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F. S. Guimaraes - One of the best experts on this subject based on the ideXlab platform.
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Tempering aversive/Traumatic Memories with cannabinoids: a review of evidence from animal and human studies
Psychopharmacology, 2019Co-Authors: Sabrina F. Lisboa, C. Vila-verde, J. Rosa, D. L. Uliana, L. J. Bertoglio, L. B. Resstel, Stern Caj, F. S. GuimaraesAbstract:Aversive learning and memory are essential to cope with dangerous and stressful stimuli present in an ever-changing environment. When this process is dysfunctional, however, it is associated with postTraumatic stress disorder (PTSD). The endocannabinoid (eCB) system has been implicated in synaptic plasticity associated with physiological and pathological aversive learning and memory. The objective of this study was to review and discuss evidence on how and where in the brain genetic or pharmacological interventions targeting the eCB system would attenuate aversive/Traumatic Memories through extinction facilitation in laboratory animals and humans. The effect size of the experimental intervention under investigation was also calculated. Currently available data indicate that direct or indirect activation of cannabinoid type-1 (CB1) receptor facilitates the extinction of aversive/Traumatic Memories. Activating CB1 receptors around the formation of aversive/Traumatic Memories or their reminders can potentiate their subsequent extinction. In most cases, the effect size has been large (Cohen’s d ≥ 1.0). The brain areas responsible for the abovementioned effects include the medial prefrontal cortex, amygdala, and/or hippocampus. The potential role of cannabinoid type-2 (CB2) receptors in extinction learning is now under investigation. Drugs augmenting the brain eCB activity can temper the impact of aversive/Traumatic experiences by diverse mechanisms depending on the moment of their administration. Considering the pivotal role the extinction process plays in PTSD, the therapeutic potential of these drugs is evident. The sparse number of clinical trials testing these compounds in stress-related disorders is a gap in the literature that needs to be addressed.
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Tempering aversive/Traumatic Memories with cannabinoids: a review of evidence from animal and human studies
Psychopharmacology, 2019Co-Authors: Sabrina F. Lisboa, C. Vila-verde, J. Rosa, D. L. Uliana, C. A. J. Stern, L. J. Bertoglio, L. B. Resstel, F. S. GuimaraesAbstract:Rationale Aversive learning and memory are essential to cope with dangerous and stressful stimuli present in an ever-changing environment. When this process is dysfunctional, however, it is associated with postTraumatic stress disorder (PTSD). The endocannabinoid (eCB) system has been implicated in synaptic plasticity associated with physiological and pathological aversive learning and memory. Objective and methods The objective of this study was to review and discuss evidence on how and where in the brain genetic or pharmacological interventions targeting the eCB system would attenuate aversive/Traumatic Memories through extinction facilitation in laboratory animals and humans. The effect size of the experimental intervention under investigation was also calculated. Results Currently available data indicate that direct or indirect activation of cannabinoid type-1 (CB1) receptor facilitates the extinction of aversive/Traumatic Memories. Activating CB1 receptors around the formation of aversive/Traumatic Memories or their reminders can potentiate their subsequent extinction. In most cases, the effect size has been large (Cohen’s d ≥ 1.0). The brain areas responsible for the abovementioned effects include the medial prefrontal cortex, amygdala, and/or hippocampus. The potential role of cannabinoid type-2 (CB2) receptors in extinction learning is now under investigation. Conclusion Drugs augmenting the brain eCB activity can temper the impact of aversive/Traumatic experiences by diverse mechanisms depending on the moment of their administration. Considering the pivotal role the extinction process plays in PTSD, the therapeutic potential of these drugs is evident. The sparse number of clinical trials testing these compounds in stress-related disorders is a gap in the literature that needs to be addressed.
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tempering aversive Traumatic Memories with cannabinoids a review of evidence from animal and human studies
Psychopharmacology, 2019Co-Authors: Sabrina F. Lisboa, J. Rosa, D. L. Uliana, L. J. Bertoglio, L. B. Resstel, Stern Caj, C Vilaverde, F. S. GuimaraesAbstract:Aversive learning and memory are essential to cope with dangerous and stressful stimuli present in an ever-changing environment. When this process is dysfunctional, however, it is associated with postTraumatic stress disorder (PTSD). The endocannabinoid (eCB) system has been implicated in synaptic plasticity associated with physiological and pathological aversive learning and memory. The objective of this study was to review and discuss evidence on how and where in the brain genetic or pharmacological interventions targeting the eCB system would attenuate aversive/Traumatic Memories through extinction facilitation in laboratory animals and humans. The effect size of the experimental intervention under investigation was also calculated. Currently available data indicate that direct or indirect activation of cannabinoid type-1 (CB1) receptor facilitates the extinction of aversive/Traumatic Memories. Activating CB1 receptors around the formation of aversive/Traumatic Memories or their reminders can potentiate their subsequent extinction. In most cases, the effect size has been large (Cohen’s d ≥ 1.0). The brain areas responsible for the abovementioned effects include the medial prefrontal cortex, amygdala, and/or hippocampus. The potential role of cannabinoid type-2 (CB2) receptors in extinction learning is now under investigation. Drugs augmenting the brain eCB activity can temper the impact of aversive/Traumatic experiences by diverse mechanisms depending on the moment of their administration. Considering the pivotal role the extinction process plays in PTSD, the therapeutic potential of these drugs is evident. The sparse number of clinical trials testing these compounds in stress-related disorders is a gap in the literature that needs to be addressed.
Naomi Josman - One of the best experts on this subject based on the ideXlab platform.
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prolonged exposure and virtual reality enhanced imaginal exposure for ptsd following a terrorist bulldozer attack a case study
Cyberpsychology Behavior and Social Networking, 2010Co-Authors: Sara Freedman, Hunter G Hoffman, Patrice L. Weiss, Sara Avitzour, Azucena Garciapalacios, Naomi JosmanAbstract:Abstract In this case study, virtual reality was used to augment imaginal exposure in a protocol based on prolonged exposure. A 29-year-old male patient developed postTraumatic stress disorder after surviving a deadly terrorist bulldozer attack on two civilian buses and several cars in Jerusalem; the traumas witnessed by the survivor included a decapitation. The crowded bus in which the patient was riding was pushed over onto its side by the terrorist, injuring, trapping, and terrifying the passengers and causing gasoline to leak. Guided by his therapist, the patient entered an immersive computer-generated virtual world to go “back” to the scene of the Traumatic event to help him gain access to his Memories of the event, process and reduce the intensity of the emotions (fear/anger) associated with his pathological Memories, and change unhealthy thought patterns. Traumatic Memories of childhood abuse and Traumatic Memories of the bulldozer terrorist attack were treated using imaginal exposure while the pat...
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Prolonged Exposure and Virtual Reality–Enhanced Imaginal Exposure for PTSD following a Terrorist Bulldozer Attack: A Case Study
Cyberpsychology behavior and social networking, 2010Co-Authors: Sara Freedman, Hunter G Hoffman, Azucena García-palacios, Patrice L. Weiss, Sara Avitzour, Naomi JosmanAbstract:Abstract In this case study, virtual reality was used to augment imaginal exposure in a protocol based on prolonged exposure. A 29-year-old male patient developed postTraumatic stress disorder after surviving a deadly terrorist bulldozer attack on two civilian buses and several cars in Jerusalem; the traumas witnessed by the survivor included a decapitation. The crowded bus in which the patient was riding was pushed over onto its side by the terrorist, injuring, trapping, and terrifying the passengers and causing gasoline to leak. Guided by his therapist, the patient entered an immersive computer-generated virtual world to go “back” to the scene of the Traumatic event to help him gain access to his Memories of the event, process and reduce the intensity of the emotions (fear/anger) associated with his pathological Memories, and change unhealthy thought patterns. Traumatic Memories of childhood abuse and Traumatic Memories of the bulldozer terrorist attack were treated using imaginal exposure while the pat...
Gustav Schelling - One of the best experts on this subject based on the ideXlab platform.
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The role of glucocorticoids, catecholamines and endocannabinoids in the development of Traumatic Memories and postTraumatic stress symptoms in survivors of critical illness
Neurobiology of learning and memory, 2013Co-Authors: Daniela Hauer, Ines Kaufmann, Claudia Strewe, Isabel Briegel, Patrizia Campolongo, Gustav SchellingAbstract:Critically ill patients are at an increased risk for Traumatic Memories and post-Traumatic stress disorder (PTSD). Memories of one or more Traumatic events play an important part in the symptom pattern of PTSD. Studies in long-term survivors of intensive care unit (ICU) treatment demonstrated a clear and vivid recall of Traumatic experiences and the incidence and intensity of PTSD symptoms increased with the number of Traumatic Memories present. Preclinical evidence has clearly shown that the consolidation and retrieval of Traumatic Memories is regulated by an interaction between the noradrenergic, the glucocorticoid and the endocannabinoid system. Critically ill patients in the ICU frequently require treatment with adrenenergic or glucocorticoid drugs and often receive sedative medications; among them propofol is known to influence endocannabinoid signaling. Critical illness could therefore represent a useful model for investigating adrenergic, glucocorticoid as well as endocannabinoid effects on Traumatic memory and PTSD development in stressed humans. The endocannabinoid system is an important regulator of HPA-axis activity during stress, an effect which has also been demonstrated in humans. Likewise, a single nucleotide polymorphism (SNP) of the glucocorticoid receptor (GR) gene (the BclI-SNP), which enhances the sensitivity of the glucocorticoid receptors to cortisol and possibly HPA-axis feedback function, was associated with enhanced emotional memory performance in healthy volunteers. The presence of the BclI-SNP increased the risk for Traumatic Memories and PTSD symptoms in patients after ICU therapy and was linked to lower basal cortisol levels. A number of small studies have demonstrated that the administration of cortisol to critically ill or injured patients results in a significant reduction of PTSD symptoms after recovery without influencing the number of Traumatic Memories. These glucocorticoid effects can possibly be explained by a cortisol-induced temporary impairment in Traumatic memory retrieval which has previously been demonstrated in both rats and humans. The hypothesis that stress doses of glucocorticoids or the pharmacologic manipulation of glucocorticoid-endocannabinoid interaction during Traumatic memory consolidation and retrieval could be useful for prophylaxis and treatment of PTSD after critical illness should be tested in larger controlled studies.
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a beta adrenergic antagonist reduces Traumatic Memories and ptsd symptoms in female but not in male patients after cardiac surgery
Psychological Medicine, 2010Co-Authors: Till Krauseneck, Florian Weis, Benno Roozendaal, Ines Kaufmann, Frank Padberg, M Grathwohl, D Hauer, M Schmoeckel, Gustav SchellingAbstract:Background. Epinephrine enhances emotional memory whereas P-adrenoceptor antagonists (beta-blockers, BBs) impair it. However, the effects of BB administration on memory are sex dependent. Therefore, we predicted differential effects of epinephrine and the BB metoprolol given to male and female patients after cardiac surgery (CS) on Traumatic Memories and post-Traumatic stress disorder (PTSD) symptoms. Method. We performed a prospective observational study and determined the number of standardized Traumatic Memories (NTRM) and PTSD symptom intensity in cardiac surgical patients at 1 day before surgery, and at 1 week and 6 months after the procedure. PTSD symptoms and NTRM were quantified using validated questionnaires. Metoprolol could be administered any time post-operatively. Results. Baseline NTRM was not significantly different between male (n=95) and female patients (n=33). One week after CS, the NTRM in male patients was significantly higher. Metoprolol had no significant effect in either sex. At 6 months, females with metoprolol (n=18) showed a significantly lower NTRM and significantly lower PTSD symptom scores than females without BBs (n=15, p=0.02). By contrast, the totally administered dosage of epinephrine correlated with NTRM in males (r=0.33, p Conclusions. beta-Adrenergic stimulation with epinephrine enhances memory for adverse experiences in males but not in females whereas beta-blockade selectively reduces memory for post-operative adverse events and PTSD symptoms in females.
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Traumatic Memories post Traumatic stress disorder and serum cortisol levels in long term survivors of the acute respiratory distress syndrome
Brain Research, 2009Co-Authors: Daniela Hauer, Gustav Schelling, Florian Weis, Till Krauseneck, Michael Vogeser, Benno RoozendaalAbstract:Survivors of the acute respiratory distress syndrome (ARDS) often report Traumatic Memories from the intensive care unit (ICU) and display a high incidence of post-Traumatic stress disorder (PTSD). As it is known that subjects with PTSD often show sustained reductions in circulating cortisol concentrations, we examined the relationship between serum cortisol, Traumatic Memories and PTSD in patients after ARDS. We evaluated 33 long-term survivors of ARDS (7.5+/-2.9 years after discharge from the ICU) for pre-defined categories of Traumatic memory from the ICU, hypothalamic-pituitary-adrenocortical axis reactivity to corticotropin and PTSD (by psychiatric interview). During evaluation, patients with multiple Traumatic Memories had significantly lower basal serum cortisol levels when compared to patients with no or only 1 category of Traumatic memory, with no differences in peak cortisol levels after corticotropin stimulation between both subgroups. There was a significant negative correlation between basal cortisol levels and the number of Traumatic Memories present. PTSD symptom scores correlated with the number of Traumatic Memories but not with cortisol levels. These findings indicate that lower baseline cortisol levels in long-term survivors of ARDS are associated with an increased incidence of Traumatic Memories from the ICU, and that more Traumatic Memories are related to a higher incidence and intensity of PTSD symptoms.
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stress doses of hydrocortisone Traumatic Memories and symptoms of postTraumatic stress disorder in patients after cardiac surgery a randomized study
Biological Psychiatry, 2004Co-Authors: Gustav Schelling, Till Krauseneck, Benno Roozendaal, Dominique J.-f. De Quervain, E Kilger, J Briegel, Alexander Dagge, Hansbernd Rothenhausler, Georg Nollert, Hanspeter KapfhammerAbstract:Abstract Background Traumatic experiences associated with cardiac surgery (CS) can result in Traumatic Memories and postTraumatic stress disorder (PTSD). Because it is known that subjects who develop PTSD often show sustained reductions in circulating cortisol concentrations, we performed a prospective, randomized study to examine whether exogenously administered stress doses of hydrocortisone during the perioperative period of CS reduces the long-term incidence of chronic stress and PTSD symptoms. Methods Patients ( n = 91) were prospectively randomized to receive either stress doses of hydrocortisone or standard treatment during the perioperative period of CS. Of 48 available patients at 6 months after CS, 26 had received stress doses of hydrocortisone and 22 standard treatment. Traumatic Memories and PTSD symptoms were diagnosed with previously validated questionnaires. Results As compared with patients after standard therapy, patients from the hydrocortisone group had significantly lower chronic stress symptom scores ( p Conclusions Stress doses of hydrocortisone in patients undergoing CS are associated with a lower intensity of chronic stress and PTSD symptoms at 6 months after CS.
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Effects of stress hormones on Traumatic memory formation and the development of postTraumatic stress disorder in critically ill patients.
Neurobiology of learning and memory, 2002Co-Authors: Gustav SchellingAbstract:A majority of patients after intensive care treatment report Traumatic Memories from their stay in the intensive care unit (ICU). Traumatic Memories can be associated with the development of postTraumatic stress disorder (PTSD) in a subpopulation of these patients. In contrast to other patient populations at risk for PTSD, patients in the ICU often receive exogenously administered stress hormones like epinephrine, norepinephrine, or cortisol for medical reasons and are extensively monitored. ICU patients therefore represent a suitable population for studying the relationship between stress hormones, Traumatic Memories, and the development of PTSD. Studies in long-term survivors of ICU treatment demonstrated a clear and vivid recall of different categories of Traumatic memory such as nightmares, anxiety, respiratory distress, or pain with little or no recall of factual events. The number of categories of Traumatic memory recalled increased with the total administered dosages of stress hormones (both catecholamines and cortisol), and the evaluation of these categories at different time points after discharge from the ICU showed better memory consolidation with higher dosages of stress hormones administered. However, the administration of stress doses of cortisol to critically ill patients resulted in more complex findings as it caused a significant reduction in PTSD symptoms measured after recovery. This effect can possibly be explained by a differential influence of cortisol on memory. Increased serum cortisol levels not only result in consolidation of emotional memory but are also known to cause a temporary impairment in memory retrieval which appears to be independent of glucocorticoid effects on memory formation. Disrupting retrieval mechanisms with glucocorticoids during critical illness may therefore act protectively against the development of PTSD by preventing recall of Traumatic Memories. Our findings indicate that stress hormones influence the development of PTSD through complex and simultaneous interactions on memory formation and retrieval. Our studies also demonstrate that animal models of aversive learning are useful in analyzing and predicting clinical findings in critically ill humans.
Sabrina F. Lisboa - One of the best experts on this subject based on the ideXlab platform.
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Tempering aversive/Traumatic Memories with cannabinoids: a review of evidence from animal and human studies
Psychopharmacology, 2019Co-Authors: Sabrina F. Lisboa, C. Vila-verde, J. Rosa, D. L. Uliana, L. J. Bertoglio, L. B. Resstel, Stern Caj, F. S. GuimaraesAbstract:Aversive learning and memory are essential to cope with dangerous and stressful stimuli present in an ever-changing environment. When this process is dysfunctional, however, it is associated with postTraumatic stress disorder (PTSD). The endocannabinoid (eCB) system has been implicated in synaptic plasticity associated with physiological and pathological aversive learning and memory. The objective of this study was to review and discuss evidence on how and where in the brain genetic or pharmacological interventions targeting the eCB system would attenuate aversive/Traumatic Memories through extinction facilitation in laboratory animals and humans. The effect size of the experimental intervention under investigation was also calculated. Currently available data indicate that direct or indirect activation of cannabinoid type-1 (CB1) receptor facilitates the extinction of aversive/Traumatic Memories. Activating CB1 receptors around the formation of aversive/Traumatic Memories or their reminders can potentiate their subsequent extinction. In most cases, the effect size has been large (Cohen’s d ≥ 1.0). The brain areas responsible for the abovementioned effects include the medial prefrontal cortex, amygdala, and/or hippocampus. The potential role of cannabinoid type-2 (CB2) receptors in extinction learning is now under investigation. Drugs augmenting the brain eCB activity can temper the impact of aversive/Traumatic experiences by diverse mechanisms depending on the moment of their administration. Considering the pivotal role the extinction process plays in PTSD, the therapeutic potential of these drugs is evident. The sparse number of clinical trials testing these compounds in stress-related disorders is a gap in the literature that needs to be addressed.
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Tempering aversive/Traumatic Memories with cannabinoids: a review of evidence from animal and human studies
Psychopharmacology, 2019Co-Authors: Sabrina F. Lisboa, C. Vila-verde, J. Rosa, D. L. Uliana, C. A. J. Stern, L. J. Bertoglio, L. B. Resstel, F. S. GuimaraesAbstract:Rationale Aversive learning and memory are essential to cope with dangerous and stressful stimuli present in an ever-changing environment. When this process is dysfunctional, however, it is associated with postTraumatic stress disorder (PTSD). The endocannabinoid (eCB) system has been implicated in synaptic plasticity associated with physiological and pathological aversive learning and memory. Objective and methods The objective of this study was to review and discuss evidence on how and where in the brain genetic or pharmacological interventions targeting the eCB system would attenuate aversive/Traumatic Memories through extinction facilitation in laboratory animals and humans. The effect size of the experimental intervention under investigation was also calculated. Results Currently available data indicate that direct or indirect activation of cannabinoid type-1 (CB1) receptor facilitates the extinction of aversive/Traumatic Memories. Activating CB1 receptors around the formation of aversive/Traumatic Memories or their reminders can potentiate their subsequent extinction. In most cases, the effect size has been large (Cohen’s d ≥ 1.0). The brain areas responsible for the abovementioned effects include the medial prefrontal cortex, amygdala, and/or hippocampus. The potential role of cannabinoid type-2 (CB2) receptors in extinction learning is now under investigation. Conclusion Drugs augmenting the brain eCB activity can temper the impact of aversive/Traumatic experiences by diverse mechanisms depending on the moment of their administration. Considering the pivotal role the extinction process plays in PTSD, the therapeutic potential of these drugs is evident. The sparse number of clinical trials testing these compounds in stress-related disorders is a gap in the literature that needs to be addressed.
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tempering aversive Traumatic Memories with cannabinoids a review of evidence from animal and human studies
Psychopharmacology, 2019Co-Authors: Sabrina F. Lisboa, J. Rosa, D. L. Uliana, L. J. Bertoglio, L. B. Resstel, Stern Caj, C Vilaverde, F. S. GuimaraesAbstract:Aversive learning and memory are essential to cope with dangerous and stressful stimuli present in an ever-changing environment. When this process is dysfunctional, however, it is associated with postTraumatic stress disorder (PTSD). The endocannabinoid (eCB) system has been implicated in synaptic plasticity associated with physiological and pathological aversive learning and memory. The objective of this study was to review and discuss evidence on how and where in the brain genetic or pharmacological interventions targeting the eCB system would attenuate aversive/Traumatic Memories through extinction facilitation in laboratory animals and humans. The effect size of the experimental intervention under investigation was also calculated. Currently available data indicate that direct or indirect activation of cannabinoid type-1 (CB1) receptor facilitates the extinction of aversive/Traumatic Memories. Activating CB1 receptors around the formation of aversive/Traumatic Memories or their reminders can potentiate their subsequent extinction. In most cases, the effect size has been large (Cohen’s d ≥ 1.0). The brain areas responsible for the abovementioned effects include the medial prefrontal cortex, amygdala, and/or hippocampus. The potential role of cannabinoid type-2 (CB2) receptors in extinction learning is now under investigation. Drugs augmenting the brain eCB activity can temper the impact of aversive/Traumatic experiences by diverse mechanisms depending on the moment of their administration. Considering the pivotal role the extinction process plays in PTSD, the therapeutic potential of these drugs is evident. The sparse number of clinical trials testing these compounds in stress-related disorders is a gap in the literature that needs to be addressed.
L. J. Bertoglio - One of the best experts on this subject based on the ideXlab platform.
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Tempering aversive/Traumatic Memories with cannabinoids: a review of evidence from animal and human studies
Psychopharmacology, 2019Co-Authors: Sabrina F. Lisboa, C. Vila-verde, J. Rosa, D. L. Uliana, L. J. Bertoglio, L. B. Resstel, Stern Caj, F. S. GuimaraesAbstract:Aversive learning and memory are essential to cope with dangerous and stressful stimuli present in an ever-changing environment. When this process is dysfunctional, however, it is associated with postTraumatic stress disorder (PTSD). The endocannabinoid (eCB) system has been implicated in synaptic plasticity associated with physiological and pathological aversive learning and memory. The objective of this study was to review and discuss evidence on how and where in the brain genetic or pharmacological interventions targeting the eCB system would attenuate aversive/Traumatic Memories through extinction facilitation in laboratory animals and humans. The effect size of the experimental intervention under investigation was also calculated. Currently available data indicate that direct or indirect activation of cannabinoid type-1 (CB1) receptor facilitates the extinction of aversive/Traumatic Memories. Activating CB1 receptors around the formation of aversive/Traumatic Memories or their reminders can potentiate their subsequent extinction. In most cases, the effect size has been large (Cohen’s d ≥ 1.0). The brain areas responsible for the abovementioned effects include the medial prefrontal cortex, amygdala, and/or hippocampus. The potential role of cannabinoid type-2 (CB2) receptors in extinction learning is now under investigation. Drugs augmenting the brain eCB activity can temper the impact of aversive/Traumatic experiences by diverse mechanisms depending on the moment of their administration. Considering the pivotal role the extinction process plays in PTSD, the therapeutic potential of these drugs is evident. The sparse number of clinical trials testing these compounds in stress-related disorders is a gap in the literature that needs to be addressed.
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Tempering aversive/Traumatic Memories with cannabinoids: a review of evidence from animal and human studies
Psychopharmacology, 2019Co-Authors: Sabrina F. Lisboa, C. Vila-verde, J. Rosa, D. L. Uliana, C. A. J. Stern, L. J. Bertoglio, L. B. Resstel, F. S. GuimaraesAbstract:Rationale Aversive learning and memory are essential to cope with dangerous and stressful stimuli present in an ever-changing environment. When this process is dysfunctional, however, it is associated with postTraumatic stress disorder (PTSD). The endocannabinoid (eCB) system has been implicated in synaptic plasticity associated with physiological and pathological aversive learning and memory. Objective and methods The objective of this study was to review and discuss evidence on how and where in the brain genetic or pharmacological interventions targeting the eCB system would attenuate aversive/Traumatic Memories through extinction facilitation in laboratory animals and humans. The effect size of the experimental intervention under investigation was also calculated. Results Currently available data indicate that direct or indirect activation of cannabinoid type-1 (CB1) receptor facilitates the extinction of aversive/Traumatic Memories. Activating CB1 receptors around the formation of aversive/Traumatic Memories or their reminders can potentiate their subsequent extinction. In most cases, the effect size has been large (Cohen’s d ≥ 1.0). The brain areas responsible for the abovementioned effects include the medial prefrontal cortex, amygdala, and/or hippocampus. The potential role of cannabinoid type-2 (CB2) receptors in extinction learning is now under investigation. Conclusion Drugs augmenting the brain eCB activity can temper the impact of aversive/Traumatic experiences by diverse mechanisms depending on the moment of their administration. Considering the pivotal role the extinction process plays in PTSD, the therapeutic potential of these drugs is evident. The sparse number of clinical trials testing these compounds in stress-related disorders is a gap in the literature that needs to be addressed.
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tempering aversive Traumatic Memories with cannabinoids a review of evidence from animal and human studies
Psychopharmacology, 2019Co-Authors: Sabrina F. Lisboa, J. Rosa, D. L. Uliana, L. J. Bertoglio, L. B. Resstel, Stern Caj, C Vilaverde, F. S. GuimaraesAbstract:Aversive learning and memory are essential to cope with dangerous and stressful stimuli present in an ever-changing environment. When this process is dysfunctional, however, it is associated with postTraumatic stress disorder (PTSD). The endocannabinoid (eCB) system has been implicated in synaptic plasticity associated with physiological and pathological aversive learning and memory. The objective of this study was to review and discuss evidence on how and where in the brain genetic or pharmacological interventions targeting the eCB system would attenuate aversive/Traumatic Memories through extinction facilitation in laboratory animals and humans. The effect size of the experimental intervention under investigation was also calculated. Currently available data indicate that direct or indirect activation of cannabinoid type-1 (CB1) receptor facilitates the extinction of aversive/Traumatic Memories. Activating CB1 receptors around the formation of aversive/Traumatic Memories or their reminders can potentiate their subsequent extinction. In most cases, the effect size has been large (Cohen’s d ≥ 1.0). The brain areas responsible for the abovementioned effects include the medial prefrontal cortex, amygdala, and/or hippocampus. The potential role of cannabinoid type-2 (CB2) receptors in extinction learning is now under investigation. Drugs augmenting the brain eCB activity can temper the impact of aversive/Traumatic experiences by diverse mechanisms depending on the moment of their administration. Considering the pivotal role the extinction process plays in PTSD, the therapeutic potential of these drugs is evident. The sparse number of clinical trials testing these compounds in stress-related disorders is a gap in the literature that needs to be addressed.
