Variation in the corticotropin-releasing hormone receptor 1 (CRHR1) gene influences fMRI signal responses during emotional stimulus processing.

The corticotropin-releasing hormone (CRH) system coordinates neuroendocrine and behavioral responses to stress and has been implicated in the development of major depressive disorder (MDD). Recent reports suggest that GG-homozygous individuals of a single nucleotide polymorphism (rs110402) in the CRH receptor 1 (CRHR1) gene show behavioral and neuroendocrine evidence of stress vulnerability. The present study explores whether those observations extend to the neuronal processing of emotional stimuli in humans.

fMRI BOLD responses to negative stimuli in the prefrontal cortex are dependent on levels of recent negative life stress in major depressive disorder.

It is poorly understood how stressors modulate neurobiological mechanisms that may contribute to the heterogeneity of major depressive disorder (MDD). Unmedicated patients diagnosed with MDD (n=15) and individually matched healthy controls (n=15) completed stress questionnaires and were studied with functional magnetic resonance imaging while viewing emotional words. Significant effects of recent negative life stressors, but not early life stress/trauma, were observed on regional blood oxygen level dependent activity during presentation of negative words in patients with MDD.

Frontal and limbic activation during inhibitory control predicts treatment response in major depressive disorder.

Background: Inhibitory control or regulatory difficulties have been explored in major depressive disorder (MDD) but typically in the context of affectively salient information. Inhibitory control is addressed specifically by using a task devoid of affectively-laden stimuli, to disentangle the effects of altered affect and altered inhibitory processes in MDD.

Methods: Twenty MDD and 22 control volunteer participants matched by age and gender completed a contextual inhibitory control task, the Parametric Go/No-go (PGNG) task during functional magnetic resonance imaging.

Dysregulation of endogenous opioid emotion regulation circuitry in major depression in women.

Context: There is extensive evidence implicating dysfunctions in stress responses and adaptation to stress in the pathophysiological mechanism of major depressive disorder (MDD) in humans. Endogenous opioid neurotransmission activating mu-opioid receptors is involved in stress and emotion regulatory processes and has been further implicated in MDD.

Objective: To examine the involvement of mu-opioid neurotransmission in the regulation of affective states in volunteers with MDD and its relationship with clinical response to antidepressant treatment.

Interface of physical and emotional stress regulation through the endogenous opioid system and mu-opioid receptors.

Unraveling the pathways and neurobiological mechanisms that underlie the regulation of physical and emotional stress responses in humans is of critical importance to understand vulnerability and resiliency factors to the development of a number of complex physical and psychopathological states. Dysregulation of central stress response circuits have been implicated in the establishment of conditions as diverse as persistent pain, mood and personality disorders and substance abuse and dependence. The present review examines the contribution of the endogenous opioid system and mu-opioid receptors to the modulation and adaptation of the organism to challenges, such as sustained pain and negative emotional states, which threaten its internal homeostasis.

Neuroreceptor imaging of stress and mood disorders.

Techniques such as positron emission tomography and single photon emission computed tomography allow for the imaging of neurotransmitter receptors and transporters in the brain. These tools have been used to investigate serotonergic, dopaminergic, and opioidergic function in healthy subjects as well as in patients with major depressive disorder, bipolar disorder, and other mood disorders. Pharmacologic challenges, such as amphetamine challenge, and physiologic stressors, such as pain challenge, have been used to further examine the function of these neurotransmitter systems.