mjn110 and anandamide

mjn110 has been researched along with anandamide* in 2 studies

Other Studies

2 other study(ies) available for mjn110 and anandamide

ArticleYear
Endocannabinoid regulation of homeostatic feeding and stress-induced alterations in food intake in male rats.
    British journal of pharmacology, 2019, Volume: 176, Issue:10

    Stress is known to reduce food intake. Many aspects of the stress response and feeding are regulated by the endocannabinoid system, but the roles of anandamide (AEA) and 2-arachidonoyl glycerol (2-AG) in stress-induced anorexia are unclear.. Effects of acute restraint stress on endocannabinoids were investigated in male Sprague-Dawley rats. Systemic and central pharmacological inhibition of fatty acid amide hydrolase (FAAH) or monoacylglycerol lipase (MAGL) was used to assess the effects of elevated AEA and 2-AG on homeostatic feeding and on food consumption after stress. Animals were pretreated with the FAAH inhibitor, PF-04457845, or the MAGL inhibitor, MJN110, before 2 h acute restraint stress or 2 h homecage period without food.. Restraint stress decreased hypothalamic and circulating AEA, with no effect in the gastrointestinal tract, while 2-AG content in the jejunum (but not duodenum) was reduced. PF-04457845 (30 μg), given i.c.v., attenuated stress-induced anorexia via CB. Our data reveal diverse roles for 2-AG and AEA in homeostatic feeding and changes in energy intake following stress.

    Topics: Amidohydrolases; Animals; Anorexia; Arachidonic Acids; Carbamates; Duodenum; Eating; Endocannabinoids; Glycerides; Homeostasis; Jejunum; Male; Monoacylglycerol Lipases; Polyunsaturated Alkamides; Rats, Sprague-Dawley; Stress, Psychological; Succinimides

2019
FAAH, but not MAGL, inhibition modulates acute TLR3-induced neuroimmune signaling in the rat, independent of sex.
    Journal of neuroscience research, 2018, Volume: 96, Issue:6

    Toll-like receptor (TLR)3 is a key component of the innate immune response to viral infection. The present study firstly examined whether sex differences exist in TLR3-induced inflammatory, endocrine, and sickness responses. The data revealed that TLR3-induced expression of interferon- or NFkB-inducible genes (IFN-α/β, IP-10, or TNF-α), either peripherally (spleen) or centrally (hypothalamus), did not differ between male and female rats, with the exception of TLR3-induced IFN-α expression in the spleen of female, but not male, rats 8 hr post TLR3 activation. Furthermore, TLR3 activation increased plasma corticosterone levels, induced fever, and reduced locomotor activity and body weight - effects independent of sex. Thus, the acute-phase inflammatory, endocrine, and sickness responses to TLR3 activation exhibit minimal sex-related differences. A further aim of this study was to examine whether enhancing endocannabinoid tone - namely, 2-arachidonylglycerol (2-AG) or N-arachidonoylethanolamine (AEA), exhibited similar effects on TLR3-induced inflammatory responses in male versus female rats. Systemic administration of the monoacylglycerol lipase (MAGL) inhibitor MJN110 and subsequent increases in 2-AG levels did not alter the TLR3-induced increase in IP-10, IRF7, or TNF-α expression in the spleen or the hypothalamus of male or female rats. In contrast, the fatty acid amide hydrolase (FAAH) inhibitor URB597 increased levels of AEA and related N-acylethanolamines, an effect associated with the attenuation of TLR3-induced inflammatory responses in the hypothalamus, but not the spleen, of male and female rats. These data support a role for FAAH, but not MAGL, substrates in the modulation of TLR3-induced neuroinflammatory responses, effects independent of sex.

    Topics: Amides; Amidohydrolases; Animals; Arachidonic Acids; Body Temperature; Carbamates; Chemokine CXCL10; Corticosterone; Endocannabinoids; Estradiol; Ethanolamines; Female; Glycerides; Immunologic Factors; Interferons; Male; Monoacylglycerol Lipases; NF-kappa B; Oleic Acids; Palmitic Acids; Poly I-C; Polyunsaturated Alkamides; Rats; Rats, Sprague-Dawley; Sex Factors; Signal Transduction; Succinimides; Toll-Like Receptor 3

2018