Long-term behavioural alterations in female rats after a single intense footshock followed by situational reminders

Louvart, Hélène; Maccari, Stefania; Ducrocq, François; Thomas, Pierre; Darnaudéry, Muriel

doi:10.1016/j.psyneuen.2004.09.003

Cited by 94 publications

(65 citation statements)

References 42 publications

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“…Indeed, startle amplitude in the shocked mice which received reminders was progressively increased with repetitions of the reminders. These original studies have recently been extended to rats by Louvart et al (Louvart et al, 2005;Louvart et al, 2006), who modified the model by using fewer (three) contextual reminders but nonetheless again demonstrated that a single exposure to inescapable footshock followed by brief weekly contextual reminders persistently increased anxiety-like behavior, altered social behavior, and increased avoidance, further demonstrating consistency between responses in this rodent [TS+R] paradigm and PTSD. In the Pynoos et al time-dependent sensitization model the repeated contextual reminders were demonstrated to play a necessary role in the progressive development of persistently increased startle and other parameters characteristic of PTSD, consistent with evidence that re-exposure to distinctive cues which had been present during a traumatic event can play an important role in development of chronic PTSD (Pitman, 1988) and that the subset of individuals who develop PTSD following trauma exhibit a progressive increase in startle reactivity over the months following the traumatic event (Shalev et al, 2000).…”

Section: Discussionmentioning

confidence: 90%

Acoustic startle amplitude predicts vulnerability to develop post-traumatic stress hyper-responsivity and associated plasma corticosterone changes in rats

Rasmussen

Crites

Burke

2008

Psychoneuroendocrinology

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SummaryFollowing exposure to trauma, a vulnerable sub-population of individuals develop post-traumatic stress disorder (PTSD) with characteristic persistent autonomic hyper-responsivity, associated increased startle response, and commonly altered hypothalamo-pituitary-adrenal regulation. A goal of this investigation was to identify a predictive marker for this vulnerability. Previous investigators have developed a model for PTSD in which male mice were exposed to a single brief episode of inescapable footshock followed by one-minute contextual reminders of this trauma at weekly intervals for six weeks. Exposure to these reminders induced a progressive and persistent increase in the amplitude of acoustic startle consistent with the persistently increased acoustic startle of individuals exhibiting PTSD. We adapted this model to adult male Wistar rats, with added characterization of initial (pre-trauma) startle response. After one episode of inescapable footshock (10 second, 2 mA) or control treatment followed by six weekly one-minute contextual reminders, acoustic startle was re-tested. Data were analyzed after dividing rats within each treatment into LOW vs MID vs HIGH (33% in each group) pre-treatment startle responders. Rats which exhibited pretreatment LOW-and MID-range acoustic startle responses did not develop increased acoustic startle responses following subsequent traumatic stress + reminders ([TS+R]) treatment. However, rats which exhibited HIGH pre-treatment startle responses exhibited further significant (p<0.01) [TS+R]-induced persistent enhancement of this already elevated startle response. Furthermore, rats exhibiting HIGH pre-treatment startle responses were also the only subgroup which exhibited increased basal plasma corticosterone levels following [TS+R] treatment. These results suggest that initial pre-stress acoustic startle response can identify subgroups of rats which are predisposed to, or resistant to, developing a PTSD-like syndrome following subsequent trauma.

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Section: Discussionmentioning

confidence: 90%

Acoustic startle amplitude predicts vulnerability to develop post-traumatic stress hyper-responsivity and associated plasma corticosterone changes in rats

Rasmussen

Crites

Burke

2008

Psychoneuroendocrinology

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“…Previous studies have shown that foot-shock exposure alone decreased social investigation for both short-and long-term, however, only when assessed in a novel environment (Short and Maier, 1993;Haller and Bakos, 2002;Haller et al, 2003;Louvart et al, 2005;Leveleki et al, 2006;Siegmund and Wotjak, 2007;Mikics et al, 2008a, b). When social investigation was assessed in the home cage, no differences were found, suggesting that the former result is due to novelty-induced anxiety (Mikics et al, 2008a).…”

Section: Discussionmentioning

confidence: 93%

“…Social defeat is used both acutely-one defeat by a dominant male and chronically-repeated defeat by several dominant males (for reviews see Huhman, 2006;Yan et al, 2010). Foot-shock exposure is used as exposure to a single (Short and Maier, 1993;Siegmund and Wotjak, 2007) or to repeated foot shocks (Haller and Bakos, 2002;Louvart et al, 2005;Mikics et al, 2008a). Although social defeat and foot-shock exposure decrease social investigation, they also lead to behavioral alterations including increased general anxiety, depression, and impaired locomotion that might account for the observed social deficit (Denmark et al, 2010;Hollis et al, 2010).…”

Section: Discussionmentioning

confidence: 99%

“…Social anxiety/avoidance is presently induced using a number of paradigms, including the social defeat paradigm-used both acutely and chronically (for reviews see Huhman, 2006;Yan et al, 2010), and foot-shock exposure (Haller and Bakos, 2002;Louvart et al, 2005;Mikics et al, 2008a). However, these paradigms are rather unspecific with respect to the behavioral alterations they induce, as increased general anxiety, depression, and impaired locomotion were found to accompany the social avoidance (Denmark et al, 2010;Hollis et al, 2010).…”

Section: Introductionmentioning

confidence: 99%

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Social Fear Conditioning: A Novel and Specific Animal Model to Study Social Anxiety Disorder

Toth

Neumann

Slattery

2012

Neuropsychopharmacol

125

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Social anxiety disorder (SAD) is a major health concern with high lifetime prevalence. The current medication is rather unspecific and, despite considerable efforts, its efficacy is still unsatisfactory. However, there are no appropriate and specific animal models available to study the underlying etiology of the disorder. Therefore, we aimed to establish a model of specific social fear in mice and use this social fear conditioning (SFC) model to assess the therapeutic efficacy of the benzodiazepine diazepam and of the antidepressant paroxetine; treatments currently used for SAD patients. We show that by administering electric foot shocks (2-5, 1 s, 0.7 mA) during the investigation of a con-specific, the investigation of unfamiliar con-specifics was reduced for both the short-and long-term, indicating lasting social fear. The induced fear was specific to social stimuli and did not lead to other behavioral alterations, such as fear of novelty, general anxiety, depression, and impaired locomotion. We show that social fear was dose-dependently reversed by acute diazepam, at doses that were not anxiolytic in a non-social context, such as the elevated plus maze. Finally, we show that chronic paroxetine treatment reversed social fear. All in all, we demonstrated robust social fear after exposure to SFC in mice, which was reversed with both acute benzodiazepine and chronic antidepressant treatment. We propose the SFC model as an appropriate animal model to identify the underlying etiology of SAD and possible novel treatment approaches.

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“…increase in the blood glucocorticoid, corticosterone (CORT), and adrenocorticothropic hormone (ACTH) levels to subsequent stress [10][11][12]. In several studies, however, an opposite effect was noted: a reduced or shortened CORT response to stressors indicating a diminished HPA axis reactivity [13][14][15]. The likely was due to a diminished reactivity of the HPA axis subsequent to the previous CVP exposure.…”

Section: Introductionmentioning

confidence: 99%

Neuroendocrine and behavioral response to amphetamine challenge after exposure to an organophosphorus pesticide

Gralewicz¹,

Lutz²,

Świercz³

et al. 2011

International Journal of Occupational Medicine and Environmental Health

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Objectives: Exposure to various stressors is known to result in sensitization to psychostimulants, a state related to the psychostimulant dependence and addiction. It has been shown in some studies that the rise in corticosterone (CORT) concentration is indispensable for both the induction and the expression of behavioral sensitization. Therefore, it might be suspected that behavioral hyposensitivity to amphetamine (AMPH) is somehow related to a reduced CORT response to the psychostimulant subsequent to the chlorphenvinphos (CVP) intoxication. Materials and Methods: The male adult Wistar rats received single i.p. injections of CVP at the doses 0.5, 1.0 or 3.0 mg/kg b.w., or pure corn oil. CORT concentration was determined in samples of blood drawn from the tail vein before and then 30, 60, 180 min and 24 h after injection. The other rats were divided into two groups and tested, three weeks after the CVP injection for the effect of AMPH (0.5 mg/kg b.w. i.p.) on the serum CORT concentration. In addition, behavioral sensitivity to AMPH was assessed by measuring locomotor activity of the animals in an open-field. Results: 1) The stressor property of CVP was confirmed. The injection resulted in up to tenfold increase in the serum CORT concentration. The magnitude and duration of this response were dose-related. 2) Three weeks after the CVP exposure, the CORT response to AMPH was significantly increased.3) The behavioral response to the psychostimulant, i.e. augmented locomotion, was significantly reduced compared to the control. Conclusions: The results confirm that CVP exposure causes behavioral hyposensitivity to AMPH. This effect, however, could not be ascribed to a diminished CORT response.

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Long-term behavioural alterations in female rats after a single intense footshock followed by situational reminders

Cited by 94 publications

References 42 publications

Acoustic startle amplitude predicts vulnerability to develop post-traumatic stress hyper-responsivity and associated plasma corticosterone changes in rats

Acoustic startle amplitude predicts vulnerability to develop post-traumatic stress hyper-responsivity and associated plasma corticosterone changes in rats

Social Fear Conditioning: A Novel and Specific Animal Model to Study Social Anxiety Disorder

Neuroendocrine and behavioral response to amphetamine challenge after exposure to an organophosphorus pesticide

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