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Review
. 2016 Jul;123(4):349-67.
doi: 10.1037/rev0000033.

Learned Helplessness at Fifty: Insights From Neuroscience

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Free PMC article
Review

Learned Helplessness at Fifty: Insights From Neuroscience

Steven F Maier et al. Psychol Rev. .
Free PMC article

Abstract

Learned helplessness, the failure to escape shock induced by uncontrollable aversive events, was discovered half a century ago. Seligman and Maier (1967) theorized that animals learned that outcomes were independent of their responses-that nothing they did mattered-and that this learning undermined trying to escape. The mechanism of learned helplessness is now very well-charted biologically, and the original theory got it backward. Passivity in response to shock is not learned. It is the default, unlearned response to prolonged aversive events and it is mediated by the serotonergic activity of the dorsal raphe nucleus, which in turn inhibits escape. This passivity can be overcome by learning control, with the activity of the medial prefrontal cortex, which subserves the detection of control leading to the automatic inhibition of the dorsal raphe nucleus. So animals learn that they can control aversive events, but the passive failure to learn to escape is an unlearned reaction to prolonged aversive stimulation. In addition, alterations of the ventromedial prefrontal cortex-dorsal raphe pathway can come to subserve the expectation of control. We speculate that default passivity and the compensating detection and expectation of control may have substantial implications for how to treat depression. (PsycINFO Database Record

Figures

Figure 1
Figure 1
Levels of serotonin (5-HT) in the dorsal raphe nucleus (DRN) measured by in vivo microdialysis before, during, and after exposure to escapable (ESC) and yoked inescapable (IS) tailshocks. Level of 5-Ht is expressed as a percentage of baseline values, and the Baseline, during stress, and Post-Stress is measured in 20 min intervals. IN produced a sustained rise in levels of extracellular 5-HT, while levels during ESC dropped rapidly as the subjects learned the controlling response.
Figure 2
Figure 2
Schematic depiction of ventromedial medial prefrontal cortex (vmPFC) dorsal raphe nucleus (DRN) interactions. Excitatory glutamatergic projections from the vmPFC synapse onto inhibitory GABAergic interneurons within the DRN that inhibit the serotonin (5-HT) neurons.
Figure 3
Figure 3
Schematic depiction of the proposed model. Serotonin (5-HT) neurons in the dorsal raphe nucleus (DRN) integrate stress-responsive inputs that encode different aspects of a stressor and then activate brain regions that are the proximate mediators of the behavioral effects of uncontrollable stress. Glut=glutamate; vmPFC=ventral medial prefrontal cortex; GABA=gamma aminobutyric acid; 5-HT=serotonin; DRN=dorsal raphe nucleus; habenula=habenula; LC=locus coeruleus; BNST=bed nucleus of the stria terminalis; PAG=periaqueductal gray; amygdala=amygdala; N. Acc.=nucleus accumbens.
Figure 4
Figure 4
Schematic depiction of experimental strategy to determine whether activation of the ventromedial prefrontal cortex (vmPFC) to dorsal raphe nucleus (DRN) pathway is necessary for the presence of behavioral control to be protective. Blockade of the vmPFC to DRN pathway would prevent behavioral control from activating the inhibitory GABAergic cells that control the 5-HT neurons.
Figure 5
Figure 5
Schematic depiction of the role of the prelimbic cortex (PL) in mediating the impact of behavioral control. Separate systems are involved in the detection of control, and then acting on this detection. The detection circuit involves bidirectional flow between the dorsomedial striatum (DMS) and the prelimbic cortex while the action circuit consists of neurons that project from the PL to the dorsal raphe nucleus (DRN).

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