Is the war on terror induced-post traumatic stress disorder; the cause of suicide attack? An approach from psycho-cognitive and neurobiological perspective

Understanding suicide attack is one of the highly complicated problems in the field of psychological disorders. Post-traumatic stress disorder (PTSD), may occur in individuals subjected to traumatic assaults like terrorism, warfare, sexual abuse or natural disaster. Individual's living within war affected area often develops PTSD, which may consequently leads to cognitive and memory impairment. The war induced PTSD patient, is under the influence of severe stress; terror and helplessness as it manipulate and retrieve the past trauma as a current threat. Substantial evidences support that PTSD patients are more prone to varying degree of neurological and psychological complications. In this correspondence, we wish to highlight the biological consequence of suicide attack from the perspective of war induced PTSD. Earlier research also supports that PTSD and suicide have some common basis like alterations in hypothalamic pituitary-adrenal axis, nitric oxide and catecholamine like norepinephrine and serotonin level. Thus it is important to uncover the risk of PTSD due to war on terror with precision towards suicide attack and minimize the detriment followed by it. PTSD through the development of depression, irritability and anger, is one amongst the major causes of suicide attack.In order to clarify the underlying psychological mechanism, there is a pressing need to address it from different aspects like disease causing synaptic plasticity and abnormal brain development. PTSD is a reaction to past traumatic events. For instance, the danger of perceived threat due to witness of deaths in a war, may develop a constellation of properties that may leads to PTSD. Usually, it initiates a sequence of behavioral and cognitive changes that can be anticipated to reduce the perceived threat. However, the consequences of perceived threat lead to cognitive changes and thus maintain a devastating disorder. Appraisals of such memory not only generate situational fear but also the avoidance, which leads to enhanced trepidation and over-activity. For example, a person exposed to a road side traumatic accident may avoid driving; for having an impractical faith that it may happen again, thereby affecting its social life.Patients suffering from PTSD due to war may interpret that the trauma will persist for long time and thus he is no longer safe. He or she may suffer from depression, irritability, anger outbursts, emotional numbing, flashbacks, and nightmares [1]. It has been reported that numbing is an ordinary reaction to traumatic events. Individuals should realize that it is a normal aspect of the recovery process, otherwise it can lead to permanent changes which may worsen their physical or psychological well-being [2-4]. Children experiencing the PTSD, usually underwent alterations in hypothalamic-pituitary-adrenal axis, catecholamine and norepinephrine, which results in pathological and detrimental brain development [5]. Interestingly, the inhibition of nitric oxide in hippocampus by antidepressant has promising outcome to alleviate the PTSD symptoms [6]. While, the augmented level of plasma nitrates in depressive patients are found to be associated with suicide attempts [7].Figure 1The intention of a suicide attack is to kill a large crowd or bringing mass destruction, even with the notion that he will die in this act. Suicide bombings termed as "suicide bombing" constitute an overall 4% of terrorist attacks, which dates back to the beginning of the 19th century. In most of the modern suicide terrorist is used against non-combatants for the accomplishment of impact on political situation. Although a suicide attack aims to annihilate a primary target, however it can be used as a weapon of psychological warfare to affect the large public population. The main target of this action is not those who are killed but those witnessed it [8]. Intriguingly, it is reported that the level of brain-derived neurotropic factor (BDNF) is directly associated with suicide while indirectly it can affect PTSD. Also, defining body of research proved that altered level of serotonin in dorsal raphe nucleus, amygdala, median raphe, frontal cortex, hypothalamus and hippocampus is associated with aggressive behavior and suicide [9]. PTSD-induce symptoms like impulsivity, violence, suicide attempts, depression, panic, and anxiety can also be associated with altered serotonin levels [10].ConclusionThe mechanism of suicide attack is still highly debated; and need much more to address. Since, PTSD through the development of depression, irritability and anger, accomplish various physiological and cognitive changes in the brain, so it might be one of the causes which increases the susceptibility of acceptance for being a volunteer to suicide attack? This discussion was put forward; as some war induced PTSD patients among temporary displaced people in different regions of the world showed strong willingness for suicide attack as a counter revenge of war. Therefore, we also need to address suicide attack from the perspective of psychological disorders like war induced PTSD

The role of opioid and nitrergic systems in dual modulation of seizure susceptibility

Epilepsy is a chronic disorder presented by recurrent episodes of seizures and affect worldwide individuals.  The underlying mechanism of seizure is still elusive. Hence, there is still a need to determine the contribution of various systems in neurobiology and treatment of seizure. Evidence shows that opioid and nitrergic systems within the brain interact to modulate various physiological and pathological conditions including memory, pain, reward, addiction, depression, and seizure. Various studies revealed that diverse dose of opioids such as morphine has dual modulation in seizure susceptibility. For instance, it is reported that morphine at lower doses (0.5, 1, and 3 mg/kg) exerts an anticonvulsant effect in experimental seizure models, whereas at higher doses (15, 30, and 60 mg/kg) it could exacerbate the seizure. Similarly, nitrergic system has also been observed to possess dual effects in modulating the seizure threshold. Therefore, understanding of opioidergic and nitrergic systems interaction in seizure seems important to achieve the successful goal of seizure management. This review aimed to clarify and provide insight into how opioidergic and nitrergic systems interact in brain and mediate seizure behavior.Keywords: Opioids; Nitric oxide; Seizures; Morphine

Risk factors associated with relapse of drug dependence after treatment and rehabilitation in areas under the influence of war on terror

Background: People exposed to war on terror are more prone to neuropsychiatric disorders and drug addiction. The present study was aimed to investigate the risk factors associated with relapse of drug dependence after treatment and rehabilitation in areas under the influence of war and terrorism.Methods: Total 57 individuals who had a relapse from the war affected area were included in current study. Retrospective data were collected from Drug Detoxification and Health Welfare Research Center, Bannu, KPK, Pakistan. Along with demographic characteristics, current study also focused on the prevalence of psychological problems due to war, in association with prevalence of relapse.Results: A total of 93% of Individuals with relapse have concurrent stress. Similarly, depression was also common in 78.9% of relapsed individuals. Relapse was more common in Polydrug abusers (66.7%) as compared to single drug abusers. As far as abstinence duration is concerned, subjects having depression and stress due to war, relapsed in less time as compared to individuals with no psychological disorders.Conclusion: Wars are related with mental and psychological problems like stress and depression and these factors significantly contribute to the relapse of drug dependence as suggested by results of current study.Keywords: Drug addiction; Relapse; War on terror; Depressio

Streptozotocin induced oxidative stress, innate immune system responses and behavioral abnormalities in male mice

Recent evidence indicates the involvement of inflammatory factors and mitochondrial dysfunction in the etiology of psychiatric disorders such as anxiety and depression. To investigate the possible role of mitochondrial-induced sterile inflammation in the co-occurrence of anxiety and depression, in this study, we treated adult male mice with the intracerebroventricular (i.c.v.) infusion of a single low dose of streptozotocin (STZ, 0.2 mg/mouse). Using valid and qualified behavioral tests for the assessment of depressive and anxiety-like behaviors, we showed that STZ-treated mice exhibited behaviors relevant to anxiety and depression 24 h following STZ treatment. We observed that the co-occurrence of anxiety and depressive-like behaviors in animals were associated with abnormal mitochondrial function, nitric oxide overproduction and, the increased activity of cytosolic phospholipase A2 (cPLA2) in the hippocampus. Further, STZ-treated mice had a significant upregulation of genes associated with the innate immune system such as toll-like receptors 2 and 4. Pathological evaluations showed no sign of neurodegeneration in the hippocampus of STZ-treated mice. Results of this study revealed that behavioral abnormalities provoked by STZ, as a cytotoxic agent that targets mitochondria and energy metabolism, are associated with abnormal mitochondrial activity and, consequently the initiation of innate-inflammatory responses in the hippocampus. Our findings highlight the role of mitochondria and innate immunity in the formation of sterile inflammation and behaviors relevant to anxiety and depression. Also, we have shown that STZ injection (i.c.v.) might be an animal model for depression and anxiety disorders based on sterile inflammation

The Antidepressant-Like Effect of the Ethanolic Extract of Mentha Piperita in Forced Swimming Test and Tail Suspension Test in Male Mice

Introduction: Previous studies have revealed analgesic, anti-inflammatory, and antioxidant properties of Mentha piperita (MP). Hence, in this study, the antidepressant effects of the ethanolic extract of MP in forced swim test (FST) and tail suspension test (TST) in male mice were investigated.   Materials & Methods: In this experimental study, 96 male mice were randomly divided into 12 groups of 8 that received normal saline (10 ml/kg), imipramine (30 mg/kg), fluoxetine (20 mg/kg), and different doses of MP (100, 200 and 400 mg/kg), respectively. In FST, immobility time, swimming time, and climbing time and immobility time in TST were recorded during 6 minutes. In this study, all the drugs and extracts were injected intraperitoneally (i.p.) at the constant volume of 10 ml/kg.   Findings: Results shows that 200 and 400 mg/kg of the extract, as well as fluoxetine and imipramine reduced immobility time compared to the control group in FST and TST (p0.05). In contrast, imipramine increased climbing time without any significant change in swimming time (p>0.05).   Discussion & Conclusions: This extract like serotonergic agents (e.g., fluoxetine) decreases immobility time and increases swimming time without any significant change in climbing time. Hence, MP compounds (especially menthol) induced their effects through serotonergic mechanism. However, further studies are needed to clarify their exact mechanism of action

Involvement of Inflammatory Cytokines in Antiarrhythmic Effects of Clofibrate in Ouabain-Induced Arrhythmia in Isolated Rat Atria

Considering the cardioprotective and anti-inflammatory properties of clofibrate, the aim of the present experiment was to investigate the involvement of local and systemic inflammatory cytokines in possible antiarrhythmic effects of clofibrate in ouabain-induced arrhythmia in rats. Rats were orally treated with clofibrate (300 mg/kg), and ouabain (0.56 mg/kg) was administered to animals intraperitoneally. After induction of anesthesia, the atria were isolated and the onset of arrhythmia and asystole was recorded. The levels of inflammatory cytokines in atria were also measured. Clofibrate significantly postponed the onset of arrhythmia and asystole when compared to control group (P≤0.05 and P≤0.01, resp.). While ouabain significantly increased the atrial beating rate in control group (P≤0.05), same treatment did not show similar effect in clofibrate-treated group (P>0.05). Injection of ouabain significantly increased the atrial and systemic levels of all studied inflammatory cytokines (P≤0.05). Pretreatment with clofibrate could attenuate the ouabain-induced elevation of IL-6 and TNF-α in atria (P≤0.01 and P≤0.05, resp.), as well as ouabain-induced increase in IL-6 in plasma (P≤0.05). Based on our findings, clofibrate may possess antiarrhythmic properties through mitigating the local and systemic inflammatory factors including IL-6 and TNF-α

D-Ala, D-Leu Enkephalin Delays Ouabain-Induced Arrhythmia In Isolated Rat Atria

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The anti-inflammatory and antipyretic effects of clove oil in healthy dogs after surgery

The current study was designed to evaluate the anti-inflammatory and antipyretic properties of clove oil in dogs. So thirty adult male dogs were used. After a surgical incision on the abdominal area, animals were divided into four group. The first group received 25 mg/kg of clove oil while the second group was considered as a control. The third and fourth groups received betamethasone (20 mg/kg) and phenylbutazone (15 mg/kg) as anti-inflammatory and anti-pyretic agents, respectively. All injections were performed for five consecutive days. All tests (measurement of edema, complete blood count, histopathology, and rectal temperature) were performed on all groups. Our results showed that in the clove oil-treated animals, the amount of edema was significantly decreased as compared to control (P ≤ 0.05). The number of white blood cells, neutrophils and band neutrophils was decreased in clove-oil treated dogs as compared to control (P ≤ 0.05). There was no significant difference in the number of red blood cells and hematocrit between clove-oil treated and vehicle-treated groups (P > 0.05). Rectal temperature significantly decreased in the clove oil-treated group as compared to control (P ≤ 0.05). Histopathology revealed that the clove oil-treatment significantly reduced the inflammation. We showed that clove oil administration has anti-inflammatory and antipyretic properties in dogs