Time-dependent protective effects of morphine against behavioral and morphological deficits in an animal model of posttraumatic stress disorder

Raise-Abdullahi, Payman; Vafaei, Abbas Ali; Ghanbari, Ali; Dadkhah, Masoomeh; Rashidy-Pour, Ali

doi:10.1016/j.bbr.2019.01.058

Cited by 19 publications

(10 citation statements)

References 91 publications

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“…The increase of thin spines in adrenalectomized rats was lower when compared to morphine-treated intact rats, with no change detected in stubby spines within the shell of NAc (Geoffroy et al 2019 ). These findings agree with the results of another report investigating the impact of morphine in the post-traumatic stress disorder (PTSD) model (RaiseAbdullahi et al 2019 ). Young–adult rats exposed to a single episode of stress have received a morphine injection at four different timepoints (0, 6, 12, 24 h).…”

Section: Opioids In General Anesthesia and Spine Remodelingsupporting

confidence: 92%

“…At 25d post-stress, morphine-treated groups showed increased dendritic spines, with the highest effects observed in the group injected with morphine 24 h after inducing a stress response. Of note, the stimulating effects of morphine on dendritic spine formation were antagonized by naloxone (RaiseAbdullahi et al 2019 ). Another study in mice also using chronic (6-day) morphine treatment followed by abstinence for 2 months showed an increase in spine density in the frontal cortex and NAc, which persisted over 2 months.…”

Section: Opioids In General Anesthesia and Spine Remodelingmentioning

confidence: 99%

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Dendritic spine remodeling and plasticity under general anesthesia

2021

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Ever since its first use in surgery, general anesthesia has been regarded as a medical miracle enabling countless life-saving diagnostic and therapeutic interventions without pain sensation and traumatic memories. Despite several decades of research, there is a lack of understanding of how general anesthetics induce a reversible coma-like state. Emerging evidence suggests that even brief exposure to general anesthesia may have a lasting impact on mature and especially developing brains. Commonly used anesthetics have been shown to destabilize dendritic spines and induce an enhanced plasticity state, with effects on cognition, motor functions, mood, and social behavior. Herein, we review the effects of the most widely used general anesthetics on dendritic spine dynamics and discuss functional and molecular correlates with action mechanisms. We consider the impact of neurodevelopment, anatomical location of neurons, and their neurochemical profile on neuroplasticity induction, and review the putative signaling pathways. It emerges that in addition to possible adverse effects, the stimulation of synaptic remodeling with the formation of new connections by general anesthetics may present tremendous opportunities for translational research and neurorehabilitation.

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Section: Opioids In General Anesthesia and Spine Remodelingsupporting

confidence: 92%

Section: Opioids In General Anesthesia and Spine Remodelingmentioning

confidence: 99%

Dendritic spine remodeling and plasticity under general anesthesia

2021

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“…However, the fish spent significant time in the non-preferred compartment due to conditioned avoidance, hence, the behavioral parameters quantified are likely to have originated from the non-preferred chamber. In rodents, the protective effect of morphine on fear memory and responses appears after 6 h but not immediately after the trauma given, and the most effective response is observed when morphine treatment is given 24 h after the traumatic event 49 . However, in the present study, single morphine treatment 30-min after AS-induced fear stimuli successfully reduced expression of ASconditioned avoidance of fish, which is much shorter time than that in rats.…”

Section: Discussionmentioning

confidence: 99%

“…Next day (Day-3), prior to post-conditioning assessment, the fish was again immersed in morphine solution for 30 min. This was because the protective effect of morphine on fear memory and responses has been demonstrated to be most effective 24 h or 48 h after the traumatic event 6,49 . The dose for morphine was chosen based on a previous study in adult zebrafish 66 .…”

Section: Post-conditioning (Day-3)mentioning

confidence: 99%

Habenula kisspeptin retrieves morphine impaired fear memory in zebrafish

Ogawa

Parhar

2020

Sci Rep

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The habenula is an evolutionarily conserved brain structure, which has recently been implicated in fear memory. In the zebrafish, kisspeptin (Kiss1) is predominantly expressed in the habenula, which has been implicated as a modulator of fear response. Hence, in the present study, we questioned whether Kiss1 has a role in fear memory and morphine-induced fear memory impairment using an odorant cue (alarm substances, AS)-induced fear avoidance paradigm in adult zebrafish, whereby the fear-conditioned memory can be assessed by a change of basal place preference (= avoidance) of fish due to AS-induced fear experience. Subsequently, to examine the possible role of Kiss1 neurons-serotonergic pathway, kiss1 mRNA and serotonin levels were measured. AS exposure triggered fear episodes and fear-conditioned place avoidance. Morphine treatment followed by AS exposure, significantly impaired fear memory with increased time-spent in AS-paired compartment. However, fish administered with Kiss1 (10–21 mol/fish) after morphine treatment had significantly lower kiss1 mRNA levels but retained fear memory. In addition, the total brain serotonin levels were significantly increased in AS- and Kiss1-treated groups as compared to control and morphine treated group. These results suggest that habenular Kiss1 might be involved in consolidation or retrieval of fear memory through the serotonin system.

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“…Low doses of opioids have been shown to reduce symptoms of air hunger and breathlessness in both acute and chronic states of dyspnea, 48,49 and an animal model of physiological and emotional stress has shown behavioral and structural neurologic benefits associated with use of morphine. 50 Propofol, a highly effective amnestic sedative, has been shown to be relatively ineffective at suppressing activation of the amygdala; that is, patients may still develop maladaptive fear responses to stimuli in the absence of conscious memories. 51,52 Although its effect on dyspnea has not been studied, deep sedation with propofol fails to diminish pain-related activations in the cerebral cortex.…”

Section: Drugs With Antidyspnea Effects May Hold Promisementioning

confidence: 99%

Dyspnea, Acute Respiratory Failure, Psychological Trauma, and Post-ICU Mental Health

Worsham

Banzett

Schwartzstein

2021

Chest

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Dyspnea is an uncomfortable sensation with the potential to cause psychological trauma. Patients presenting with acute respiratory failure, particularly when tidal volume is restricted during mechanical ventilation, may experience the most distressing form of dyspnea known as air hunger. Air hunger activates brain pathways known to be involved in post-traumatic stress disorder (PTSD), anxiety, and depression. These conditions are considered part of the post-intensive care syndrome. These sequelae may be even more prevalent among patients with acute respiratory distress syndrome (ARDS). Low tidal volume, a mainstay of modern therapy for ARDS is difficult to avoid and is likely to cause air hunger despite sedation. Adjunctive neuromuscular blockade does not prevent or relieve air hunger, but it does prevent the patient from communicating discomfort to caregivers. Consequently, paralysis may also contribute to the development of PTSD. Although research has identified post-ARDS PTSD as a cause for concern and investigators have taken steps to quantify the burden of disease, there is little information to guide mechanical ventilation strategies designed to reduce its occurrence. We suggest such efforts will be more successful if they are directed at the known mechanisms of air hunger. Investigation of the anti-dyspnea effects of sedative and analgesic drugs commonly used in the ICU and their impact on post-ARDS PTSD symptoms is a logical next step. While in practice we often accept negative consequences of life-saving therapies as unavoidable, we must understand the negative sequalae of our therapies and work to minimize them under our primary directive to “first, do no harm” to our patients.

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Time-dependent protective effects of morphine against behavioral and morphological deficits in an animal model of posttraumatic stress disorder

Cited by 19 publications

References 91 publications

Dendritic spine remodeling and plasticity under general anesthesia

Dendritic spine remodeling and plasticity under general anesthesia

Habenula kisspeptin retrieves morphine impaired fear memory in zebrafish

Dyspnea, Acute Respiratory Failure, Psychological Trauma, and Post-ICU Mental Health

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