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In depression, the hypothalamic-pituitary-adrenal axis is upregulated with a down-regulation of its negative feedback controls. Corticotropin-releasing factor (CRF) is hypersecreted from the hypothalamus and induces the release of adrenocorticotropin hormone (ACTH) from the pituitary.

Dopamine is released from the presynaptic terminal, diffuses over the synaptic cleft and activates Dopaminergic receptors (D1-D5 receptors).

There are two different types of adrenoreceptor – the α and β receptors. The α receptors are further classified into α1 and α2 subtypes and α2 receptors are widely distributed throughout the body and are found in adrenergic neurons, blood vessels, the pancreas and in smooth muscle.

Benzodiazepines bind to the gamma sub-unit of the GABA-A receptor, causing an allosteric (structural) modification of the receptor that results in an increase in GABA A receptor activity.

The action of noradrenaline at the synapse is terminated by its re-uptake across the pre-synaptic membrane. This is an energy dependent process.

Antagonist binding to the α2 noradrenaline receptor induces noradrenaline release.