Electric Shock as Model of Post-Traumatic Stress Disorder in Rodents

Aliczki, Manó; Haller, József

doi:10.1007/978-3-319-08359-9_132

Cited by 3 publications

(7 citation statements)

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“…Electric footshocks induced marked acute and conditioned fear responses in our studies consistent with earlier reports (Aliczki and Haller, 2016). Conditioned fear responses disappeared during the seven consecutive contextual reminders and did not return 28 days after conditioning in shocked control subjects.…”

Section: Discussionsupporting

confidence: 93%

“…A number of studies assessed eCB effects in laboratory rodents employing electric footshocks to induce changes resembling the symptomatology of PTSD, most importantly conditioned fear responses to the trauma-associated context (Aliczki and Haller, 2016). While all of these studies concluded that eCB signaling is directly involved in the neurobiological basis of trauma-induced behavioral changes, eCB effects on conditioned fear are still to be clarified in details.…”

Section: Introductionmentioning

confidence: 99%

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Endocannabinoid interactions in the regulation of acquisition of contextual conditioned fear

Balogh

Szente

Biró

et al. 2019

Progress in Neuro-Psychopharmacology and Biological Psychiatry

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Endocannabinoids (eCBs) anandamide (AEA) and 2-arachidonoylglycerol (2-AG) were shown to be involved in the basis of trauma-induced behavioral changes, particularly contextual conditioned fear, however, their ligand-specific effects and possible interactions are poorly understood. Here we assessed specific eCB effects and interactions on acquisition of contextual conditioned fear employing electric footshocks in a rat model. We selectively increased eCB levels by pharmacological blockade of the degrading enzymes of AEA by URB597 and 2-AG by JZL184 before traumatization either systemically or locally in relevant brain areas, the prelimbic cortex (PrL), ventral hippocampus (vHC) and basolateral amygdala (BLA). Following traumatization, a series of contextual reminders were conducted during which conditioned fear was assessed. While systemic URB597-treatment during traumatization only slightly enhanced the acquisition of contextual conditioned fear, administration of the compound in the PrL and vHC led to the acquisition of stable, lasting conditioned fear, resistant to extinction. These effects of URB597 were blocked by simultaneous administration of JZL184. Similar treatment effects did not occur in the BLA. Treatment effects were not secondary to alterations in locomotor activity or nociception. Our findings suggest that AEA and 2-AG functionally interact in the regulation of acquisition of contextual conditioned fear. AEA signaling in the PrL and vHC is a crucial promoter of fear acquisition while 2-AG potentially modulates this effect. The lack of eCB effects in the BLA suggests functional specificity of eCBs at distinct brain sites.

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Section: Discussionsupporting

confidence: 93%

Section: Introductionmentioning

confidence: 99%

Endocannabinoid interactions in the regulation of acquisition of contextual conditioned fear

Balogh

Szente

Biró

et al. 2019

Progress in Neuro-Psychopharmacology and Biological Psychiatry

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“…Currents and durations were typically larger than those applied in fear conditioning (0.5-1.5 mA, 0.5-2 s) aiming to investigate short-term fear learning. Currently, learning and trauma protocols are not clearly differentiated as there is no clear evidence for separating "nontraumatic" shocks that are within a rodent's coping capacity from "traumatic" shocks that are beyond its coping capacity 22 . However, this stressor is more frequently used to study learning and memory, its initial application, rather than to model PTSD.…”

Section: Electric Shockmentioning

confidence: 99%

“…Advantages of electric shock as a PTSD model are its controllable delivery and shock parameters (current intensity, duration, number, and interstimulus interval), reproducible context and cues, adjustable environmental cues, and reducible stress habituation 28 . For review of electric shock, see Aliczki and Bali & Jaggi 22,29 .…”

Section: Electric Shockmentioning

confidence: 99%

Rodent models of post-traumatic stress disorder: behavioral assessment

2020

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Although the etiology and expression of psychiatric disorders are complex, mammals show biologically preserved behavioral and neurobiological responses to valent stimuli which underlie the use of rodent models of post-traumatic stress disorder (PTSD). PTSD is a complex phenotype that is difficult to model in rodents because it is diagnosed by patient interview and influenced by both environmental and genetic factors. However, given that PTSD results from traumatic experiences, rodent models can simulate stress induction and disorder development. By manipulating stress type, intensity, duration, and frequency, preclinical models reflect core PTSD phenotypes, measured through various behavioral assays. Paradigms precipitate the disorder by applying physical, social, and psychological stressors individually or in combination. This review discusses the methods used to trigger and evaluate PTSD-like phenotypes. It highlights studies employing each stress model and evaluates their translational efficacies against DSM-5, validity criteria, and criteria proposed by Yehuda and Antelman's commentary in 1993. This is intended to aid in paradigm selection by informing readers about rodent models, their benefits to the clinical community, challenges associated with the translational models, and opportunities for future work. To inform PTSD model validity and relevance to human psychopathology, we propose that models incorporate behavioral test batteries, individual differences, sex differences, strain and stock differences, early life stress effects, biomarkers, stringent success criteria for drug development, Research Domain Criteria, technological advances, and cross-species comparisons. We conclude that, despite the challenges, animal studies will be pivotal to advances in understanding PTSD and the neurobiology of stress. Introduction Post-traumatic stress disorder (PTSD) is an incapacitating chronic disorder. With a 3.9% lifetime prevalence rate worldwide and a 6.4-7.8% rate in the USA, PTSD's health burden is substantial 1-5. Based on the World Mental Health Surveys, 69.7% worldwide (82.7% in the USA) reported exposure to a traumatic experience. While trauma exposure is a required criterion for PTSD diagnosis, only 5.6% worldwide (8.3% in the USA) of those who experienced trauma developed the disorder 1. This is due to numerous factors, including trauma type, variation in trauma response, social support, and endogenous factors of individuals. For adults, adolescents, and children older than six years, eight diagnostic criteria, defined in the 5th edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5), specify measures concerning the victim's perception of trauma and symptoms. For children six years and younger, Criteria C and D (described below) are combined, making for seven diagnostic criteria 6. Criterion A: Exposure to actual or threatened death, serious injury, or sexual violence; one or more ways (e.g., direct experience, witnessing others, learning of close family member's or friend's trauma...

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“…For example, foot shocks of varying intensity produce behavioral and neurochemical changes which model depression, anxiety, and post-traumatic stress disorder (PTSD) [1,2]. Specifically, electric shocks delivered during fear conditioning in both learning-and trauma-imitating protocols (compared in [3]) were shown to result in increased avoidance, cognitive and mood alterations, increased arousal, social avoidance and sleep disturbance (summarized in [4])…”

Section: Introductionmentioning

confidence: 99%

Increased Vocalization of Rats in Response to Ultrasonic Playback as a Sign of Hypervigilance Following Fear Conditioning

et al. 2021

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We investigated the effects of prior stress on rats’ responses to 50-kHz (appetitive) and 22-kHz (aversive) ultrasonic playback. Rats were treated with 0, 1, 6 or 10 shocks (1 s, 1.0 mA each) and were exposed to playbacks the following day. Previous findings were confirmed: (i) rats moved faster during 50-kHz playback and slowed down after 22-kHz playback; (ii) they all approached the speaker, which was more pronounced during and following 50-kHz playback than 22-kHz playback; (iii) 50-kHz playback caused heart rate (HR) increase; 22-kHz playback caused HR decrease; (iv) the rats vocalized more often during and following 50-kHz playback than 22-kHz playback. The previous shock affected the rats such that singly-shocked rats showed lower HR throughout the experiment and a smaller HR response to 50-kHz playback compared to controls and other shocked groups. Interestingly, all pre-shocked rats showed higher locomotor activity during 50-kHz playback and a more significant decrease in activity following 22-kHz playback; they vocalized more often, their ultrasonic vocalizations (USV) were longer and at a higher frequency than those of the control animals. These last two observations could point to hypervigilance, a symptom of post-traumatic stress disorder (PTSD) in human patients. Increased vocalization may be a valuable measure of hypervigilance used for PTSD modeling.

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Electric Shock as Model of Post-Traumatic Stress Disorder in Rodents

Cited by 3 publications

References 58 publications

Endocannabinoid interactions in the regulation of acquisition of contextual conditioned fear

Endocannabinoid interactions in the regulation of acquisition of contextual conditioned fear

Rodent models of post-traumatic stress disorder: behavioral assessment

Increased Vocalization of Rats in Response to Ultrasonic Playback as a Sign of Hypervigilance Following Fear Conditioning

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