Learned helplessness at fifty: Insights from neuroscience.

In the paper

“Second, it is trans-situational and so inescapable shock in one situation blocks the passivity/anxiety caused by even stressors that do not involve shock in different situations.”

What the sources say

• Disputed

  The Discussion reports that prior escapable shock blocked the behavioral effects of later social defeat, a stressor involving no shock. It explicitly says yoked inescapable shock did not have this effect and slightly, though not significantly, exaggerated those effects. The claim reverses which initial shock condition was protective. (LLM, conf=0.95)

  Checked by a reasoning model — may be wrong.

  cites Amat et al. (2010) sourceExperimental — accuracy not yet measured

In the paper

“Moreover, perceived control in these pain studies increases ventromedial prefrontal cortex activity (Salomons, Johnstone, Backonja, & Davidson, 2004).”

What the sources say

• Disputed

  The fMRI section defines the reported contrast as uncontrollable minus controllable pain (UC − C). Table 1 lists prefrontal activation under that contrast, indicating greater activity with perceived uncontrollability, not an increase with perceived control. The paper does not identify a vmPFC increase. (LLM, conf=0.84)

  Checked by a reasoning model — may be wrong.

  cites Salomons, Johnstone, Backonja, & Davidson, 2004 sourceExperimental — accuracy not yet measured

In the paper

“A number of studies employing painful stimuli have found that providing control, or inducing perceived control, reduces the experienced intensity of the painful stimulus.”

What the sources say

• Disputed

  The Behavioral results report virtually identical pain ratings in the uncontrollable and controllable conditions (7.19 versus 7.20), with no significant difference. The Discussion says the neural-activity differences were not attributable to a difference in perceived pain. Thus, this study does not find that perceived control reduced experienced pain intensity. (LLM, conf=0.94)

  Checked by a reasoning model — may be wrong.

  cites Salomons, Johnstone, Backonja, & Davidson, 2004 sourceExperimental — accuracy not yet measured

In the paper

“inescapable shock reduces later social investigation of a juvenile, a putative measure of anxiety”

What the sources say

• Supported

  The Discussion reports that inescapable shock (IS), but not escapable shock, reduced subsequent social exploration with a juvenile. It also says the procedure was sensitive to anxiogenic and anxiolytic drugs, supporting the interpretation of reduced exploration as a measure of anxiety. (LLM, conf=0.94)

  cites Christianson, Paul, et al., 2008 source

In the paper

“However, the mere presence of a juvenile leads to a large increase in 5-HT within the amygdala in a subject that has experienced inescapable shock, but not escapable shock previously”

What the sources say

• Supported

  The Results section, “Extracellular BLA 5-HT during and following social exploration,” reports that a five-minute juvenile encounter increased extracellular 5-HT in the basolateral amygdala after inescapable shock, but not after escapable shock. The Discussion describes the increase after inescapable shock as large and sustained. (LLM, conf=0.94)

  cites Christianson et al., 2010 source

In the paper

“So, the conclusion is that the dorsal raphe nucleus does not receive any heightened excitation from inescapable shock relative to escapable shock.”

What the sources say

• Partly supported

  The Discussion (page not provided) says the dorsal raphe shows reduced activity during controllable stress and describes an inhibitory pathway activated under that condition. This supports inhibition during escapable shock as an explanation for the activity difference, but it does not establish that inescapable shock produces no greater excitatory input. (LLM, conf=0.82)

  cites McDevitt et al., 2009 sourceExperimental — accuracy not yet measured
• ?Not checked — no full text of the sourcecites Grahn et al., 2002 source
• ?Not checked — no full text of the sourcecites Weiss & Simson, 1988 source

In the paper

“Direct electrophysiological measurement of projecting prelimbic neurons indicates that escapable shock, but not inescapable shock increases their excitability (Varela, Wang, Christianson, Maier, & Cooper, 2012).”

What the sources say

• Supported

  The Introduction identifies the measured cells as prelimbic projection neurons and describes electrophysiological measurements after escapable or inescapable tail shock. The Discussion reports increased excitability after escapable shock and no observable change after inescapable shock. (LLM, conf=0.93)

  cites Varela, Wang, Christianson, Maier, & Cooper, 2012 source

In the paper

“Thus, stimulation of the infralimbic region should inhibit fear expression, and it does (Sierra-Mercado, Padilla-Coreano, & Quirk, 2011).”

What the sources say

• Partly supported

  The Discussion (‘Fear expression: PL not IL’; page unavailable) suggests that IL helps inhibit fear responses during extinction. But the Results report inactivation, not stimulation: IL inactivation did not change freezing at the start of the session, though it impaired extinction. The paper therefore does not demonstrate that stimulating IL inhibits initial fear expression. (LLM, conf=0.83)

  cites Sierra-Mercado, Padilla-Coreano, & Quirk, 2011 sourceExperimental — accuracy not yet measured

In the paper

“the dorsal raphe nucleus receives virtually all of its cortical input from the prelimbic region (PL) of the ventromedial prefrontal cortex (vmPFC) (Peyron, Petit, Rampon, Jouvet, & Luppi, 1997; Vertes, 2004).”

What the sources say

• ?Not matched

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

  cites Peyron, Petit, Rampon, Jouvet, & Luppi, 1997
• Partly supported

  The Prelimbic cortex results (p. 8) report fairly dense PL innervation of the dorsal raphe nucleus. But the Infralimbic cortex results (p. 6) also report light-to-moderate innervation, and the paper does not establish that virtually all cortical input comes from PL. (LLM, conf=0.86)

  cites Vertes, 2004 sourceExperimental — accuracy not yet measured

In the paper

“Indeed, microinjection of 5-HT2C antagonists directly into these structures does block the passivity and increased anxiety (Christianson et al., 2010; Strong et al., 2011).”

What the sources say

• Partly supported

  The Results (Intra-BLA 5-HT2C receptor antagonism; page unavailable) report that microinjecting the antagonist into the basolateral amygdala before testing reversed the anxiety-like reduction in social exploration after inescapable shock. The Discussion says that whether the basolateral amygdala is involved in the antagonist’s effect on shuttle-box escape deficits remains to be determined. This paper therefore does not support the claim that microinjection blocked passivity. (LLM, conf=0.90)

  cites Christianson et al., 2010 sourceExperimental — accuracy not yet measured
• Partly supported

  Results §3.4 (page not provided) reports that injecting a 5-HT2C antagonist into the basolateral amygdala before testing partially reduced the escape deficit after uncontrollable stress. It did not reduce exaggerated freezing, the paper’s measure of stress-induced fear. Results §3.2 likewise reports that dorsal-striatum injection improved escape behavior but not exaggerated fear, so this source does not support the claim that the injections blocked both passivity and increased anxiety. (LLM, conf=0.92)

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

In the paper

“Briefly, the association between a stimulus predicting shock and the shock forms in basolateral regions of the amygdala.”

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 caption in Conclusions (page not specified) says tone and shock inputs converge in the lateral amygdala, producing potentiated responses to the tone. The paper defines the basolateral amygdala as including the lateral nucleus, supporting the cited paraphrase. (LLM, conf=0.90)

  cites Maren & Quirk, 2004 source

In the paper

“Increases in these particular proteins (e.g., phosphorylated extracellular signal-regulated kinase) are indeed induced in the prelimbic region of theventromedial prefrontal cortex by escapable shock (Christianson et al., 2014)”

What the sources say

• Supported

  The Results section, “Escapable stress induced ERK phosphorylation in the PL and IL,” reports significant increases in phosphorylated ERK1 and ERK2 in the prelimbic (PL) region after escapable stress. Figure 2 likewise reports increased phosphorylated ERK1/2 in PL samples after 25 trials. (LLM, conf=0.94)

  cites Christianson et al., 2014 source

In the paper

“Of special note, the infralimbic region sends excitatory glutamatergic projections to a region of the amygdala known as the intercalated cell region.”

What the sources say

• Supported

  The Abstract says intercalated neurons receive glutamatergic afferents from the infralimbic cortex, and the Discussion says the cortex sends substantial projections to intercalated cell masses. The Abstract also reports results suggesting these inputs activate intercalated neurons. Page numbers are not provided in our copy. (LLM, conf=0.92)

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

In the paper

“As this conclusion also predicts, inactivating the dorsolateral striatum and the habit system did not reduce the protective effects of escapability.”

What the sources say

• Partly supported

  The Results (Juvenile social exploration at 24 h after stress) report that D-AP5 injected into the dorsolateral striatum before escapable shock did not diminish the behavioral protection afforded by control. The Discussion identifies the dorsolateral striatum with the habit system. However, the experiment blocked NMDA receptors in that region; it did not establish the effect of inactivating the entire region or habit system. (LLM, conf=0.85)

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

In the paper

“Inhibitors of just these plasticity proteins prevent immunization when microinjected in the prelimbic area (Christianson et al., 2014)”

What the sources say

• Supported

  The Results report that intra-PL U0126 completely prevented behavioral immunization. The Discussion also states that NMDAR blockade in the PL prevented immunization, supporting the claim about inhibitors microinjected into the prelimbic area. (LLM, conf=0.91)

  cites Christianson et al., 2014 source

In the paper

“As expected, perceived control over the snake presentation reduced anticipatory anxiety on snake trials.”

What the sources say

• Partly supported

  The Introduction (page unavailable) describes controllable and uncontrollable snake-video trials, and the Abstract reports greater anticipatory vmPFC activity when participants had control. The copy does not report that perceived control reduced anticipatory anxiety on snake trials; its reported finding is a difference in neural activity, not a measured reduction in anxiety. (LLM, conf=0.84)

  cites Kerr, McLaren, Mathy, and Nitschke (2012) sourceExperimental — accuracy not yet measured

In the paper

“Finally, there was a negative relationship between ventromedial prefrontal cortex and amygdala activity on snake trials.”

What the sources say

• Partly supported

  The Results (fMRI context-dependent connectivity/gPPI results; page unavailable) report vmPFC–amygdala connectivity during anticipation of snake videos, including greater connectivity for controllable snake than controllable fish trials. They do not report a negative relationship between the regions’ activity on snake trials. The Discussion also cautions that PPI cannot conclusively establish the direction of their association. (LLM, conf=0.85)

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

In the paper

“Moreover, these effects of prior control depended on the ventromedial prefrontal cortex (Baratta, Lucero, Amat, Watkins, & Maier, 2008)”

What the sources say

• Supported

  The paper’s Abstract states that the effect of prior behavioral control on subsequent conditioned fear depends on ventral medial prefrontal cortex activation. It further reports that infralimbic cortex inactivation before testing, but not before conditioning, blocked the fear-reducing effect, locating that dependence in fear expression rather than learning. (LLM, conf=0.93)

  cites Baratta, Lucero, Amat, Watkins, & Maier, 2008 source

In the paper

“Importantly, behavioral sequelae of IS such as escape deficits and anxiety also persist for just this period of time”

What the sources say

• ?Not checked — no full text of the sourcecites Maier, 2001 source

In the paper

“the ESC and the 0 group learned to escape equally well”

In the paper

“Placing a juvenile into an adult's rat cage, as is done in this test, produces no increase in 5-HT activity at all in control subjects.”

In the paper

“Both inescapable shock and escapable shock led to a rapid and large release of 5-HT.”

In the paper

“However, 5-HT dropped precipitously as the escapable subjects learned the instrumental wheel-turn escape response, even though the shocks continued.”

In the paper

“This elevated level of 5-HT within the dorsal raphe nucleus was maintained even after the session ended for the inescapable subjects.”

In the paper

“We know that the part of the brain that DETECTs control is a circuit formed by the prelimbic area of the ventromedial prefrontal cortex and the dorsal medial striatum.”

In the paper

“The data suggest that there are two important circuits within the ventromedial prefrontal cortex engaged by control that mediate the protective effects of control—a prelimbic-dorsomedial striatum pathway and a prelimbic-dorsal raphe nucleus pathway.”

In the paper

“The passivity produced by inescapable shock is transient, lasting for only a few days after the inescapable shock.”

In the paper

“Since Baratta (2015) has shown that the prelimbic neurons that participate in these two circuits are quite discrete”

What the sources say

• ?Not matched

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

  cites Baratta (2015)

In the paper

“Here we have reviewed research that indicates that the experience of behavioral control over a stressor also has an enduring impact”

In the paper

“it is learned very rapidly. Indeed, rodents escape with almost asymptotically fast latencies by the second or third trial (e.g., Grahn, Watkins, & Maier, 2000).”

What the sources say

• ?Not checked — no full text of the sourcecites Grahn, Watkins, & Maier, 2000 source

In the paper

“When this system was inactivated so that control/lack of control information could not be detected and subjects were exposed to escapable shock or inescapable shock, the rats reacted to the shock as if it were inescapable – both in terms of passivity/anxiety and of neurochemistry.”

In the paper

“If the rats first experience is with escape the organism is immunized and reacts to subsequent stressors in new situations as if they are escapable.”

In the paper

“Interestingly, these receptors are desensitized or downregulated by high levels of 5-HT.”

In the paper

“with the activity of the medial prefrontal cortex, which subserves the detection of control”

In the paper

“This 5-HT comes from axon collaterals from neighboring 5-HT cells within the dorsal raphe nucleus.”

In the paper

“Hence we discarded contiguity accounts of helplessness.”

In the paper

“When common cues are shared between the first environment and the test environment, processes such as fear conditioning could mediate the behavioral change.”

In the paper

“However, it should be clearly understood that this EXPECTATION may not be a cognitive process or entity as psychologists tend to view them. It is a circuit that provides an expectational function”

In the paper

“Thus, 5-HT released within the dorsal raphe nucleus during the strong dorsal raphe nucleus 5-HT activation produced by inescapable shock could desensitize these receptors, leading to a loss of the normal inhibitory restraint on these cells, thereby sensitizing them.”

In the paper

“Aversive shock, among its other neural actions, activates serotonergic (5-HT) neurons in the dorsal raphe nucleus (DRN).”

In the paper

“many of the behavioral consequences seemed to be captured as either inhibited fight/flight (poor escape, reduced aggression, reduced social dominance) or exaggerated fear/anxiety”

In the paper

“When shock is initially escapable, the presence of control is DETECTed. This is accomplished by a circuit involving projections from the prelimbic region of the ventromedial prefrontal cortex (the PL) to the dorsal medial striatum (the DMS), and back.”

In the paper

“Second, the initial stressor must occur in an environment very different from the test environment since one of the hallmarks of learned helplessness is trans-situationality.”

In the paper

“Thus, it is not enough to compare only inescapable shock and non-shocked controls.”

In the paper

“alterations of the ventromedial prefrontal cortex-dorsal raphe pathway can come to subserve the expectation of control”

In the paper

“This is now a circuit that EXPECTS control.”

In the paper

“If the rat has previously had control, now even inescapable shock or other uncontrollable stressors activate this prelimbic- dorsal raphe nucleus pathway, which they would not otherwise do.”

In the paper

“Importantly, activation of dorsal raphe nucleus 5-HT neurons also occurs robustly during other essentially uncontrollable stressors such as social defeat”

What the sources say

• ?Not matched

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

  cites Amat, Aleksejev, Paul, Watkins, & Maier, 2010

In the paper

“Learned helplessness in the laboratory – combining the animal and human experimental results – produced eight of the nine symptoms, with the only exception being suicide and suicidal thoughts”

What the sources say

• ?Not matched

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

  cites Seligman, 1974; Simson & Weiss, 1988

In the paper

“the dogs often failed to escape altogether in the shuttlebox and passively waited the shock out”

What the sources say

• ?Not matched

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

  cites Leaf, 1964; Overmier & Leaf, 1965

In the paper

“Maier found that this escapable shock group easily learned to escape in the shuttlebox by jumping the barrier.”

What the sources say

• ?Not checked — no full text of the sourcecites Maier (1970) source

In the paper

“When these circuits are inactive the organism reacts passively and fearfully if the aversive event is prolonged.”

In the paper

“This learned “mastery” effect foreshadows the main findings of the neuroscientific work below, in which first learning about escapable shock inhibits the default response of passivity.”

In the paper

“Passivity in response to shock is not learned.”

In the paper

“This passivity can be overcome by learning control”

In the paper

“So animals learn that they can control aversive events”

In the paper

“It is the default, unlearned response to prolonged aversive events”

In the paper

“leading to the automatic inhibition of the dorsal raphe nucleus”

In the paper

“it is mediated by the serotonergic activity of the dorsal raphe nucleus”

In the paper

“This is caused by prolonged exposure to aversive stimulation per se.”

In the paper

“These predictions were tested and largely borne out”

What the sources say

• ?Not checked — no full text of the sourcecites Alloy et al., 1984 source

In the paper

“After detection of control, a separate and distinct population of prelimbic neurons are activated that here we call ACT.”

In the paper

“These treatments all prevented inescapable shock from producing its usual poor escape and heightened anxiety, and these subjects behaved as did non-shocked controls.”

What the sources say

• ?Not matched

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

  cites Maier et al., 1993
• ?Not checked — no full text of the sourcecites Will et al., 2004 source
• ?Not checked — no full text of the sourcecites Maier, Grahn, & Watkins, 1995 source

In the paper

“So it is the presence of control, not the absence of control, that is detected by prelimbic medial prefrontal circuits, leading to consequent prelimbic-mediated inhibition of stress-responsive brainstem structures such as the dorsal raphe nucleus.”

In the paper

“which in turn inhibits escape”

In the paper

“So it seemed as if the subjects that received inescapable shock later behaved as if they had inhibited dorsal periaqueductal gray function and exaggerated amygdala/BNST function.”

In the paper

“First, control over the stressor must be manipulated to determine whether any neural change measured is indeed a consequence of the uncontrollability/controllability of the event.”

In the paper

“the addition of external stimuli such as a light or a tone occurring immediately after each INESC prevented the occurrence of later failure to learn to escape”

What the sources say

• ?Not matched

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

  cites Minor et al., 1990; Weiss, 1971

In the paper

“a wide range of other behavioral changes followed INESC including reduced aggression, reduced social dominance, reduced food and water intake, exaggerated attention to external cues, reduced preference for sweet tastes, potentiated fear conditioning, slowed fear extinction, neophobia, anxious behavior on measures such as juvenile social exploration, potentiated opioid reward, exaggerated stereotyp”

• Also stated in: § Animals · plain

  “Importantly, none of these occurred if the shocks were escapable”

What the sources say

• ?Not checked — no full text of the sourcecites Maier & Watkins, 2005 source

In the paper

“Thus, it is not turning the wheel and actually escaping the shock by wheel turning that is necessary to prevent later passivity, but rather the detection of escapability by the prelimbic-dorsal medial striatum act/outcome system.”

In the paper

“It is known that without prior escapable shock activation of the prelimbic-dorsal raphe nucleus ACT pathway requires the detection of control by the prelimbic-dorsal medial striatum DETECT circuit.”

In the paper

“We conclude from this that the prelimbic-dorsal raphe nucleus ACT pathway can be modified over several hours after the joint experience of control and aversive stimulation, to respond to stressors in general as if they were controllable”

In the paper

“Furthermore, when these prelimbic neurons were inactivated during the inescapable shock via the microinjection of inhibitory pharmacological agents, immunization no longer occurred (Amat, Paul, Zarza, Watkins, & Maier, 2006).”

What the sources say

• ?Not matched

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

  cites Amat, Paul, Zarza, Watkins, & Maier, 2006

In the paper

“The work above indicates that dorsal raphe nucleus 5-HT neurons are selectively activated if the shock is inescapable, and that this activation is necessary and sufficient to produce passivity and anxiety.”

In the paper

“Initial exposure to escapable shock prevents or reduces the passivity/anxiety induced by later inescapable shock, a phenomenon we called immunization (Maier et al., 1969).”

What the sources say

• ?Not matched

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

  cites Maier et al., 1969

In the paper

“Dramatically, inescapable shock now does activate these cells as if the inescapable shock was escapable shock – if the organism had experienced immunizing control seven days earlier!”

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. (2009)

In the paper

“Remarkably, now immunization occurred. That is, inescapable shock produces immunization as long as the prelimbic pathway is activated during shock.”

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

“and this is compatible with the idea that this altered pathway subserves the EXPECTation that shock will be controllable in new aversive situations.”

In the paper

“Here an antagonist to the 5-HT1A receptor was microinjected into the dorsal raphe nucleus during inescapable shock, and as above these subjects behaved later as if they had not received the inescapable shock.”

In the paper

“There was no colocalization at all, indicating that these are separate populations of prelimbic neurons.”

What the sources say

• ?Not matched

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

  cites M. Barratta (unpublished)

In the paper

“For example, the central nucleus of the amygdala projects to regions of the periaqueductal gray that produce freezing, a behavioral component of conditioned fear.”

In the paper

“Direct activation of the dorsal raphe nucleus by microinjection of the GABA antagonist picrotoxin or the benzodiazepine receptor antagonist beta-carboline both produce the typical behavioral outcomes that are produced by inescapable shock (Maier, Grahn, Maswood, & Watkins, 1995; Short & Maier, 1993).”

What the sources say

• ?Not matched

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

  cites Maier, Grahn, Maswood, & Watkins, 1995
• ?Not checked — no full text of the sourcecites Short & Maier, 1993 source

In the paper

“Thus, the same prelimbic-dorsal raphe nucleus pathway that operates as ACT can later operate as EXPECT.”

In the paper

“The dorsal raphe nucleus is a site of convergence that sums inputs from a number of structures themselves activated by shock (Figure 3).”

In the paper

“So the presence of control activates descending inhibition of shock-induced dorsal raphe nucleus activation and thereby blocks passivity and anxiety.”

In the paper

“Indeed, escapable shock but not exactly equal inescapable shock, increased c-fos protein in the labeled projecting neurons.”

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. (2009)

In the paper

“Thus, the experience of escapable shock (control) produced a specific and persistent change in the prelimbic-dorsal raphe nucleus circuit that led to the inhibition of the dorsal raphe nucleus and prevented passivity in response to even uncontrollable stress.”

In the paper

“These findings provide some support for generalizing the animal data reviewed above to humans.”

In the paper

“It also appears that the passivity and increased anxiety that follows uncontrollable stressors for several days is not produced by any expectancy at all, but rather is an unlearned reaction to prolonged aversive stimulation that sensitizes a specific set of neurons.”

In the paper

“The non-difference between the zero group and the escapable shock group led us to believe that organisms expected controllability as the basic “default option”.”

In the paper

“Given our caution about the multifarious functions and structures of the ventromedial prefrontal cortex, it has not escaped our notice that one such function is prospection, the representation of possible futures (Seligman et al., 2013).”

What the sources say

• ?Not checked — no full text of the sourcecites Seligman et al., 2013 source

In the paper

“In the present case, the detailed knowledge concerning neural processes enabled the testing and major revision of the original psychological theory of learned helplessness—refinements that could not have happened without knowing the neural circuitry”

In the paper

“That is, the findings that we have reviewed do not imply that the brain does not have circuitry to detect non-contingency between events that include actions and outcomes.”

In the paper

“the non-shocked controls learn control before 5-HT levels that could induce passivity have accumulated in regions such as the dPAG and striatum.”

In the paper

“There is no question that the presence of safety signals that predict a period of time free from shock can reduce the behavioral impact of aversive events.”

In the paper

“However, the neural basis of inescapable and escapable shock effects does not support this general schema.”

In the paper

“In addition, plasticity is induced in the prelimbic-to dorsal raphe nucleus circuit so that the system is biased to initially react to aversive events as if they are controllable, thereby prolonging the duration of active responding.”

In the paper

“This suggests that if the DETECT control circuit is absent the animal invariably reverts to the default of helplessness following exposure to any prolonged stressor.”

In the paper

“However, if control is possible this is detected and leads to the inhibition of this process so that active responding can continue.”

In the paper

“Importantly, the presence of control aborts this process.”

In the paper

“However, expectancy does play a role, but it does in the immunization process. Here, an expectancy of control does blunt the impact of subsequent stressors.”

In the paper

“Given this pattern we inferred that detecting and expecting a lack of control was the active ingredient.”

In the paper

“Retrograde and anterograde tracing studies indicate that the dorsal raphe nucleus does not send a major projection to the paraventricular nucleus of the hypothalamus, and perhaps none at all (Larsen, Hay-Schmidt, Vrang, & Mikkelsen, 1996).”

What the sources say

• ?Not matched

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

  cites Larsen, Hay-Schmidt, Vrang, & Mikkelsen, 1996

In the paper

“passivity/anxiety is explained by 5-HT accumulation during the testing in projection regions of the dorsal raphe nucleus that mediate these behaviors.”

In the paper

“Thus, the dorsal raphe nucleus is not a major source of the hypothalamo-pituitary-adrenal activation during stress (Herman & Cullinan, 1997).”

What the sources say

• ?Not checked — no full text of the sourcecites Herman & Cullinan, 1997 source

In the paper

“showing that this structure exerts top-down inhibition of more than just the dorsal raphe nucleus”

In the paper

“However, the part of the dimension that is detected or expected seems now to be the presence of control, not the absence of control.”

In the paper

“A default of helplessness eventually overcome by the experience of mastery over aversive events is compatible with the ontogeny of the human species: beginning life in a state of almost utter helplessness and only gradually learning to control bad events.”

In the paper

“Treatment can only buffer against past and present events with moves that produce control over bad events in the future: These are therapy's end-runs around bad events.”

In the paper

“Furthermore, the critical dorsal raphe nucleus5-HT neurons that are involved in mediating the effects of uncontrollable stress and that are inhibited from the prelimbic by control are restricted to the caudal dorsal raphe nucleus (Grahn et al., 1999), maybe 8,000 neurons in the rat and 50,000 in the human.”

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

“It was behavioral work and psychological theorizing that led to the isolation of behavioral control/lack of control as being the key feature of the Pavlovian conditioning that led to the failure to learn”

In the paper

“First, Maier's group was able to test hypotheses that did not seem testable at the psychological level.”

In the paper

“The neural evidence strongly suggests that activation and sensitization of the dorsal raphe nucleus leads to the passivity and anxiety characteristic of learned helplessness.”

In the paper

“This is too small a number of cells by at least an order of magnitude to be imaged currently.”

In the paper

“Rather passivity and heightened anxiety are the default mammalian reaction to prolonged bad events.”

In the paper

“What can be learned is cortical—that bad events will be controllable in the future.”

In the paper

“The top-down circuitry that descends from the ventromedial prefrontal cortex down to the dorsal raphe nucleus and other structures acts to inhibit this default.”

In the paper

“In conclusion, the neural circuitry underlying the phenomenon of learned helplessness strongly suggests that helplessness was not learned in the original experiments.”