14 research outputs found
Neutral endopeptidase (3.4.24.11) in plasma and synovial fluid of patients with rheumatoid arthritis. A marker of disease activity or a regulator of pain and inflammation?
Drugs Inhibiting the Metabolism and Inactivation of Atrial Natriuretic Factor: Pharmacological Actions and Therapeutic Implications
Utility of CD10 in Distinguishing between Endometrial Stromal Sarcoma and Uterine Smooth Muscle Tumors: An Immunohistochemical Comparison of 34 Cases
Selective effects of benzodiazepines on the acquisition of conditioned taste aversion compared to attenuation of neophobia in C57BL/6 mice
Memory formation orchestrates the wiring of adult-born hippocampal neurons into brain circuits
Neuropeptides (Neurokinins, Bombesin, Neurotensin, Cholecystokinins, Opioids) and Smooth Muscle
Targeting the intracellular signaling "STOP" and "GO" pathways for the treatment of alcohol use disorders.
In recent years, research has identified the molecular and neural substrates underlying the transition of moderate "social" consumption of alcohol to the characteristic alcohol use disorder (AUD) phenotypes including excessive and compulsive alcohol use which we define in the review as the GO signaling pathways. In addition, growing evidence points to the existence of molecular mechanisms that keep alcohol consumption in check and that confer resilience for the development of AUD which we define herein as the STOP signaling pathways. In this review, we focus on examples of the GO and the STOP intracellular signaling pathways and discuss our current knowledge of how manipulations of these pathways may be used for the treatment of AUD