Locatelli, Sonia / Castro-Zavala, Adriana / Castilla-Ortega, Estela / Rodríguez de Fonseca, Fernando / Decara, Juan / Rivera, Patricia

International journal of molecular sciences

2024 Volume 25, Issue 4

Abstract: Paracetamol, or acetaminophen (N-acetyl-para-aminophenol, APAP), is an analgesic and antipyretic drug that is commonly used worldwide, implicated in numerous intoxications due to overdose, and causes serious liver damage. APAP can cross the blood-brain ... ...

Abstract	Paracetamol, or acetaminophen (N-acetyl-para-aminophenol, APAP), is an analgesic and antipyretic drug that is commonly used worldwide, implicated in numerous intoxications due to overdose, and causes serious liver damage. APAP can cross the blood-brain barrier and affects brain function in numerous ways, including pain signals, temperature regulation, neuroimmune response, and emotional behavior; however, its effect on adult neurogenesis has not been thoroughly investigated. We analyze, in a mouse model of hepatotoxicity, the effect of APAP overdose (750 mg/kg/day) for 3 and 4 consecutive days and after the cessation of APAP administration for 6 and 15 days on cell proliferation and survival in two relevant neurogenic zones: the subgranular zone of the dentate gyrus and the hypothalamus. The involvement of liver damage (plasma transaminases), neuronal activity (c-Fos), and astroglia (glial fibrillar acidic protein, GFAP) were also evaluated. Our results indicated that repeated APAP overdoses are associated with the inhibition of adult neurogenesis in the context of elevated liver transaminase levels, neuronal hyperactivity, and astrogliosis. These effects were partially reversed after the cessation of APAP administration for 6 and 15 days. In conclusion, these results suggest that APAP overdose impairs adult neurogenesis in the hippocampus and hypothalamus, a fact that may contribute to the effects of APAP on brain function.
MeSH term(s)	Mice ; Male ; Animals ; Acetaminophen/pharmacology ; Chemical and Drug Induced Liver Injury/metabolism ; Transaminases/metabolism ; Drug Overdose ; Neurogenesis ; Liver/metabolism ; Mice, Inbred C57BL
Chemical Substances	Acetaminophen (362O9ITL9D) ; Transaminases (EC 2.6.1.-)
Language	English
Publishing date	2024-02-06
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms25041964
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Article ; Online: Sex-based differences in growth-related IGF1 signaling in response to PAPP-A2 deficiency: comparative effects of rhGH, rhIGF1 and rhPAPP-A2 treatments.

Fernández-Arjona, María Del Mar / Navarro, Juan Antonio / López-Gambero, Antonio Jesús / de Ceglia, Marialuisa / Rodríguez, Miguel / Rubio, Leticia / Rodríguez de Fonseca, Fernando / Barrios, Vicente / Chowen, Julie A / Argente, Jesús / Rivera, Patricia / Suárez, Juan

Biology of sex differences

2024 Volume 15, Issue 1, Page(s) 34

Abstract: Background: Children with pregnancy-associated plasma protein-A2 (PAPP-A2) mutations resulting in low levels of bioactive insulin-like growth factor-1 (IGF1) and progressive postnatal growth retardation have improved growth velocity and height following ...

Abstract	Background: Children with pregnancy-associated plasma protein-A2 (PAPP-A2) mutations resulting in low levels of bioactive insulin-like growth factor-1 (IGF1) and progressive postnatal growth retardation have improved growth velocity and height following recombinant human (rh)IGF1 treatment. The present study aimed to evaluate whether Pappa2 deficiency and pharmacological manipulation of GH/IGF1 system are associated with sex-specific differences in growth-related signaling pathways. Methods: Plasma, hypothalamus, pituitary gland and liver of Pappa2 Results: Reduced body and femur length of Pappa2 Conclusions: Sex-specific differences in IGF1 system and signaling pathways are associated with Pappa2 deficiency, pointing to rhPAPP-A2 as a promising drug to alleviate postnatal growth retardation underlying low IGF1 bioavailability in a female-specific manner.
MeSH term(s)	Humans ; Male ; Child ; Mice ; Female ; Animals ; Pregnancy-Associated Plasma Protein-A/genetics ; Pregnancy-Associated Plasma Protein-A/metabolism ; Proto-Oncogene Proteins c-akt ; Growth Disorders/metabolism ; Piperazines
Chemical Substances	Pregnancy-Associated Plasma Protein-A (EC 3.4.24.-) ; LY 165163 (8HAJ699EWG) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1) ; Piperazines
Language	English
Publishing date	2024-04-08
Publishing country	England
Document type	Journal Article
ZDB-ID	2587352-0
ISSN	2042-6410 ; 2042-6410
ISSN (online)	2042-6410
ISSN	2042-6410
DOI	10.1186/s13293-024-00603-5
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Article ; Online: Attenuation of oleoylethanolamide-induced reduction of alcohol consumption in adult rats exposed intermittently to alcohol during adolescence.

Sánchez-Marín, Laura / Pavón-Morón, Francisco J / Rodríguez de Fonseca, Fernando / Serrano, Antonia

Neuroscience letters

2022 Volume 781, Page(s) 136670

Abstract: Oleoylethanolamide (OEA) is an endogenous N-acylethanolamine that reduces both food and alcohol intake through the activation of peripheral sensory nerves in the gut. These effects are opposite to those of anandamide, a main endogenous cannabinoid type 1 ...

Abstract	Oleoylethanolamide (OEA) is an endogenous N-acylethanolamine that reduces both food and alcohol intake through the activation of peripheral sensory nerves in the gut. These effects are opposite to those of anandamide, a main endogenous cannabinoid type 1 receptor (CB
MeSH term(s)	Alcohol Drinking ; Animals ; Endocannabinoids/pharmacology ; Ethanol/pharmacology ; Oleic Acids/pharmacology ; Rats ; Rats, Wistar ; Rimonabant/pharmacology
Chemical Substances	Endocannabinoids ; Oleic Acids ; oleoylethanolamide (1HI5J9N8E6) ; Ethanol (3K9958V90M) ; Rimonabant (RML78EN3XE)
Language	English
Publishing date	2022-04-29
Publishing country	Ireland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	194929-9
ISSN	1872-7972 ; 0304-3940
ISSN (online)	1872-7972
ISSN	0304-3940
DOI	10.1016/j.neulet.2022.136670
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Article ; Online: Oleoylethanolamide attenuates cocaine-primed reinstatement and alters dopaminergic gene expression in the striatum.

González-Portilla, Macarena / Mellado, Susana / Montagud-Romero, Sandra / Rodríguez de Fonseca, Fernando / Pascual, María / Rodríguez-Arias, Marta

Behavioral and brain functions : BBF

2023 Volume 19, Issue 1, Page(s) 8

Abstract: The lipid oleoylethanolamide (OEA) has been shown to affect reward-related behavior. However, there is limited experimental evidence about the specific neurotransmission systems OEA may be affecting to exert this modulatory effect. The aim of this study ... ...

Abstract	The lipid oleoylethanolamide (OEA) has been shown to affect reward-related behavior. However, there is limited experimental evidence about the specific neurotransmission systems OEA may be affecting to exert this modulatory effect. The aim of this study was to evaluate the effects of OEA on the rewarding properties of cocaine and relapse-related gene expression in the striatum and hippocampus. For this purpose, we evaluated male OF1 mice on a cocaine-induced CPP procedure (10 mg/kg) and after the corresponding extinction sessions, we tested drug-induced reinstatement. The effects of OEA (10 mg/kg, i.p.) were evaluated at three different timepoints: (1) Before each cocaine conditioning session (OEA-C), (2) Before extinction sessions (OEA-EXT) and (3) Before the reinstatement test (OEA-REINST). Furthermore, gene expression changes in dopamine receptor D1 gene, dopamine receptor D2 gene, opioid receptor µ, cannabinoid receptor 1, in the striatum and hippocampus were analyzed by qRT-PCR. The results obtained in the study showed that OEA administration did not affect cocaine CPP acquisition. However, mice receiving different OEA treatment schedules (OEA-C, OEA-EXT and OEA-REINST) failed to display drug-induced reinstatement. Interestingly, the administration of OEA blocked the increase of dopamine receptor gene D1 in the striatum and hippocampus caused by cocaine exposure. In addition, OEA-treated mice exhibited reduced striatal dopamine receptor gene D2 and cannabinoid receptor 1. Together, these findings suggest that OEA may be a promising pharmacological agent in the treatment of cocaine use disorder.
MeSH term(s)	Male ; Animals ; Mice ; Neostriatum ; Cocaine/pharmacology ; Dopamine ; Receptors, Cannabinoid ; Gene Expression
Chemical Substances	oleoylethanolamide (1HI5J9N8E6) ; oleoyl ethanolamine ; Cocaine (I5Y540LHVR) ; Dopamine (VTD58H1Z2X) ; Receptors, Cannabinoid
Language	English
Publishing date	2023-05-24
Publishing country	England
Document type	Journal Article
ZDB-ID	2185773-8
ISSN	1744-9081 ; 1744-9081
ISSN (online)	1744-9081
ISSN	1744-9081
DOI	10.1186/s12993-023-00210-1
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Article ; Online: Oleoylethanolamide attenuates the stress-mediated potentiation of rewarding properties of cocaine associated with an increased TLR4 proinflammatory response.

González-Portilla, Macarena / Moya, Marta / Montagud-Romero, Sandra / de Fonseca, Fernando Rodríguez / Orio, Laura / Rodríguez-Arias, Marta

Progress in neuro-psychopharmacology & biological psychiatry

2023 Volume 124, Page(s) 110722

Abstract: The lipid-derived messenger oleoylethanolamide (OEA) has been involved in multiple physiological functions including metabolism and the immune response. More recently, OEA has been observed to affect reward-related behavior. Stress is a major risk factor ...

Abstract	The lipid-derived messenger oleoylethanolamide (OEA) has been involved in multiple physiological functions including metabolism and the immune response. More recently, OEA has been observed to affect reward-related behavior. Stress is a major risk factor for drug use and a predictor of drug relapse. In the laboratory, social stress has been largely studied using the social defeat (SD) model. Here, we explored the effects of different OEA administration schedules on the increased rewarding properties of cocaine induced by SD. In addition, we evaluated the anti-inflammatory action of OEA pretreatment in TLR4 expression caused by SD in the cerebellum, a novel brain structure that has been involved in the development of cocaine addiction. Adult OF1 mice were assigned to an experimental group according to the stress condition (exploration or SD) and treatment (OEA before SD, OEA before conditioning or subchronic OEA treatment). Mice were administered with OEA i.p (10 mg/kg) 10 min previously to the corresponding event. Three weeks after the last SD encounter, conditioned place preference (CPP) was induced by a subthreshold cocaine dose (1 mg/kg). As expected, socially defeated mice presented greater vulnerability to the cocaine reinforcing effects and expressed CPP. Conversely, this effect was not observed under a non-stressed condition. Most importantly, we observed that OEA pretreatment before SD or before conditioning prevented cocaine CPP in defeated mice. Biochemical analysis showed that OEA administration before SD decreased proinflammatory TLR4 upregulation in the cerebellum caused by social stress. In summary, our results suggest that OEA may have a protective effect on stress-induced increased cocaine sensitivity by exerting an anti-inflammatory action.
MeSH term(s)	Mice ; Animals ; Cocaine/pharmacology ; Toll-Like Receptor 4 ; Reward ; Oleic Acids/pharmacology
Chemical Substances	Cocaine (I5Y540LHVR) ; oleoylethanolamide (1HI5J9N8E6) ; Toll-Like Receptor 4 ; Oleic Acids ; Tlr4 protein, mouse
Language	English
Publishing date	2023-01-29
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	781181-0
ISSN	1878-4216 ; 0278-5846
ISSN (online)	1878-4216
ISSN	0278-5846
DOI	10.1016/j.pnpbp.2023.110722
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Article: Novel insights into D-Pinitol based therapies: a link between tau hyperphosphorylation and insulin resistance.

Medina-Vera, Dina / López-Gambero, Antonio Jesús / Navarro, Juan Antonio / Sanjuan, Carlos / Baixeras, Elena / Decara, Juan / de Fonseca, Fernando Rodríguez

Neural regeneration research

2023 Volume 19, Issue 2, Page(s) 289–295

Abstract: Alzheimer's disease is a neurodegenerative disorder characterized by the amyloid accumulation in the brains of patients with Alzheimer's disease. The pathogenesis of Alzheimer's disease is mainly mediated by the phosphorylation and aggregation of tau ... ...

Abstract	Alzheimer's disease is a neurodegenerative disorder characterized by the amyloid accumulation in the brains of patients with Alzheimer's disease. The pathogenesis of Alzheimer's disease is mainly mediated by the phosphorylation and aggregation of tau protein. Among the multiple causes of tau hyperphosphorylation, brain insulin resistance has generated much attention, and inositols as insulin sensitizers, are currently considered candidates for drug development. The present narrative review revises the interactions between these three elements: Alzheimer's disease-tau-inositols, which can eventually identify targets for new disease modifiers capable of bringing hope to the millions of people affected by this devastating disease.
Language	English
Publishing date	2023-07-18
Publishing country	India
Document type	Journal Article ; Review
ZDB-ID	2388460-5
ISSN	1876-7958 ; 1673-5374
ISSN (online)	1876-7958
ISSN	1673-5374
DOI	10.4103/1673-5374.379015
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Article ; Online: Special issue honoring the legacy of Loren H. Parsons.

Roberto, Marisa / Rodríguez de Fonseca, Fernando

Addiction biology

2018 Volume 23, Issue 6, Page(s) 1203

Language	English
Publishing date	2018-10-31
Publishing country	United States
Document type	Journal Article
ZDB-ID	1324314-7
ISSN	1369-1600 ; 1355-6215
ISSN (online)	1369-1600
ISSN	1355-6215
DOI	10.1111/adb.12693
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