Noradrenaline binding to α2 noradrenaline receptor inhibits noradrenaline release. The α2 noradrenaline receptor is coupled to inhibitory G-proteins. Following agonist binding, the G-protein dissociates from the receptor and inhibits adenylyl cyclase. This causes the inactivation of adenylyl cyclase, resulting in a decrease of cyclic adenosine monophosphate (cAMP) produced from ATP. As cAMP is inhibited, potassium efflux through calcium-activated channels prevents calcium ions from entering the nerve terminal, leading to hyperpolarization and a suppression of neural firing and neurotransmitter release.1
Related content
Major Depressive Disorder (MDD) is a highly prevalent psychiatric condition with significant individual and socio-economic burden. Despite the broad availability of numerous effective therapeutic interventions, up to 30% of patients fail to achieve adequate symptom relief and are classified as having treatment-resistant depression (TRD). TRD represents a significant clinical challenge, affecting approximately 30% of individuals with MDD who fail to respond to at least two adequate antidepressant trials.
Sequential treatment optimization scheme for major depressive disorder generated according to international evidence.
Key steps for managing factors that may confound antidepressant treatment response, including dose, side effects, comorbidities, stressors, adherence, pharmacogenomics, interactions, and treatment algorithms.