Dear Colleagues,

Depression is the most common psychiatric disorder, and by virtue will be experienced by many people throughout their life time. Associated with a heterogenous symptomatology and varied severity, according to the World Health Organisation it is the second most leading cause for disability adjusted life-years worldwide.

My research fascination with depression began over 30 years ago when undertaking my PhD which focused on the role of stress in the etiology of one of the core symptoms of depression i.e. the inability to experience pleasure or anhedonia. Of particular interest was the use of preclinical models of depression to elucidate the role of the dopaminergic reward circuitry in mediating the mood enhancing properties of a range of pharmacologically diverse antidepressant drugs. 

Since this time, huge advances have been made in understanding the neural basis of a disorder that is inherently characterised by decreased responsiveness to reward and an increased responsiveness to punishment. Research has shown that depression is underpinned by complex and wide neural circuitry changes which parallel the heterogenous symptomatology associated with the disorder. It has also become evident that the neurobiological mechanisms underlying depression cannot simply be equated to the neurobiological mechanisms underpinning the therapeutic effects of antidepressants. Very briefly, treatment advances have included cognitive behavioural therapy becoming much more of a mainstay option and newer pharmacological approaches have been targeted towards more specific monoaminergic neurotransmitter sites. Although not necessarily boosting clinical efficacy, the beneficial effects of these newer antidepressants have been increased tolerability and reduced side effect profiles. The ability of acute and controlled doses of the NMDA antagonist ketamine to address treatment resistant depression has continued to shed light on the glutamate system being a plausible alternative neurobiological approach for antidepressant action. However, some key themes remain, notably the continued reliance of effective antidepressants on enhancing monoaminergic activity, limited efficacy and the time lag to onset of therapeutic action. Thus, the search for more efficacious treatments for major depression continues. 

Authors are invited to submit relevant original research articles based on primary or longitudinal collaborative datasets (e.g., UK Biobank). Preclinical and translational research which focuses on a high degree of originality, significance and is underpinned by methodological rigor is welcomed. Opinion and review papers that help to inform on how to bridge the current gap between the advanced knowledge gained on the neurobiology of depression and antidepressants vs. developing alternative pharmacological treatment options for this disorder are also encouraged.

Dr. Survjit Cheeta
Dr. Andrew J Grottick
Guest Editors

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• anhedonia
• animal models of depression
• antidepressants
• cognition/cognitive biases
• cognitive behavioural therapy
• diathesis/stress model
• depression
• emotional processing
• mood
• neurobiology of antidepressants
• neurobiology of depression
• stress
• treatment-resistant depression
• vulnerability to depression