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2016 ; 10
(ä): 571
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Circuits Regulating Pleasure and Happiness-Mechanisms of Depression
#MMPMID27891086
Loonen AJ
; Ivanova SA
Front Hum Neurosci
2016[]; 10
(ä): 571
PMID27891086
show ga
According to our model of the regulation of appetitive-searching vs.
distress-avoiding behaviors, the motivation to display these essential conducts
is regulated by two parallel cortico-striato-thalamo-cortical, re-entry circuits,
including the core and the shell parts of the nucleus accumbens, respectively. An
entire series of basal ganglia, running from the caudate nucleus on one side, to
the centromedial amygdala on the other side, controls the intensity of these
reward-seeking and misery-fleeing behaviors by stimulating the activity of the
(pre)frontal and limbic cortices. Hyperactive motivation to display behavior that
potentially results in reward induces feelings of hankering (relief leads to
pleasure). Hyperactive motivation to exhibit behavior related to avoidance of
misery results in dysphoria (relief leads to happiness). These two systems
collaborate in a reciprocal fashion. In clinical depression, a mismatch exists
between the activities of these two circuits: the balance is shifted to the
misery-avoiding side. Five theories have been developed to explain the mechanism
of depressive mood disorders, including the monoamine, biorhythm,
neuro-endocrine, neuro-immune, and kindling/neuroplasticity theories. This paper
describes these theories in relationship to the model (described above) of the
regulation of reward-seeking vs. misery-avoiding behaviors. Chronic stress that
leads to structural changes may induce the mismatch between the two systems. This
mismatch leads to lack of pleasure, low energy, and indecisiveness, on one hand,
and dysphoria, continuous worrying, and negative expectations on the other hand.
The neuroplastic effects of monoamines, cortisol, and cytokines may mediate the
induction of these structural alterations. Long-term exposure to stressful
situations (particularly experienced during childhood) may lead to increased
susceptibility for developing this condition. This hypothesis opens up the
possibility of treating depression with psychotherapy. Genetic and other
biological factors (toxic, infectious, or traumatic) may increase sensitivity to
the induction of relevant neuroplastic changes. Reversal or compensation of these
neuroplastic adjustments may explain the effects of biological therapies in
treating depression.
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