Learned helplessness at fifty: Insights from neuroscience.

In the paper

“Greenwood, Strong, and Fleshner (2010) have shown this to be the case. In their studies, manipulations that reduce fear conditioning reduce the shuttle escape deficit when the prior inescapable shocks were administered in the shuttlebox, but not when they were administered outside the shuttlebox.”

What the sources say

• Partly supported

  Split into 2 atoms — 1 confirmed, 1 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.

  cites Greenwood, Strong, and Fleshner (2010) sourceExperimental — accuracy not yet measured

In the paper

“Inescapable shock, but not exactly equal escapable shock, desensitizes these receptors so that dorsal raphe nucleus5-HT neurons are sensitized for a number of days and to a remarkably large extent.”

What the sources say

• Supported

  The Results (Experiment 1; page not provided) report impaired serotonin-mediated inhibition of dorsal raphe neurons 24 hours after inescapable shock, but not after escapable shock. The Introduction says inescapable shock sensitizes these neurons for 24–72 hours, with exaggerated subsequent serotonin release; the Discussion explains that reduced 5-HT1A receptor function would sensitize them. (LLM, conf=0.90)

  cites Rozeske et al., 2011 source

In the paper

“Of course, the desensitization of 5-HT1A receptors is not permanent, and recovers to normal within 3 days”

What the sources say

• Partly supported

  Results, Experiment 4 (page unavailable), show impaired 5-HT1A-receptor-mediated inhibition at 24 hours but no significant difference from controls at 7 days. The paper did not test receptor function at 3 days; its reference to effects lasting 24–72 hours concerns behavior, not measured receptor recovery. Thus, recovery by 3 days is not established. (LLM, conf=0.88)

  cites Rozeske et al., 2011 sourceExperimental — accuracy not yet measured

In the paper

“That is, activating the ventromedial prefrontal cortex-to-dorsal raphe nucleus pathway turned an animal without control into an animal with control.”

What the sources say

• Supported

  The Discussion reports that activating mPFCv during inescapable shock blocked DRN activation and prevented subsequent escape-learning failure, reproducing the protective effects of behavioral control. The paper describes the mPFCv-to-DRN projection as the proposed mechanism; the citing sentence is a functional analogy, not a claim that the animal gained actual control. (LLM, conf=0.90)

  cites Amat, Paul, Watkins, and Maier (2008) source

In the paper

“First, inactivating the dorsal medial striatum did not interfere with the learning and performance of the escape response. This suggests that the rats could use the “dumber” habit system to acquire and perform the escape response.”

What the sources say

• Partly supported

  The Results (Wheel-turn escape learning) report that rats given D-AP5 in the DMS learned and performed the escape response as efficiently as controls, and the Discussion suggests they did so through the habit system. But this finding concerns NMDA-receptor blockade during escapable shock, not DMS inactivation during both escapable and inescapable shock. The Experimental design section also says that a different DMS-inactivating drug, muscimol, prevented rats from learning to escape. (LLM, conf=0.88)

  cites Amat et al. (2014) sourceExperimental — accuracy not yet measured

In the paper

“As would be predicted, Amat et al. (2014) found that escapable shock, but not inescapable shock activates the contingency-sensitive dorsal medial striatum, but not the habit-oriented contingency-insensitive dorsal lateral striatum.”

What the sources say

• Supported

  The Results section (“Dorsomedial striatum Fos immunoreactivity”; page unavailable) reports a large Fos increase in the DMS after escapable shock but not inescapable shock. Neither condition produced a statistically significant group difference in the DLS, supporting the claimed contrast in activation, though the paper notes a small DLS increase after both conditions. (LLM, conf=0.91)

  cites Amat et al. (2014) source

In the paper

“One system, called the “act/outcome” system, is sensitive to the contingency between response and reinforcer.”

• Also stated in: § Detection of control · plain

  “A second system, the “habit” system, is a mere habit that is not sensitive to contingency but only to the temporal pairing between response and reward, and it produces inflexible learning that is not sensitive to changes in the contingency of the reward (Balleine & Dickinson, 1998).”

What the sources say

• Supported

  The Contingency Degradation section says response–outcome (R–O) learning is sensitive to contingency rather than mere contiguity. It contrasts this with stimulus–response (S–R) learning, which it describes as contiguity-driven and insensitive to non-contiguous outcome delivery. The paper specifies that the relevant temporal pairing for S–R learning is between stimuli and responses. (LLM, conf=0.91)

  cites Balleine & O'Doherty, 2010 source
• ?Not checked — no full text of the sourcecites Balleine & Dickinson, 1998 source

In the paper

“For example, Amat et al. (2010) reported that experience with escapable shock blocked the passivity in shuttle escape and also blocked the reduced social investigation (anxiety) produced by social defeat occurring seven days later.”

What the sources say

• Supported

  The Experimental Designs section specifies that social defeat occurred seven days after escapable shock. The Results sections on Escape learning and Social exploration report that prior escapable shock blocked both the shuttlebox escape deficit and the decrease in social investigation caused by social defeat. Page numbers are unavailable in our copy. (LLM, conf=0.94)

  cites Amat et al. (2010) source

In the paper

“Importantly, the act/outcome system involves a corticostriatal circuit consisting of the prelimbic area within the ventromedial prefrontal cortex and the posterior dorsal medial striatum (DMS), while the”

• Also stated in: § Detection of control · plain

  “habit system has no prefrontal cortical involvement, but instead involves the sensorimotor cortex and the dorsal lateral striatum (DLS).”

What the sources say

• Partly supported

  The Neural Substrates of Goal-Directed Learning section identifies a rat prelimbic–dorsomedial striatal circuit for goal-directed learning, and the Figure 2 caption (Future Directions) links sensorimotor cortical inputs to dorsolateral striatum with habits. The paper describes rodent prelimbic cortex as analogous to human vmPFC, not as an area within it, and the cited passages do not specify the posterior dorsomedial striatum. (LLM, conf=0.83)

  cites Balleine & O'Doherty, 2010 sourceExperimental — accuracy not yet measured

In the paper

“As would be expected, social defeat also increased dorsal raphe nucleus 5-HT activity, and this increase was prevented by the prior escapable shock (Amat et al., 2010).”

What the sources say

• Supported

  The Results section on extracellular 5-HT in the caudal DRN reports that social defeat increased 5-HT efflux in rats. Its “Immunizing effect of ES” subsection states that prior escapable shock blocked that increase; page numbers are unavailable in our copy. (LLM, conf=0.95)

  cites Amat et al., 2010 source

In the paper

“Dramatically, even though the escapable subjects performed the controlling escape response perfectly, this was not protective against passivity/anxiety later.”

• Also stated in: § Detection of control · plain

  “That is, the dorsal raphe nucleus was activated as if the shocks were uncontrollable and passivity/anxiety followed.”

What the sources say

• Partly supported

  The Results (Wheel-turn escape learning; Juvenile social exploration at 24 h after stress) show that rats given intra-DMS D-AP5 escaped as efficiently as controls but lost the usual protection against later anxiety-like behavior. The paper also reports loss of the usual suppression of dorsal raphe serotonin release. It blocked DMS NMDA receptors rather than fully inactivating the DMS, and it did not test later passivity or establish literally perfect escape performance. (LLM, conf=0.85)

  cites Amat et al. (2014) sourceExperimental — accuracy not yet measured

In the paper

“Thus, lesion, NMDA receptor blockade, and inactivation of either the prelimbic area or the dorsal medial striatum prevents contingency sensitive act/outcome learning. Responses can be learned, but only the habit system is then used, and so the learning is insensitive to contingency (Shiflett & Balleine, 2011).”

What the sources say

• Partly supported

  In “Striatal ERK signaling and instrumental learning” (page unavailable), the paper says that pDMS inactivation leaves rats capable of instrumental responding but makes their responses outcome-insensitive; it also reports that inhibiting glutamate receptors in the dorsal striatum interferes with action–outcome encoding. The References identify a study of NMDA-receptor blockade in the DMS. Our copy does not establish the claimed effects of prelimbic lesions or inactivation, or show that every listed intervention leaves only contingency-insensitive habit learning; its behavioral evidence here concerns sensitivity to outcome devaluation. (LLM, conf=0.85)

  cites Shiflett & Balleine, 2011 sourceExperimental — accuracy not yet measured

In the paper

“The cells in this region are GABAergic and project to and inhibit the central nucleus of the amygdala (Berretta, Pantazopoulos, Caldera, Pantazopoulos, & Pare, 2005).”

What the sources say

• Supported

  The Discussion states that intercalated neurons send a GABAergic projection to the central amygdala and generate feedforward inhibition in its neurons. The passage directly supports all three parts of the citing sentence. (LLM, conf=0.93)

  cites Berretta, Pantazopoulos, Caldera, Pantazopoulos, & Pare, 2005 source

In the paper

“From there the information passes to the central nucleus of the amygdala, which in turns projects to the regions that control the behaviors and physiological responses that are the symptoms of fear (Davis, Rainnie, & Cassell, 1994; LeDoux, 2003; Maren & Quirk, 2004).”

What the sources say

• ?Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  cites Davis, Rainnie, & Cassell, 1994
• ?Not checked — no full text of the sourcecites LeDoux, 2003 source
• Supported

  The figure description in Conclusions states that the lateral amygdala projects to the central nucleus directly and via the basal amygdala, and that central-nucleus outputs to brainstem and hypothalamic structures trigger fear responses. The section on fear-related plasticity in the lateral amygdala also describes information relayed through basal amygdaloid nuclei to the central nucleus. (LLM, conf=0.93)

  cites Maren & Quirk, 2004 source

In the paper

“It is straightforward to ask whether the protective effects of safety signals also requires the ventromedial prefrontal cortex, and the answer is no.”

• Also stated in: § Hypothesis Testing · plain

  “Instead, safety signals had their impact via the insular cortex and insular cortex lesions eliminated the protective effects of safety signals.”

What the sources say

• Supported

  The Results (Ventromedial Prefrontal Cortex Inhibition) report that inhibiting the vmPFC did not affect the safety signal’s protection against reduced social investigation after tail-shock. The Results (Sensory Insular Lesions and Safety Signals) report that sensory insular lesions completely blocked that protective effect. These findings concern the paper’s measured stress-buffering effect, not every possible effect of safety signals. (LLM, conf=0.92)

  cites Christianson, Benison, et al., 2008 source

In the paper

“ventromedial prefrontal cortex lesions eliminated the ability of behavioral control to blunt the passivity and fear caused by inescapable shock, but these lesions did not even reduce the passivity and fear blunting impact of safety signals (Christianson, Benison, et al., 2008).”

What the sources say

• Partly supported

  The Discussion (page not provided) says vmPFC inhibition with muscimol abolished behavioral control’s effects in prior work but had no effect on safety signals; the Results confirm the latter finding for social exploration after tail-shock. The claim overstates the evidence as vmPFC lesions affecting passivity and fear: this paper used temporary vmPFC inhibition and explicitly says it did not measure fear inhibition. (LLM, conf=0.88)

  cites Christianson, Benison, et al., 2008 sourceExperimental — accuracy not yet measured

In the paper

“Importantly, there was one condition that selectively excited ventromedial prefrontal cortex activity – snake controllable trials. Control did not increase ventromedial prefrontal cortex activity on neutral fish trials, even though the subjects pressed. Ventromedial prefrontal cortex activity was higher on controllable snake trials than in any of the other conditions.”

What the sources say

• Partly supported

  The Results (fMRI activation results; page unavailable) report greater anticipatory vmPFC activation for controllable than uncontrollable snake trials, but no significant vmPFC difference between controllable and uncontrollable fish trials. They do not establish that vmPFC activity on controllable snake trials was higher than in every other individual condition; the reported snake-versus-fish vmPFC comparison collapses across controllability. (LLM, conf=0.84)

  cites Kerr et al. (2012) sourceExperimental — accuracy not yet measured

In the paper

“Thus, these behavioral changes should exist only as long as the receptors remain desensitized, which proved to be for only a few days (Rozeske et al., 2011).”

What the sources say

• Supported

  Results, Experiment 4 (page unavailable), reports receptor desensitization at 24 hours after uncontrollable stress but not at seven days, and states that the associated behavioral effects are observed at 24–72 hours. The Abstract (page unavailable) likewise says desensitization was observed only at timepoints when the behavioral effects are present. This supports the citing sentence’s hedged inference, although the experiment did not pinpoint the exact day desensitization ended. (LLM, conf=0.86)

  cites Rozeske et al., 2011 source

In the paper

“In primitive organisms threats engage defensive reflexes (Walters & Erickson, 1986).”

• Also stated in: § What Did Original Learned Helplessness Theory Get Right and What Did It Get Wrong? · hedged

  “However, these reflexes are energy intensive, and so if unsuccessful it might be adaptive to inhibit them and conserve energy for use in physiological adjustments that promote survival, such as altering the responsivity of the immune system to be better able to fight any infection or wound that might occur after an attack (Frank, Watkins, & Maier, 2013).”

What the sources say

• ?Not checked — no full text of the sourcecites Walters & Erickson, 1986 source
• Partly supported

  The Introduction says that physically present threats produce defensive behaviors such as fleeing and fighting. It does not specify primitive organisms or defensive reflexes. Its discussion of energy costs concerns immune responses, not reflexes, and it does not say that unsuccessful reflexes are inhibited to conserve energy. (LLM, conf=0.78)

  cites Frank, Watkins, & Maier, 2013 sourceExperimental — accuracy not yet measured

In the paper

“However, insular lesions did not reduce the passivity blunting effects of having an escape response, thereby demonstrating a double dissociation (Christianson, Benison, et al., 2008).”

What the sources say

• Supported

  The Results section, “Sensory Insular Lesions and Behavioral Control” (page not provided), reports that escapable shock prevented the reduction in social exploration regardless of insular lesion treatment. The companion Results section, “Sensory Insular Lesions and Safety Signals” (page not provided), reports that the lesions completely blocked the safety signal’s protective effect, supporting the stated double dissociation. (LLM, conf=0.93)

  cites Christianson, Benison, et al., 2008 source

In the paper

“The failure to escape produced by inescapable shock occurs for some number of days (see below for discussion of time course), but the elevation in 5-HT within regions such as the amygdala does not persist for this period of time.”

In the paper

“two-thirds of the animals from the INESC group failed to learn to escape, whereas 90% of the animals in both the ESC and 0 groups easily learned to escape.”

What the sources say

• ?Not checked — no full text of the sourcecites Seligman & Maier, 1967 source

In the paper

“This argument would suggest that in tasks in which the non-shocked control is not at ceiling a difference between the previously escapably shocked and non-shocked controls might emerge, and this appears to be the case (Baratta et al., 2007).”

What the sources say

• ?Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  cites Baratta et al., 2007

In the paper

“we found that as the original theory claimed, organisms are sensitive to the dimension of control, and this dimension is critical.”

In the paper

“Inescapable shock does not provide more excitatory input—both forms of shock produce equal excitation of the dorsal raphe nucleus.”

In the paper

“Thus, the activation of a dorsal raphe nucleus 5-HT neuron can lead to the inhibition of its neighbors, and so dorsal raphe nucleus 5-HT activity is under self-restraint.”

In the paper

“The most proximate mediator of fight/flight seemed to be the dorsal periaqueductal gray (dPAG), while the extended amygdala (bed nucleus of the stria terminalis, BNST, together with the amygdala proper) mediated fear/anxiety.”

In the paper

“The intense activation of the dorsal raphe nucleus by shock sensitizes these neurons and this sensitization lasts for a few days and results in poor escape (passivity) and heightened anxiety.”

In the paper

“These neurons project to the dorsal raphe nucleus and inhibit the 5-HT cells that are activated by aversive stimulation, thus preventing dorsal raphe nucleus activation and thereby preventing sensitization of these cells, eliminating passivity and exaggerated fear.”

In the paper

“Abramson et al. (1978) claimed that inescapability itself was not sufficient to produce anything more than momentary helplessness. Rather, the explanations that subjects made of the causes of their helplessness predicted the time course and the extent of helplessness.”

What the sources say

• ?Not checked — no full text of the sourcecites Abramson, Seligman, & Teasdale, 1978 source

In the paper

“So, inescapable shock is not being detected as uncontrollable, but it is being responded to as if it were controllable.”

In the paper

“The excitation of the dorsal raphe nucleus is necessary and sufficient for passivity and heightened fear”

In the paper

“Receptors of the 5-HT1A subtype are expressed on the soma and dendrites of 5-HT cells within the dorsal raphe nucleus. These are inhibitory autoreceptors – 5-HT binding to these receptors inhibits 5-HT neuronal activity.”

In the paper

“The dorsal raphe nucleus sends 5-HT projections to both the dorsal periaqueductal gray and to the amygdala, with 5-HT released in the dorsal periaqueductal gray inhibiting its function and 5-HT in the amygdala potentiating its function”

What the sources say

• ?Not checked — no full text of the sourcecites Graeff, Guimarães, De Andrade, & Deakin, 1996 source

In the paper

“It would also have to be true that escapable shock does not activate the dorsal raphe nucleus.”

In the paper

“The mechanism of learned helplessness is now very well-charted biologically and the original theory got it backwards.”

In the paper

“5-HT released in the periaqueductal gray and striatum acts at 5-HT receptors to inhibit active escape behavior, while 5-HT released in the amygdala acts at receptors to potentiate fear/anxiety.”

In the paper

“if inescapable shock were to produce a powerful activation of the dorsal raphe nucleus 5-HT neurons and lead to the release of 5-HT in structures such as the amygdala and dorsal periaqueductal gray, then this structure would hold the potential to be a crucial node in any learned helplessness circuit.”

In the paper

“After the prelimbic-dorsal raphe nucleus ACT circuit is activated a set of changes that require several hours occurs in this pathway and involves the formation of new proteins related to plasticity.”

In the paper

“most of the people from the yoked group failed to escape in the shuttlebox, whereas people from the escapable group and the zero group escaped well in the shuttlebox. Importantly the same pattern in the shuttlebox emerged when preceded by solvable and unsolvable anagrams”

What the sources say

• ?Not checked — no full text of the sourcecites Hiroto & Seligman, 1975 source

In the paper

“The detection of uncontrollability is not necessary nor is it sufficient for passivity.”

In the paper

“There is a structure—the dorsal raphe nucleus – that projects to both, inhibiting one and potentiating the other when it itself is activated.”

In the paper

“she was able to show that inescapable shock activated the neurons in the dorsal raphe nucleus that contained 5-HT, and exactly equal escapable shock did not.”

What the sources say

• ?Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  cites Grahn et al. (1999)

In the paper

“He and his colleagues showed that INESC depletes norepinephrine (NE) in the region of the locus coeruleus (LC)”

• Also stated in: § Animals · plain

  “depletion of NE within this structure actually increases the activity of NE neurons, and Weiss had shown this to be important in the development of learned helplessness”

What the sources say

• ?Not checked — no full text of the sourcecites Weiss & Simson, 1988 source

In the paper

“Volpicelli, Ulm, Altenor, and Seligman (1983) using a triadic design found that the ESC group was much superior to the zero group and the INESC group. During later inescapable shock, the ESC group which had first learned to bar press to escape shock continued to run in a shuttlebox during long duration inescapable shock.”

What the sources say

• ?Not checked — no full text of the sourcecites Volpicelli, Ulm, Altenor, and Seligman (1983) source

In the paper

“Depressed people, who had not received inescapable events, behaved in the laboratory as if they had—showing passivity in the shuttlebox and giving up on cognitive problems”

What the sources say

• ?Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  cites Klein, Fencil-Morse, & Seligman, 1976; Klein & Seligman, 1976; Miller & Seligman, 1976

In the paper

“Overall learned helplessness by mapping into the symptoms of depression seemed like a plausible laboratory model.”

In the paper

“In sum, a number of inputs to the dorsal raphe nucleus, using a number of different transmitters, was necessary to produce learned helplessness behaviors, but these inputs did not discriminate inescapable from escapable shock.”

In the paper

“Inescapable shock potentiated later fear conditioning, a well-known phenomenon (Rau, DeCola, & Fenselow, 2005). It would not have been surprising if initial control merely prevented this potentiating effect, but it did more than that: Instead prior escapable shock actually retarded fear conditioning and facilitated fear extinction.”

What the sources say

• ?Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  cites Rau, DeCola, & Fenselow, 2005
• ?Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  cites Baratta et al. (2007)

In the paper

“That is, inactivating the ventromedial prefrontal cortex-to-dorsal raphe nucleus pathway turned an animal with control into an animal without control.”

What the sources say

• ?Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  cites Amat et al. (2005)

In the paper

“Thus, the joint occurrence of shock and control might induce increased connectivity so that later just the presence of the shock, without control, is sufficient to activate the pathway.”

In the paper

“If inescapable shock produces a much greater activation of dorsal raphe nucleus 5-HT neurons than does escapable shock, but both provide equivalent excitatory input, then there is only one obvious possibility left—the presence of control must somehow inhibit dorsal raphe nucleus 5-HT neurons that would otherwise be activated by shock per se without regard to controllability.”

In the paper

“In sum, the prelimbic region of the ventromedial prefrontal cortex is involved in two separable functions-the DETECTion of control in a circuit with the dorsal medial striatum and then ACTing to inhibit the dorsal raphe nucleus (see Figure 5).”

In the paper

“Interestingly, this definition of instrumental contingency is identical to the definition of control that Maier and Seligman (1976) provided, although Maier and Seligman were referring to shock rather than food.”

What the sources say

• ?Not checked — no full text of the sourcecites Maier and Seligman (1976) source

In the paper

“To test this idea Amat et al. (2006) activated this pathway directly by microinjecting a pharmacological agent with no actual escapable shock present, but this did not produce the persistent pathway change or produce immunization.”

What the sources say

• ?Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  cites Amat et al. (2006)

In the paper

“However, the dorsal raphe nucleus 5-HT neurons are under the inhibitory control of the prelimbic region of the ventromedial prefrontal cortex, and the detection of escapable shock activates this top-down inhibition of the dorsal raphe nucleus.”

In the paper

“blockade of new protein synthesis in the prelimbic area after the escapable shock experience prevents immunization (Amat et al., 2006).”

• Also stated in: § Immunization and EXPECTation · plain

  “Importantly, control still blunts the impact of the stressor being experienced, but longer-term immunization is eliminated”

What the sources say

• ?Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  cites Amat et al., 2006

In the paper

“Thus, DETECT escapability and ACT to pass this information that then inhibits the dorsal raphe nucleus are subserved by different populations of ventromedial prefrontal cortex cells and so are truly different functions.”

In the paper

“Notice that the top-down process from the prelimbic to the dorsal raphe nucleus captures the notion of EXPECTing that future bad events will be controllable.”

In the paper

“Thus, measuring a global ventromedial prefrontal cortex fMRI signal will not remotely imply activation of the control-related critical prelimbic neurons.”

In the paper

“there has to be a pathway from somewhere in the prelimbic-dorsomedial striatum circuit that projects to and activates the prelimbic neurons in the prelimbic- dorsal raphe nucleus pathway, and this pathway is as yet unknown.”

In the paper

“In their review of prospection research Gilbert and Wilson (2007) conclude “An extensive body shows that prefeeling depends critically on the ventromedial prefrontal cortex and that people with damage to this area find it difficult to predict the hedonic consequences of future events” (p. 1352).”

What the sources say

• ?Not checked — no full text of the sourcecites Gilbert and Wilson (2007) source

In the paper

“Instead, the presence of control seems to be the active ingredient, leading to the inhibition of threat-induced changes in limbic and brainstem structures.”

In the paper

“The prelimbic-dorsomedial striatum circuit detects control (DETECT) when control is present, and then activates the prelimbic-dorsal raphe nucleus pathway (ACT) to then blunt the behavioral effects of stress.”

In the paper

“Thus, control cannot be reduced to safety.”

• Also stated in: § Hypothesis Testing · plain

  “but only that stressor control and safety signals exert their effects via different neural mechanisms.”

In the paper

“Even if there were a slight difference in 5-HT, the shuttle response is learned so rapidly that there is a ceiling effect.”

In the paper

“First, defensive behavior will be elicited. The aversive event would activate structures such as the dorsal raphe nucleus. This is a cumulative process with 5-HT building over time, and if the transmitter reaches some threshold in target structures, defensive behaviors become inhibited and energy flow is shifted.”

In the paper

“when shock is escapable this is DETECTed by the ventromedial prefrontal cortex-dorsal medial striatum circuit, and then the ventromedial prefrontal cortex ACTs, sending inputs to the dorsal raphe nucleus that inhibit it, thereby turning off the activation produced by shock per se.”

In the paper

“As organisms became more complex, they could detect and identify threats at a distance. And so they developed rich behavioral and cognitive skills that could be used to cope with threats. Control became possible even against threats that persist over time.”

In the paper

“Thus, the fact that in an aversive situation the brain seems to detect control as the active ingredient rather than a lack of control, does not mean that the brain cannot detect lack of control in other types of circumstances, such as uncontrollable food or unsolvable cognitive problems, or even loud noise.”

In the paper

“there is nothing in the brain that is selectively turned on by a lack of control, only something that turns things off when there is the presence of control.”

In the paper

“It is important to note that 5-HT is phylogenetically very old (Hen, 1993).”

• Also stated in: § What Did Original Learned Helplessness Theory Get Right and What Did It Get Wrong? · plain

  “Moreover, 5-HT has, from the beginning, been involved in controlling and shifting the balance and flow of energy (see Andrews, Bharwani, Lee, Fox, & Thomson, 2015, for review).”

What the sources say

• ?Not checked — no full text of the sourcecites Hen, 1993 source
• ?Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  cites Andrews, Bharwani, Lee, Fox, & Thomson, 2015

In the paper

“This circuit is about the future and it buffers against, but does not annihilate, the default reaction of the dorsal raphe nucleus.”

In the paper

“Thus, we would expect that control would not modulate the HPA axis response to stress because the paraventricular nucleus is not informed about controllability by the ACT circuit.”

In the paper

“aversive events per se (either controllable or uncontrollable) excite the dorsal raphe nucleus, but control over stress actively turns this off.”

In the paper

“This suggests that the rat EXPECTs that shock will be escapable in the new situation and that plasticity in the prelimbic-dorsal raphe nucleus subserves this expectation and inhibits the dorsal raphe nucleus, thus blocking learned helplessness.”

In the paper

“Reappraisal as a tool of therapy is behavioral control. It blunts the impact of a negative event, and likely involves top-down inhibition from the ventro to lower structures.”

In the paper

“The basic result was that the subjects without control later revealed passivity and a number of other behavioral changes, while those with control did not and appeared to be similar to non-shocked controls.”

In the paper

“The default reaction to past and present bad events may be concurrent passivity and heightened anxiety. These cannot be undone directly or annihilated. They can, however, be inhibited by top-down cortical, control.”

In the paper

“The second is that top-down higher cortical processes from the ventromedial prefrontal cortex inhibit this default response.”

In the paper

“However, it was difficult to separate these two possibilities with behavioral experiments, and the idea that uncontrollability was learned remained the dominant view.”

In the paper

“and have suggested that this occurs because that experience induces plasticity in ventromedial prefrontal cortex neurons that project to midbrain and brainstem stress-responsive structures, leading to their later inhibition.”

In the paper

“The passivity occurs because excessive 5-HT is released in projection regions of the dorsal raphe nucleus, and this occurs because dorsal raphe nucleus 5-HT neurons have become sensitized due to the desensitization of 5-HT1A receptors on the soma and dendrites of these cells.”

In the paper

“For complex organisms behavioral control can be possible over threats that are repeated, intermittent, and so persist across time. Thus, conservation/withdrawal and other energy adjustments set in motion by the continuation of threat should be inhibited.”

In the paper

“The first is that the default response of higher organisms to prolonged bad events seems to be passivity and heightened anxiety and that this is caused by the activation of the dorsal raphe nucleus.”

In the paper

“The passivity and heightened anxiety symptoms of learned helplessness map quite well into symptoms of depression (Seligman 1975; Weiss, Simson, Ambrose, Webster, & Hoffman, 1985) and perhaps those of posttraumatic stress disorder (LoLordo & Overmier, 2011).”

What the sources say

• ?Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  cites Seligman 1975
• ?Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  cites Weiss, Simson, Ambrose, Webster, & Hoffman, 1985
• ?Not checked — no full text of the sourcecites LoLordo & Overmier, 2011 source

In the paper

“Thus, the existing neural evidence although strong, it is not conclusive.”

In the paper

“Rather, it may be that this processing can occur, but is not deployed in situations that are highly aversive such as the original helplessness experiments.”

In the paper

“We are mindful that in the theory of explanatory style, “hope” consists largely in the habit of expecting that future bad events will not be permanent, global, and uncontrollable, rather they will be temporary, local and controllable (Seligman, 1991, pp. 48-49).”

What the sources say

• ?Not checked — no full text of the sourcecites Seligman, 1991

In the paper

“Indeed much of cognitive behavioral therapy is actually future–oriented, even if it is not taught in this way.”

In the paper

“Such expectations are likely the best natural defense against helplessness”