Spanish and Catalan Versions of the eHealth Literacy Questionnaire: Translation, Cross-Cultural Adaptation, and Validation Study.

Background: The rise of digital health services, especially following the outbreak of COVID-19, has led to a need for health literacy policies that respond to people's needs. Spain is a country with a highly developed digital health infrastructure, but there are currently no tools available to measure digital health literacy fully. A well-thought-through questionnaire with strong psychometric properties such as the eHealth Literacy Questionnaire (eHLQ) is important to assess people's eHealth literacy levels, especially in the context of a fast-growing field such as digital health.

Absence of LPA1 signaling results in defective cortical development.

Lysophosphatidic acid (LPA) is a simple phospholipid with extracellular signaling properties mediated by specific G protein-coupled receptors. At least 2 LPA receptors, LPA(1) and LPA(2), are expressed in the developing brain, the former enriched in the neurogenic ventricular zone (VZ), suggesting a normal role in neurogenesis. Despite numerous studies reporting the effects of exogenous LPA using in vitro neural models, the first LPA(1) loss-of-function mutants reported did not show gross cerebral cortical defects in the 50% that survived perinatal demise.

The cannabinoid CB1 receptor antagonist SR141716A (Rimonabant) enhances the metabolic benefits of long-term treatment with oleoylethanolamide in Zucker rats.

Anandamide and oleoylethanolamide (OEA) are lipid mediators that regulate feeding and lipid metabolism. While anandamide, a cannabinoid CB1 receptor agonist, promotes feeding and lipogenesis, oleoylethanolamide, an endogenous agonist of peroxisome proliferator activated receptor alpha (PPAR-alpha), decreases food intake and activates lipid mobilization and oxidation. The treatment with a cannabinoid CB1 receptor antagonist results in reduction of body weight gain and cholesterol in obese humans and rodents.

Acute delta9-tetrahydrocannabinol exposure facilitates quinpirole-induced hyperlocomotion.

The endogenous cannabinoid system works as a feedback signal controlling dopamine-induced facilitation of motor behaviors. The present study explored whether a single acute stimulation of CB1 cannabinoid receptors with (-)-Delta9-tetrahydrocannabinol (THC, 5 mg kg(-1) i.p.

Cannabinoid CB1 receptor antagonism reduces conditioned reinstatement of ethanol-seeking behavior in rats.

The endocannabinoid system is involved in a variety of effects of drugs of misuse, and blockade of the cannabinoid CB1 receptor by selective antagonists elicits marked reductions in opioid and alcohol self-administration. The present study was designed to extend our knowledge of the role of the cannabinoid CB1 receptor in the modulation of alcohol misuse vulnerability in rats. Accordingly, using nonselected Wistar rats and genetically selected Marchigian Sardinian alcohol-preferring (msP) rats, we investigated the effect of the CB1 antagonist SR141716A on operant alcohol self-administration and on reinstatement of alcohol-seeking behavior by environmental conditioning factors.

The endocannabinoid system: physiology and pharmacology.

The endogenous cannabinoid system is an ubiquitous lipid signalling system that appeared early in evolution and which has important regulatory functions throughout the body in all vertebrates. The main endocannabinoids (endogenous cannabis-like substances) are small molecules derived from arachidonic acid, anandamide (arachidonoylethanolamide) and 2-arachidonoylglycerol. They bind to a family of G-protein-coupled receptors, of which the cannabinoid CB(1) receptor is densely distributed in areas of the brain related to motor control, cognition, emotional responses, motivated behaviour and homeostasis.

Cannabinoid receptor antagonist reduces heroin self-administration only in dependent rats.

Functionality of the endogenous cannabinoid system undergoes relevant changes in reward-related brain areas in animal models of opiate addiction. By using a limited access heroin self-administration paradigm we show that cannabinoid CB(1) receptor antagonist N-(piperidin-1-yl)-5-(4-chlorophenyl)-1-(2,4-dichlorophenyl)-4-methyl-1H-pyrazole-3-carboxamide hydrochloride (SR141716A, 0.03-3.

A peripheral mechanism for CB1 cannabinoid receptor-dependent modulation of feeding.

Recent studies suggest that the endocannabinoid system modulates feeding. Despite the existence of central mechanisms for the regulation of food intake by endocannabinoids, evidence indicates that peripheral mechanisms may also exist. To test this hypothesis, we investigated (1) the effects of feeding on intestinal anandamide accumulation; (2) the effects of central (intracerebroventricular) and peripheral (intraperitoneal) administration of the endocannabinoid agonist anandamide, the synthetic cannabinoid agonist R-(+)-(2,3-dihydro-5-methyl-3-[(4-morpholinyl)methyl]pyrol[1,2,3-de]-1,4-benzoxazin-6-yl)(1-naphthalenyl) methanone monomethanesulfonate (WIN55,212-2), and the CB1-selective antagonist N-piperidino-5-(4-chlorophenyl)-1-(2,4-dichlorophenyl)-4-methylpyrazole-3-carboxamide (SR141716A) on food intake in rats; and (3) the effects of sensory deafferentation on the modulation of feeding by cannabinoids.

Attenuation of spontaneous opiate withdrawal in mice by the anandamide transport inhibitor AM404.

The endogenous cannabinoid, anandamide, has been shown to attenuate naloxone-precipitated opiate withdrawal in rodents. Here we show that the spontaneous, but not the naloxone-precipitated withdrawal syndrome in morphine-dependent mice is attenuated by the inhibitor of carrier-mediated anandamide transport N-(4-hydroxyphenyl) arachidonylethanolamide (AM404) (2 and 10 mg/kg, i.p.