Hippocampal low-frequency stimulation and chronic mild stress similarly disrupt fear extinction memory in rats

García, René; Spennato, Guillaume; Nilsson-Todd, Linda; Moreau, Jean‐Luc; Deschaux, Olivier

doi:10.1016/j.nlm.2007.10.005

Cited by 117 publications

(93 citation statements)

References 39 publications

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“…In this case, impaired communication between the hippocampus and sgACC may reduce contextual gating of the expression of conditioned fear, leading to more generalized and persistent negative affect states. In rodents, both the IL cortex and hippocampus are required for the recall of fearextinction memory (22,32,33), which involves enhanced synaptic plasticity between the hippocampus and medial PFC (mPFC) (21,34). Furthermore, chronic stress in rodents blocks extinctionrelated enhancement of hippocampus-mPFC plasticity and the recall of fear extinction (21).…”

Section: Discussionmentioning

confidence: 99%

“…In rodents, both the IL cortex and hippocampus are required for the recall of fearextinction memory (22,32,33), which involves enhanced synaptic plasticity between the hippocampus and medial PFC (mPFC) (21,34). Furthermore, chronic stress in rodents blocks extinctionrelated enhancement of hippocampus-mPFC plasticity and the recall of fear extinction (21). Our findings are consistent with this effect and suggest that experiences of maltreatment during childhood may reduce the capacity of the hippocampus to engage PFC-mediated recall of fear extinction, thereby leading to greater internalizing symptoms.…”

Section: Discussionmentioning

confidence: 99%

“…The ventromedial (vm)PFC inhibits amygdala-based expression of fear responses and is required for fear extinction (14), whereas the hippocampus contextually limits fear responses via connections to both the amygdala and vmPFC (20). In rats, chronic stress impairs hippocampus-vmPFC longterm potentiation, which is required for the proper gating of conditioned fear (21,22). Together, these findings suggest that prolonged exposure to stress may impair connectivity among the components of the fear circuitry, thereby impairing the regulation of emotion and amplifying fear responses.…”

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confidence: 99%

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Childhood maltreatment is associated with altered fear circuitry and increased internalizing symptoms by late adolescence

Herringa

Birn

Ruttle

et al. 2013

Proc. Natl. Acad. Sci. U.S.A.

364

314

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Maltreatment during childhood is a major risk factor for anxiety and depression, which are major public health problems. However, the underlying brain mechanism linking maltreatment and internalizing disorders remains poorly understood. Maltreatment may alter the activation of fear circuitry, but little is known about its impact on the connectivity of this circuitry in adolescence and whether such brain changes actually lead to internalizing symptoms. We examined the associations between experiences of maltreatment during childhood, resting-state functional brain connectivity (rs-FC) of the amygdala and hippocampus, and internalizing symptoms in 64 adolescents participating in a longitudinal community study. Childhood experiences of maltreatment were associated with lower hippocampus-subgenual cingulate rs-FC in both adolescent females and males and lower amygdalasubgenual cingulate rs-FC in females only. Furthermore, rs-FC mediated the association of maltreatment during childhood with adolescent internalizing symptoms. Thus, maltreatment in childhood, even at the lower severity levels found in a community sample, may alter the regulatory capacity of the brain's fear circuit, leading to increased internalizing symptoms by late adolescence. These findings highlight the importance of fronto-hippocampal connectivity for both sexes in internalizing symptoms following maltreatment in childhood. Furthermore, the impact of maltreatment during childhood on both fronto-amygdala and -hippocampal connectivity in females may help explain their higher risk for internalizing disorders such as anxiety and depression.child maltreatment | sex differences | ventromedial prefrontal cortex I n both clinical and community samples, maltreatment during childhood represents one of the strongest risk factors for developing depression and anxiety (1-3). Childhood maltreatment and other adversities account for up to a third of the risk for mood and anxiety disorders (4). Further, depression and anxiety disorders are major public health problems, affecting 15 and 32% of youth, respectively, by the age of 18 y (5). The burden of these disorders is significant, representing the second and fifth leading causes, respectively, of years lived with disability in the United States (6). Some evidence suggests that maltreatment may impart greater risk for the development of internalizing symptoms in females than in males (e.g., refs. 7-9). This differential risk could account, in part, for the higher incidence of internalizing problems in females than in males (10, 11). However, the neurobiological pathways from maltreatment during childhood to the expression of internalizing problems, including potential differences for females and males, remain poorly understood. Such information is crucial for improving the treatment of depression and anxiety disorders and for mitigating the effects of maltreatment during childhood.Both maltreatment during childhood (12) and internalizing disorders (13, 14) have been associated with altered activity in specific b...

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

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Childhood maltreatment is associated with altered fear circuitry and increased internalizing symptoms by late adolescence

Herringa

Birn

Ruttle

et al. 2013

Proc. Natl. Acad. Sci. U.S.A.

364

314

View full text Add to dashboard Cite

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“…A deregulation of conditioned fear responses has been observed in acutely and/or repeatedly stressed animals. Indeed, repeatedly stressed rats and mice that were cued fear-conditioned 1 or 7 days after the last stress session displayed an increased fear expression and/or impaired recall of extinction memory, compared with unstressed animals (Izquierdo et al, 2006;Miracle et al, 2006;Garcia et al, 2008). Interestingly, these stress-elicited changes in fear memory were more obvious when unstressed animals had reached extinction and were not accounted for by changes in acquisition during the conditioning sessions (Izquierdo et al, 2006;Miracle et al, 2006;Garcia et al, 2008; but see Rau and Fanselow, 2009).…”

Section: Discussionmentioning

confidence: 99%

Genetic Dissection of the Role of Cannabinoid Type-1 Receptors in the Emotional Consequences of Repeated Social Stress in Mice

Dubreucq

Matías

Cardinal

et al. 2012

Neuropsychopharmacol

133

117

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The endocannabinoid system (ECS) tightly controls emotional responses to acute aversive stimuli. Repeated stress alters ECS activity but the role played by the ECS in the emotional consequences of repeated stress has not been investigated in detail. This study used social defeat stress, together with pharmacology and genetics to examine the role of cannabinoid type-1 (CB 1 ) receptors on repeated stressinduced emotional alterations. Seven daily social defeat sessions increased water (but not food) intake, sucrose preference, anxiety, cued fear expression, and adrenal weight in C57BL/6N mice. The first and the last social stress sessions triggered immediate brain regiondependent changes in the concentrations of the principal endocannabinoids anandamide and 2-arachidonoylglycerol. Pretreatment before each of the seven stress sessions with the CB 1 receptor antagonist rimonabant prolonged freezing responses of stressed mice during cued fear recall tests. Repeated social stress abolished the increased fear expression displayed by constitutive CB 1 receptordeficient mice. The use of mutant mice lacking CB 1 receptors from cortical glutamatergic neurons or from GABAergic neurons indicated that it is the absence of the former CB 1 receptor population that is responsible for the fear responses in socially stressed CB 1 mutant mice. In addition, stress-induced hypolocomotor reactivity was amplified by the absence of CB 1 receptors from GABAergic neurons. Mutant mice lacking CB 1 receptors from serotonergic neurons displayed a higher anxiety but decreased cued fear expression than their wild-type controls. These mutant mice failed to show social stress-elicited increased sucrose preference. This study shows that (i) release of endocannabinoids during stress exposure impedes stress-elicited amplification of cued fear behavior, (ii) social stress opposes the increased fear expression and delayed between-session extinction because of the absence of CB 1 receptors from cortical glutamatergic neurons, and (iii) CB 1 receptors on central serotonergic neurons are involved in the sweet consumption response to repeated stress.

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“…We recently showed (Akirav and Maroun, 2007) that 30 min of exposure to the elevated platform stressor disrupts the extinction of both auditory and contextual fear conditioning. Others have reported that stress reduces cued fear extinction (Shumake et al, 2005;Izquierdo et al, 2006;Maren and Chang, 2006) or impairs its recall (Maren and Chang, 2006;Miracle et al, 2006;Garcia et al, 2008). In parallel, exposure to stress facilitates the initial fear learning, thus further enhancing the fear response (Shors et al, 1992;Cordero et al, 2003).…”

Section: Introductionmentioning

confidence: 99%

Cannabinoid Receptor Activation in the Basolateral Amygdala Blocks the Effects of Stress on the Conditioning and Extinction of Inhibitory Avoidance

Ganon-Elazar¹,

Akirav²

2009

J. Neurosci.

154

137

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Hippocampal low-frequency stimulation and chronic mild stress similarly disrupt fear extinction memory in rats

Cited by 117 publications

References 39 publications

Childhood maltreatment is associated with altered fear circuitry and increased internalizing symptoms by late adolescence

Childhood maltreatment is associated with altered fear circuitry and increased internalizing symptoms by late adolescence

Genetic Dissection of the Role of Cannabinoid Type-1 Receptors in the Emotional Consequences of Repeated Social Stress in Mice

Cannabinoid Receptor Activation in the Basolateral Amygdala Blocks the Effects of Stress on the Conditioning and Extinction of Inhibitory Avoidance

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