Clinical Therapeutic Strategy and Neuronal Mechanism Underlying Post-Traumatic Stress Disorder (PTSD)

Abstract

Post-traumatic stress disorder (PTSD) is characterized by an exaggerated response to contextual memory and impaired fear extinction, with or without mild cognitive impairment, learning deficits, and nightmares. PTSD is often developed by traumatic events, such as war, terrorist attack, natural calamities, etc. Clinical and animal studies suggest that aberrant susceptibility of emotion- and fear-related neurocircuits, including the amygdala, prefrontal cortex (PFC), and hippocampus may contribute to the development and retention of PTSD symptoms. Psychological and pharmacological therapy, such as cognitive behavioral therapy (CBT), and treatment with anti-depressive agents and/or antipsychotics significantly attenuate PTSD symptoms. However, more effective therapeutics are required for improvement of quality of life in PTSD patients. Previous studies have reported that ω3 long-chain polyunsaturated fatty acid (LCPUFA) supplements can suppress the development of PTSD symptoms. Fatty acid binding proteins (FABPs) are essential for LCPUFA intracellular trafficking. In this review, we have introduced Fabp3 null mice as an animal model of PTSD with impaired fear extinction. Moreover, we have addressed the neuronal circuits and novel therapeutic strategies for PTSD symptoms.

Towards an understanding of psychedelic-induced neuroplasticity

“…Depression in particular is characterized by reduced cortical neuroplasticity [56,[126][127][128], synapse atrophy in the PFC [18,[129][130][131], and a reduced ability of the PFC to regulate limbic areas [132,133]. Additionally, PTSD, social anxiety disorder, and generalized anxiety have been associated with fewer synaptic connections between the medial PFC and the amygdala, compromising the PFC's ability to regulate fear responses [134][135][136]. In addiction, neuroplasticity in the circuits between the PFC and the nucleus accumbens, striatum, and limbic system becomes impaired, reducing PFC modulation of these regions [137].…”

Blunted Nocturnal Salivary Melatonin Secretion Profiles in Military-Related Posttraumatic Stress Disorder

“…The work reported here indicates that PTSD should be added to this evolving list of disorders/diseases that result in blunted production of endogenous melatonin, and work investigating the efficiency of supplementation with exogenous melatonin in PTSD sufferers should be undertaken soonest. There is also recent evidence that long-chain polyunsaturated fatty acids can be beneficial in attenuating PTSD symptomology (69). These and other antioxidant strategies for treating PTSD should also be investigated.…”

Nabilone for the Treatment of Post-Traumatic Stress Disorder: A 2021 Update

“…4 Cognitive behavioural therapy is a form of psychotherapy that is used to treat patients with PTSD. 2,4,5 Pharmacological therapies such as selective serotonin reuptake inhibitors (e.g., fluoxetine, paroxetine, sertraline) and serotonin and noradrenaline reuptake inhibitors (e.g., venlafaxine, duloxetine) have also been recommended for the treatment of PTSD. 2,4 Other pharmacological options for the treatment of PTSD include atypical antipsychotic drugs (e.g., risperidone, olanzapine, aripiprazole), antidepressants (e.g., mirtazapine, bupropion), and others (e.g., gabapentin, topiramate).…”

“…2,4 Other pharmacological options for the treatment of PTSD include atypical antipsychotic drugs (e.g., risperidone, olanzapine, aripiprazole), antidepressants (e.g., mirtazapine, bupropion), and others (e.g., gabapentin, topiramate). 2,5 Recently, cannabinoids have emerged as a potential treatment option for patients with PTSD. 6 Cannabinoids is an umbrella term for the components of the cannabis plant and their synthetic analogues.…”