The Platelet α2-Adrenoceptor as a Potential Biological Marker in Depression

Publisher Website
Google Scholar
Abstract
Insights into the cellular and molecular mechanisms of action of anti-depressant drugs have led to the study of possible dysfunctions of monoamine neurotransmitter receptors in endogenous depression. Presynaptic receptors play an important role in the regulation of transmitter release from neurons. The major mechanism that regulates the release of noradrenaline appears to be feedback inhibition by the neurotransmitter located in the synaptic cleft. This inhibition is mediated by stimulation of a presynaptic autoreceptor, the inhibitory α2-adrenoceptor. When this is stimulated, further release of noradrenaline is inhibited; therefore, increased autoreceptor sensitivity could result in insufficient neuronal release of noradrenaline, and lead to depression.