Valproic acid effects in the hippocampus and prefrontal cortex in an animal model of post-traumatic stress disorder

Wilson, C. Brad; McLaughlin, Leslie D.; Ebenezer, Philip J.; Nair, Anand; Francis, Joseph

doi:10.1016/j.bbr.2014.03.029

Cited by 66 publications

(36 citation statements)

References 68 publications

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“…A variety of animal paradigms have been adopted to mimic the behavioral and cognitive impairments in patients with PTSD, including predator-scent stress (PSS), trauma witness model (TWM) and single-prolonged stress (SPS) [27][28][29]. Here, we used a restressed single-prolonged stress model (RSPS), initially proposed by Liberzon et al, as it replicated the specific neuroendocrinological abnormalities observed in PTSD patients, such as enhanced glucocorticoid negative feedback [5,30].…”

Section: Introductionmentioning

confidence: 91%

Activation of Sigma-1 receptor ameliorates anxiety-like behavior and cognitive impairments in a rat model of post-traumatic stress disorder

Peng

et al. 2016

Behavioural Brain Research

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Section: Introductionmentioning

confidence: 91%

Activation of Sigma-1 receptor ameliorates anxiety-like behavior and cognitive impairments in a rat model of post-traumatic stress disorder

Peng

et al. 2016

Behavioural Brain Research

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“…In another rat model of PTSD, treatment with valproic acid, a histone deacetylase inhibitor, normalized the levels of indices of oxidative stress and of pro-inflammatory cytokines in hippocampus and pre-frontal cortex of stressed animals. In addition, valproic acid treatment reduced anxiety in experimental animals, and restored neurotransmitters levels to normal values (Wilson et al, 2014). Valproic acid has several functions, including raising GABA levels, blocking Naþ channels, and maintaining IP3 levels.…”

Section: Oxidative Stress In Ptsdmentioning

confidence: 96%

Common biochemical defects linkage between post-traumatic stress disorders, mild traumatic brain injury (TBI) and penetrating TBI

Prasad¹,

Bondy

2015

Brain Research

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AnxietyPsychological damage a b s t r a c t Post-traumatic stress disorder (PTSD) is a complex mental disorder with psychological and emotional components, caused by exposure to single or repeated extreme traumatic events found in war, terrorist attacks, natural or man-caused disasters, and by violent personal assaults and accidents. Mild traumatic brain injury (TBI) occurs when the brain is violently rocked back and forth within the skull following a blow to the head or neck as in contact sports, or when in close proximity to a blast pressure wave following detonation of explosives in the battlefield. Penetrating TBI occurs when an object penetrates the skull and damages the brain, and is caused by vehicle crashes, gunshot wound to the head, and exposure to solid fragments in the proximity of explosions, and other combat-related head injuries. Despite clinical studies and improved understanding of the mechanisms of cellular damage, prevention and treatment strategies for patients with PTSD and TBI remain unsatisfactory. To develop an improved plan for treating and impeding progression of PTSD and TBI, it is important to identify underlying biochemical changes that may play key role in the initiation and progression of these disorders. This review identifies three common biochemical events, namely oxidative stress, chronic inflammation and excitotoxicity that participate in the initiation and progression of these conditions. While these features are separately discussed, in many instances, they overlap. This review also addresses the goal of developing novel treatments and drug regimens, aimed at combating this triad of events common to, and underlying, injury to the brain.

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“…HDAC treatment is relevant to persistent PTSD effects, as it can modify genetic transcription and diminish oxidative stress and levels of pro-inflammatory cytokines. These investigators reported that VA reversed the psychosocial stress-induced increase in anxiety-like behavior and restored the stress-induced alterations of neurotransmitter levels, oxidative stress and inflammation to control values (Wilson et al, 2014c). Particularly important is that the reversal of these changes occurred in the hippocampus and PFC, emphasizing that the neurochemical alterations in these brain regions might underlie the anxiogenic and cognitive effects of the PPS model.…”

Section: Accepted Manuscriptmentioning

confidence: 97%

Predator-based psychosocial stress animal model of PTSD: Preclinical assessment of traumatic stress at cognitive, hormonal, pharmacological, cardiovascular and epigenetic levels of analysis

Zoladz

Diamond

2016

Experimental Neurology

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Valproic acid effects in the hippocampus and prefrontal cortex in an animal model of post-traumatic stress disorder

Cited by 66 publications

References 68 publications

Activation of Sigma-1 receptor ameliorates anxiety-like behavior and cognitive impairments in a rat model of post-traumatic stress disorder

Activation of Sigma-1 receptor ameliorates anxiety-like behavior and cognitive impairments in a rat model of post-traumatic stress disorder

Common biochemical defects linkage between post-traumatic stress disorders, mild traumatic brain injury (TBI) and penetrating TBI

Predator-based psychosocial stress animal model of PTSD: Preclinical assessment of traumatic stress at cognitive, hormonal, pharmacological, cardiovascular and epigenetic levels of analysis

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