Pub Date : 2022-01-01Epub Date: 2022-11-18DOI: 10.1159/000526805
Ke Chen, Maria Garbusow, Miriam Sebold, Hilmar G Zech, Ulrich Zimmermann, Andreas Heinz
Introduction: Positively conditioned Pavlovian cues tend to promote approach and negative cues promote withdrawal in a Pavlovian-to-instrumental transfer (PIT) paradigm, and the strength of this PIT effect was associated with the subsequent relapse risk in alcohol-dependent (AD) patients. When investigating the effect of alcohol-related background cues, instrumental approach behavior was inhibited in subsequent abstainers but not relapsers. An automatic approach bias towards alcohol can be modified using a cognitive bias modification (CBM) intervention, which has previously been shown to reduce the relapse risk in AD patients. Here we examined the effects of such CBM training on PIT effects and explored its effect on the relapse risk in detoxified AD patients.
Methods: N = 81 recently detoxified AD patients performed non-drug-related and drug-related PIT tasks before and after CBM versus placebo training. In addition, an alcohol approach/avoidance task (aAAT) was performed before and after the training to assess the alcohol approach bias. Patients were followed up for 6 months.
Results: A stronger alcohol approach bias as well as a stronger non-drug-related PIT effect predicted relapse status in AD patients. No significant difference regarding relapse status or the number of heavy drinking days was found when comparing the CBM training group versus the placebo group. Moreover, there was no significant modulation effect of CBM training on any PIT effect or the aAAT.
Conclusion: A higher alcohol approach bias in the aAAT and a stronger non-drug-related PIT effect both predicted relapse in AD patients, while treatment outcome was not associated with the drug-related PIT effect. Unlike expected, CBM training did not significantly interact with the non-drug-related or the drug-related PIT effects or the alcohol approach bias.
{"title":"Automatic Approach Behaviors in Alcohol Dependence: Does a Cognitive Bias Modification Training Affect Pavlovian-to-Instrumental Transfer Effects?","authors":"Ke Chen, Maria Garbusow, Miriam Sebold, Hilmar G Zech, Ulrich Zimmermann, Andreas Heinz","doi":"10.1159/000526805","DOIUrl":"https://doi.org/10.1159/000526805","url":null,"abstract":"<p><strong>Introduction: </strong>Positively conditioned Pavlovian cues tend to promote approach and negative cues promote withdrawal in a Pavlovian-to-instrumental transfer (PIT) paradigm, and the strength of this PIT effect was associated with the subsequent relapse risk in alcohol-dependent (AD) patients. When investigating the effect of alcohol-related background cues, instrumental approach behavior was inhibited in subsequent abstainers but not relapsers. An automatic approach bias towards alcohol can be modified using a cognitive bias modification (CBM) intervention, which has previously been shown to reduce the relapse risk in AD patients. Here we examined the effects of such CBM training on PIT effects and explored its effect on the relapse risk in detoxified AD patients.</p><p><strong>Methods: </strong>N = 81 recently detoxified AD patients performed non-drug-related and drug-related PIT tasks before and after CBM versus placebo training. In addition, an alcohol approach/avoidance task (aAAT) was performed before and after the training to assess the alcohol approach bias. Patients were followed up for 6 months.</p><p><strong>Results: </strong>A stronger alcohol approach bias as well as a stronger non-drug-related PIT effect predicted relapse status in AD patients. No significant difference regarding relapse status or the number of heavy drinking days was found when comparing the CBM training group versus the placebo group. Moreover, there was no significant modulation effect of CBM training on any PIT effect or the aAAT.</p><p><strong>Conclusion: </strong>A higher alcohol approach bias in the aAAT and a stronger non-drug-related PIT effect both predicted relapse in AD patients, while treatment outcome was not associated with the drug-related PIT effect. Unlike expected, CBM training did not significantly interact with the non-drug-related or the drug-related PIT effects or the alcohol approach bias.</p>","PeriodicalId":19239,"journal":{"name":"Neuropsychobiology","volume":null,"pages":null},"PeriodicalIF":3.2,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40477316","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"心理学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Introduction: Since decades, the "Mozart effect" has been studied. However, the diverse effects of Mozart's music components have not been yet defined. Authors aimed to identify a differential response to short-term exposure to Mozart's music, or to its rhythmic signature only, on subjective and objective measures.
Methods: The Mozart Sonata in A major K 331 (Mozart), the same piece consisting only of beat (Destructured), and duration-matched silence were administered to 25 healthy young adults, stood supine in a relaxing setting. The Italian Mood Scale questionnaire was administered before and after each listening. Heart rate variability (HRV) metrics were calculated from ECG recording, and breath flow was registered during experiments.
Results: After Destructured, there was no change of fatigue and tension. After Mozart, fatigue was significantly reduced (and a tendency appeared for tension), whereas vigor was not. Breathing rate tended to be higher during Mozart. The nonlinear parameter HFD of HRV analysis, even though not significantly, was slightly lower during Destructured; Poincaré plots SD1 and SD2 tended to be lower during Mozart.
Discussion/conclusion: Mozart's music may allow to maintain arousal during relaxing condition. Psychological response of music and physiological dynamics were not necessarily entangled. Musical pieces based on individual physiological signature may lead musical psychological interventions.
{"title":"Neurovegetative and Emotional Modulation Induced by Mozart's Music.","authors":"Margherita Di Cesare, Alessandro Tonacci, Danilo Bondi, Vittore Verratti, Giulia Prete, Gianluca Malatesta, Tiziana Pietrangelo","doi":"10.1159/000525360","DOIUrl":"https://doi.org/10.1159/000525360","url":null,"abstract":"<p><strong>Introduction: </strong>Since decades, the \"Mozart effect\" has been studied. However, the diverse effects of Mozart's music components have not been yet defined. Authors aimed to identify a differential response to short-term exposure to Mozart's music, or to its rhythmic signature only, on subjective and objective measures.</p><p><strong>Methods: </strong>The Mozart Sonata in A major K 331 (Mozart), the same piece consisting only of beat (Destructured), and duration-matched silence were administered to 25 healthy young adults, stood supine in a relaxing setting. The Italian Mood Scale questionnaire was administered before and after each listening. Heart rate variability (HRV) metrics were calculated from ECG recording, and breath flow was registered during experiments.</p><p><strong>Results: </strong>After Destructured, there was no change of fatigue and tension. After Mozart, fatigue was significantly reduced (and a tendency appeared for tension), whereas vigor was not. Breathing rate tended to be higher during Mozart. The nonlinear parameter HFD of HRV analysis, even though not significantly, was slightly lower during Destructured; Poincaré plots SD1 and SD2 tended to be lower during Mozart.</p><p><strong>Discussion/conclusion: </strong>Mozart's music may allow to maintain arousal during relaxing condition. Psychological response of music and physiological dynamics were not necessarily entangled. Musical pieces based on individual physiological signature may lead musical psychological interventions.</p>","PeriodicalId":19239,"journal":{"name":"Neuropsychobiology","volume":null,"pages":null},"PeriodicalIF":3.2,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40399530","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"心理学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2022-01-01Epub Date: 2021-09-02DOI: 10.1159/000517329
Franziska C Weber, Thomas C Wetter
Sleep disorders and nightmares are core symptoms of post-traumatic stress disorder (PTSD). The relationship seems to be bidirectional, and persistent disturbed sleep may influence the course of the disorder. With regard to sleep quality, insomnia and nocturnal anxiety symptoms, as well as nightmares and stressful dreams, are the most prominent sleep symptoms. Polysomnographic measurements reveal alterations of the sleep architecture and fragmentation of rapid eye movement sleep. In addition, sleep disorders, such as sleep-related breathing disorders and parasomnias are frequent comorbid conditions. The complex etiology and symptomatology of trauma-related sleep disorders with frequent psychiatric comorbidity require the application of multimodal treatment concepts, including psychological and pharmacological interventions. However, there is little empirical evidence on the effectiveness of long-term drug treatment for insomnia and nightmares. For nondrug interventions, challenges arise from the current lack of PTSD-treatment concepts integrating sleep- and trauma-focused therapies. Effective therapy for sleep disturbances may consequently also improve well-being during the day and probably even the course of PTSD. Whether early sleep interventions exert a preventive effect on the development of PTSD remains to be clarified in future studies.
{"title":"The Many Faces of Sleep Disorders in Post-Traumatic Stress Disorder: An Update on Clinical Features and Treatment.","authors":"Franziska C Weber, Thomas C Wetter","doi":"10.1159/000517329","DOIUrl":"10.1159/000517329","url":null,"abstract":"<p><p>Sleep disorders and nightmares are core symptoms of post-traumatic stress disorder (PTSD). The relationship seems to be bidirectional, and persistent disturbed sleep may influence the course of the disorder. With regard to sleep quality, insomnia and nocturnal anxiety symptoms, as well as nightmares and stressful dreams, are the most prominent sleep symptoms. Polysomnographic measurements reveal alterations of the sleep architecture and fragmentation of rapid eye movement sleep. In addition, sleep disorders, such as sleep-related breathing disorders and parasomnias are frequent comorbid conditions. The complex etiology and symptomatology of trauma-related sleep disorders with frequent psychiatric comorbidity require the application of multimodal treatment concepts, including psychological and pharmacological interventions. However, there is little empirical evidence on the effectiveness of long-term drug treatment for insomnia and nightmares. For nondrug interventions, challenges arise from the current lack of PTSD-treatment concepts integrating sleep- and trauma-focused therapies. Effective therapy for sleep disturbances may consequently also improve well-being during the day and probably even the course of PTSD. Whether early sleep interventions exert a preventive effect on the development of PTSD remains to be clarified in future studies.</p>","PeriodicalId":19239,"journal":{"name":"Neuropsychobiology","volume":null,"pages":null},"PeriodicalIF":2.3,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9153357/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39378697","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"心理学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Introduction: The interaction of environmental and inherited factors determines how a young person becomes involved in problem behaviours such as drinking alcohol. We have investigated whether the association of family relationships with early experience with alcohol is related to variation in the serotonin transporter gene promoter region (5-HTTLPR).
Methods: We used data of the two birth cohorts of the Estonian Personality Behaviour and Health Study (original n = 1,238) at age 15 and 18 years. Data were self-reported in a laboratory setting.
Results: Family relationships at age 15 years were significantly related to the frequency of drinking alcohol. Specifically, association of Warmth in Family (closeness and support within family) with consuming alcohol was in a negative, while maltreatment (misprize and abuse) in a positive relationship with alcohol consumption. At age 18 years, the effects of family relationships on consuming alcohol were lower and no longer statistically significant (p values >0.10). The associations between family relations and alcohol use at age 15 years varied by the 5-HTTLPR genotype: at this age, the impact of the family relations, both Warmth and Maltreatment, on the frequency of drinking alcohol was statistically significant among participants with the S/L genotype, and while rather similar results were obtained for the S/S genotype, no relations were apparent between family relations and consuming alcohol in subjects with the L/L genotype.
Conclusion: These findings reveal that family relations are related to alcohol consumption, dependent upon the 5-HTTLPR genotype. This is compatible with the hypothesis that the S-allele carriers are more malleable by the environment.
{"title":"Family Relationships and Alcohol Consumption: Interaction with the Serotonin Transporter Promoter Polymorphism (5-HTTLPR).","authors":"Farzaneh Zareei, Toomas Veidebaum, Jaanus Harro","doi":"10.1159/000526004","DOIUrl":"https://doi.org/10.1159/000526004","url":null,"abstract":"<p><strong>Introduction: </strong>The interaction of environmental and inherited factors determines how a young person becomes involved in problem behaviours such as drinking alcohol. We have investigated whether the association of family relationships with early experience with alcohol is related to variation in the serotonin transporter gene promoter region (5-HTTLPR).</p><p><strong>Methods: </strong>We used data of the two birth cohorts of the Estonian Personality Behaviour and Health Study (original n = 1,238) at age 15 and 18 years. Data were self-reported in a laboratory setting.</p><p><strong>Results: </strong>Family relationships at age 15 years were significantly related to the frequency of drinking alcohol. Specifically, association of Warmth in Family (closeness and support within family) with consuming alcohol was in a negative, while maltreatment (misprize and abuse) in a positive relationship with alcohol consumption. At age 18 years, the effects of family relationships on consuming alcohol were lower and no longer statistically significant (p values >0.10). The associations between family relations and alcohol use at age 15 years varied by the 5-HTTLPR genotype: at this age, the impact of the family relations, both Warmth and Maltreatment, on the frequency of drinking alcohol was statistically significant among participants with the S/L genotype, and while rather similar results were obtained for the S/S genotype, no relations were apparent between family relations and consuming alcohol in subjects with the L/L genotype.</p><p><strong>Conclusion: </strong>These findings reveal that family relations are related to alcohol consumption, dependent upon the 5-HTTLPR genotype. This is compatible with the hypothesis that the S-allele carriers are more malleable by the environment.</p>","PeriodicalId":19239,"journal":{"name":"Neuropsychobiology","volume":null,"pages":null},"PeriodicalIF":3.2,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10716192","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"心理学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2022-01-01Epub Date: 2021-10-15DOI: 10.1159/000514076
Mi Su, Yongyan Song
Background: Genetic factors were suggested to have influence on the development of post-traumatic stress disorder (PTSD). The possible association between catechol-O-methyltransferase (COMT) Val158Met polymorphism and PTSD has been evaluated in several studies. But the results were still controversial. Therefore, we conduct this meta-analysis to address these issues.
Methods: The PubMed, EMBASE, Cochrane Library, and Web of Science databases were searched for eligible studies. The pooled odds ratio (OR) with 95% confidence interval (CI) was calculated to estimate the association between COMT Val158Met polymorphism and PTSD.
Results: Five articles including 6 studies with 893 cases and 968 controls were finally included in the present meta-analysis. The pooled analyses did not demonstrate a significant association between the COMT Val158Met polymorphism and PTSD in any of the selected genetic models: allele model (OR = 1.13, 95% CI: 0.97-1.31), dominant model (OR = 1.17, 95% CI: 0.93-1.46), recessive model (OR = 1.44, 95% CI: 0.78-2.66), and additive model (OR = 1.54, 95% CI: 0.85-2.80). Subgroup analyses suggested that the Hardy-Weinberg equilibrium status of genotype distributions could influence the relationship of COMT Val158Met polymorphism and PTSD.
Conclusions: The present meta-analysis suggested that the COMT Val158Met polymorphism may not be associated with the PTSD risk. Further large-scale and population-representative studies are warranted to evaluate the impact of the COMT Val158Met polymorphism on the risk of PTSD.
{"title":"The Association between COMT Val158Met Polymorphism and the Post-Traumatic Stress Disorder Risk: A Meta-Analysis.","authors":"Mi Su, Yongyan Song","doi":"10.1159/000514076","DOIUrl":"https://doi.org/10.1159/000514076","url":null,"abstract":"<p><strong>Background: </strong>Genetic factors were suggested to have influence on the development of post-traumatic stress disorder (PTSD). The possible association between catechol-O-methyltransferase (COMT) Val158Met polymorphism and PTSD has been evaluated in several studies. But the results were still controversial. Therefore, we conduct this meta-analysis to address these issues.</p><p><strong>Methods: </strong>The PubMed, EMBASE, Cochrane Library, and Web of Science databases were searched for eligible studies. The pooled odds ratio (OR) with 95% confidence interval (CI) was calculated to estimate the association between COMT Val158Met polymorphism and PTSD.</p><p><strong>Results: </strong>Five articles including 6 studies with 893 cases and 968 controls were finally included in the present meta-analysis. The pooled analyses did not demonstrate a significant association between the COMT Val158Met polymorphism and PTSD in any of the selected genetic models: allele model (OR = 1.13, 95% CI: 0.97-1.31), dominant model (OR = 1.17, 95% CI: 0.93-1.46), recessive model (OR = 1.44, 95% CI: 0.78-2.66), and additive model (OR = 1.54, 95% CI: 0.85-2.80). Subgroup analyses suggested that the Hardy-Weinberg equilibrium status of genotype distributions could influence the relationship of COMT Val158Met polymorphism and PTSD.</p><p><strong>Conclusions: </strong>The present meta-analysis suggested that the COMT Val158Met polymorphism may not be associated with the PTSD risk. Further large-scale and population-representative studies are warranted to evaluate the impact of the COMT Val158Met polymorphism on the risk of PTSD.</p>","PeriodicalId":19239,"journal":{"name":"Neuropsychobiology","volume":null,"pages":null},"PeriodicalIF":3.2,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39524146","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"心理学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2022-01-01Epub Date: 2021-11-02DOI: 10.1159/000519534
Mohammadali Amini, Zohreh Abdolmaleki
Introduction: Using nanoparticle (NP) drugs can have better effects on the target tissue in various diseases. Alzheimer's disease (AD) is one of the degenerative neurological diseases that due to its high prevalence, requires the use of more appropriate treatments. Therefore, the aim of this study was consideration of the effect of cannabidiol (CBD) coated by nano-chitosan on learning and memory, hippocampal cannabinoid receptor type 1 (CB1) and cannabinoid receptor type 1 (CB2) levels, and amyloid plaques in an AD rat model.
Material and methods: Thirty-five male Wistar rats were randomly divided into 5 groups (n = 7 in each): control, Alzheimer's disease model that received the beta-amyloid (Aβ) peptide (Alz), Alz + nano-chitosan (NP) Alz + CBD, and Alz + NP + CBD. Alz was induced by injection of the Aβ1-42 peptide into the hippocampal area cornu ammonis1. After confirmation of Alz, 1 μL of CBD and NP + CBD were administered by oral gavage daily in rats for 1 month. The Morris water maze (MWM) test was used to assess learning and memory of animals. Cresyl violet staining was used for consideration of dead cells. Gene and protein expression of CB1 and CB2 was performed by real-time PCR and immunohistochemistry methods.
Results: Induction of Alz significantly increased Aβ plaques and dead cells compared to the control group (p < 0.001). Results of MWM in the day test show that Alz + NP + CBD significantly decrease escape latency (p < 0.01), travelled distance (p < 0.001), and significantly increased spending time (p < 0.001) compared to the Alz group. Protein expression of CB1 and CB2 significantly increased in Alz + CBD and Alz + NP + CBD compared to the Alz group (p < 0.05).
Conclusion: It seems that CBD coated by nano-chitosan has good potential for reducing Aβ plaques, increasing brain CB1 and levels CB2, and improving learning and memory in Alz rats.
{"title":"The Effect of Cannabidiol Coated by Nano-Chitosan on Learning and Memory, Hippocampal CB1 and CB2 Levels, and Amyloid Plaques in an Alzheimer's Disease Rat Model.","authors":"Mohammadali Amini, Zohreh Abdolmaleki","doi":"10.1159/000519534","DOIUrl":"https://doi.org/10.1159/000519534","url":null,"abstract":"<p><strong>Introduction: </strong>Using nanoparticle (NP) drugs can have better effects on the target tissue in various diseases. Alzheimer's disease (AD) is one of the degenerative neurological diseases that due to its high prevalence, requires the use of more appropriate treatments. Therefore, the aim of this study was consideration of the effect of cannabidiol (CBD) coated by nano-chitosan on learning and memory, hippocampal cannabinoid receptor type 1 (CB1) and cannabinoid receptor type 1 (CB2) levels, and amyloid plaques in an AD rat model.</p><p><strong>Material and methods: </strong>Thirty-five male Wistar rats were randomly divided into 5 groups (n = 7 in each): control, Alzheimer's disease model that received the beta-amyloid (Aβ) peptide (Alz), Alz + nano-chitosan (NP) Alz + CBD, and Alz + NP + CBD. Alz was induced by injection of the Aβ1-42 peptide into the hippocampal area cornu ammonis1. After confirmation of Alz, 1 μL of CBD and NP + CBD were administered by oral gavage daily in rats for 1 month. The Morris water maze (MWM) test was used to assess learning and memory of animals. Cresyl violet staining was used for consideration of dead cells. Gene and protein expression of CB1 and CB2 was performed by real-time PCR and immunohistochemistry methods.</p><p><strong>Results: </strong>Induction of Alz significantly increased Aβ plaques and dead cells compared to the control group (p < 0.001). Results of MWM in the day test show that Alz + NP + CBD significantly decrease escape latency (p < 0.01), travelled distance (p < 0.001), and significantly increased spending time (p < 0.001) compared to the Alz group. Protein expression of CB1 and CB2 significantly increased in Alz + CBD and Alz + NP + CBD compared to the Alz group (p < 0.05).</p><p><strong>Conclusion: </strong>It seems that CBD coated by nano-chitosan has good potential for reducing Aβ plaques, increasing brain CB1 and levels CB2, and improving learning and memory in Alz rats.</p>","PeriodicalId":19239,"journal":{"name":"Neuropsychobiology","volume":null,"pages":null},"PeriodicalIF":3.2,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39584307","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"心理学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2022-01-01Epub Date: 2022-01-11DOI: 10.1159/000521234
Else Refsgaard, Anne Vibeke Schmedes, Klaus Martiny
Introduction: The hypothalamic-pituitary-adrenal axis function in depression has been the subject of considerable interest, and its function has been tested with a variety of methods. We investigated associations between saliva cortisol at awakening and the 24-h urine cortisol output, both measured at study baseline, with endpoint depression scores.
Methods: Patients were admitted to a psychiatric inpatient ward with a major depressive episode and were started on fixed duloxetine treatment. They delivered saliva samples at awakening and 15, 30, and 60 min post-awakening and sampled urine for 24 h. Subsequently, they started a daily exercise program maintained for a 9-week period. Clinician-rated depression severity was blindly assessed with the Hamilton Depression Rating 6-item subscale (HAM-D6). The cortisol awakening response was quantified by the area under the curve with respect to the ground (AUCG) and with respect to the rise (AUCI) using saliva cortisol levels in the 1-h period after awakening. Analysis of expected associations between depression severity, AUCG, AUCI, exercise, and 24-h cortisol output was performed in a general linear model.
Results: In all, 35 participants delivered saliva or 24-h urine samples. The mean age was 49.0 years (SD = 11.0) with 48.6% females with a mean baseline HAM-D6 score of 12.2 (SD = 2.3). In a statistical model investigating the association between HAM-D6 at week 9 as a dependent variable and AUCI, concurrent HAM-D6, gender, smoking, and exercise volume as covariates, we found a significant effect of AUCI, concurrent HAM-D6, and exercise. The following statistics were found: AUCI (regression coefficient 0.008; F value = 9.1; p = 0.007), concurrent HAM-D6 (regression coefficient 0.70; F value = 8.0; p = 0.01), and exercise (regression coefficient -0.005; F value = 5.7; p = 0.03). The model had an R2 of 0.43. The association between HAM-D6 endpoint scores and the AUCI showed that higher AUCI values predicted higher HAM-D6 endpoint values. The association between HAM-D6 endpoint scores and the exercise level showed that a high exercise level was associated with lower HAM-D6 endpoint values.
Conclusion: The results thus showed that high AUCI values predicted less improvement of depression and high exercise levels predicted more improvement of depression. These findings need to be confirmed in larger samples to test if more covariates can improve prediction of depression severity.
{"title":"Salivary Cortisol Awakening Response as a Predictor for Depression Severity in Adult Patients with a Major Depressive Episode Performing a Daily Exercise Program.","authors":"Else Refsgaard, Anne Vibeke Schmedes, Klaus Martiny","doi":"10.1159/000521234","DOIUrl":"https://doi.org/10.1159/000521234","url":null,"abstract":"<p><strong>Introduction: </strong>The hypothalamic-pituitary-adrenal axis function in depression has been the subject of considerable interest, and its function has been tested with a variety of methods. We investigated associations between saliva cortisol at awakening and the 24-h urine cortisol output, both measured at study baseline, with endpoint depression scores.</p><p><strong>Methods: </strong>Patients were admitted to a psychiatric inpatient ward with a major depressive episode and were started on fixed duloxetine treatment. They delivered saliva samples at awakening and 15, 30, and 60 min post-awakening and sampled urine for 24 h. Subsequently, they started a daily exercise program maintained for a 9-week period. Clinician-rated depression severity was blindly assessed with the Hamilton Depression Rating 6-item subscale (HAM-D6). The cortisol awakening response was quantified by the area under the curve with respect to the ground (AUCG) and with respect to the rise (AUCI) using saliva cortisol levels in the 1-h period after awakening. Analysis of expected associations between depression severity, AUCG, AUCI, exercise, and 24-h cortisol output was performed in a general linear model.</p><p><strong>Results: </strong>In all, 35 participants delivered saliva or 24-h urine samples. The mean age was 49.0 years (SD = 11.0) with 48.6% females with a mean baseline HAM-D6 score of 12.2 (SD = 2.3). In a statistical model investigating the association between HAM-D6 at week 9 as a dependent variable and AUCI, concurrent HAM-D6, gender, smoking, and exercise volume as covariates, we found a significant effect of AUCI, concurrent HAM-D6, and exercise. The following statistics were found: AUCI (regression coefficient 0.008; F value = 9.1; p = 0.007), concurrent HAM-D6 (regression coefficient 0.70; F value = 8.0; p = 0.01), and exercise (regression coefficient -0.005; F value = 5.7; p = 0.03). The model had an R2 of 0.43. The association between HAM-D6 endpoint scores and the AUCI showed that higher AUCI values predicted higher HAM-D6 endpoint values. The association between HAM-D6 endpoint scores and the exercise level showed that a high exercise level was associated with lower HAM-D6 endpoint values.</p><p><strong>Conclusion: </strong>The results thus showed that high AUCI values predicted less improvement of depression and high exercise levels predicted more improvement of depression. These findings need to be confirmed in larger samples to test if more covariates can improve prediction of depression severity.</p>","PeriodicalId":19239,"journal":{"name":"Neuropsychobiology","volume":null,"pages":null},"PeriodicalIF":3.2,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39811090","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"心理学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2022-01-01Epub Date: 2022-07-15DOI: 10.1159/000525579
Maria Garbusow, Claudia Ebrahimi, Carlotta Riemerschmid, Luisa Daldrup, Marcus Rothkirch, Ke Chen, Hao Chen, Matthew J Belanger, Angela Hentschel, Michael N Smolka, Andreas Heinz, Maximilan Pilhatsch, Michael A Rapp
A mechanism known as Pavlovian-to-instrumental transfer (PIT) describes a phenomenon by which the values of environmental cues acquired through Pavlovian conditioning can motivate instrumental behavior. PIT may be one basic mechanism of action control that can characterize mental disorders on a dimensional level beyond current classification systems. Therefore, we review human PIT studies investigating subclinical and clinical mental syndromes. The literature prevails an inhomogeneous picture concerning PIT. While enhanced PIT effects seem to be present in non-substance-related disorders, overweight people, and most studies with AUD patients, no altered PIT effects were reported in tobacco use disorder and obesity. Regarding AUD and relapsing alcohol-dependent patients, there is mixed evidence of enhanced or no PIT effects. Additionally, there is evidence for aberrant corticostriatal activation and genetic risk, e.g., in association with high-risk alcohol consumption and relapse after alcohol detoxification. In patients with anorexia nervosa, stronger PIT effects elicited by low caloric stimuli were associated with increased disease severity. In patients with depression, enhanced aversive PIT effects and a loss of action-specificity associated with poorer treatment outcomes were reported. Schizophrenic patients showed disrupted specific but intact general PIT effects. Patients with chronic back pain showed reduced PIT effects. We provide possible reasons to understand heterogeneity in PIT effects within and across mental disorders. Further, we strengthen the importance of reliable experimental tasks and provide test-retest data of a PIT task showing moderate to good reliability. Finally, we point toward stress as a possible underlying factor that may explain stronger PIT effects in mental disorders, as there is some evidence that stress per se interacts with the impact of environmental cues on behavior by selectively increasing cue-triggered wanting. To conclude, we discuss the results of the literature review in the light of Research Domain Criteria, suggesting future studies that comprehensively assess PIT across psychopathological dimensions.
{"title":"Pavlovian-to-Instrumental Transfer across Mental Disorders: A Review.","authors":"Maria Garbusow, Claudia Ebrahimi, Carlotta Riemerschmid, Luisa Daldrup, Marcus Rothkirch, Ke Chen, Hao Chen, Matthew J Belanger, Angela Hentschel, Michael N Smolka, Andreas Heinz, Maximilan Pilhatsch, Michael A Rapp","doi":"10.1159/000525579","DOIUrl":"https://doi.org/10.1159/000525579","url":null,"abstract":"<p><p>A mechanism known as Pavlovian-to-instrumental transfer (PIT) describes a phenomenon by which the values of environmental cues acquired through Pavlovian conditioning can motivate instrumental behavior. PIT may be one basic mechanism of action control that can characterize mental disorders on a dimensional level beyond current classification systems. Therefore, we review human PIT studies investigating subclinical and clinical mental syndromes. The literature prevails an inhomogeneous picture concerning PIT. While enhanced PIT effects seem to be present in non-substance-related disorders, overweight people, and most studies with AUD patients, no altered PIT effects were reported in tobacco use disorder and obesity. Regarding AUD and relapsing alcohol-dependent patients, there is mixed evidence of enhanced or no PIT effects. Additionally, there is evidence for aberrant corticostriatal activation and genetic risk, e.g., in association with high-risk alcohol consumption and relapse after alcohol detoxification. In patients with anorexia nervosa, stronger PIT effects elicited by low caloric stimuli were associated with increased disease severity. In patients with depression, enhanced aversive PIT effects and a loss of action-specificity associated with poorer treatment outcomes were reported. Schizophrenic patients showed disrupted specific but intact general PIT effects. Patients with chronic back pain showed reduced PIT effects. We provide possible reasons to understand heterogeneity in PIT effects within and across mental disorders. Further, we strengthen the importance of reliable experimental tasks and provide test-retest data of a PIT task showing moderate to good reliability. Finally, we point toward stress as a possible underlying factor that may explain stronger PIT effects in mental disorders, as there is some evidence that stress per se interacts with the impact of environmental cues on behavior by selectively increasing cue-triggered wanting. To conclude, we discuss the results of the literature review in the light of Research Domain Criteria, suggesting future studies that comprehensively assess PIT across psychopathological dimensions.</p>","PeriodicalId":19239,"journal":{"name":"Neuropsychobiology","volume":null,"pages":null},"PeriodicalIF":3.2,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40596910","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"心理学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2022-01-01Epub Date: 2022-01-13DOI: 10.1159/000521184
Tayllon Dos Anjos-Garcia, Alexandre Kanashiro, Alline Cristina de Campos, Norberto Cysne Coimbra
Introduction: Environmental enrichment (EE) is a useful and sophisticated tool that improves rodents' well-being by stimulating social behaviour and cognitive, motor, and sensory functions. Exposure to EE induces neuroplasticity in different brain areas, including the limbic system, which has been implicated in the control of anxiety and fear. However, the effects of EE on ethologically relevant naturalistic behaviours, such as those displayed by prey in the presence of predators, remain largely unexplored.
Material and methods: In the present study, we investigated anxiety- and panic attack-like behaviours in a predator (cat)-prey confrontation paradigm and compared them with those in classical assays, such as the elevated plus-maze (EPM), marble-burying, and open field tests (OFTs), using C57BL/6J male mice housed in enriched or standard environments for 6 weeks.
Results: We observed that EE exposure caused enhancement of the levels of anxiety-like behaviours in the EPM and OFTs, increasing risk assessment (an anxiety-related response), and decreasing escape (a panic attack-like response) behaviours during exposure to the predator versus prey confrontation paradigm.
Conclusion: Taken together, our findings suggest that enriched external environments can modify the processing of fear- and anxiety-related stimuli in dangerous situations, changing the decision-making defensive strategy.
{"title":"Environmental Enrichment Facilitates Anxiety in Conflict-Based Tests but Inhibits Predator Threat-Induced Defensive Behaviour in Male Mice.","authors":"Tayllon Dos Anjos-Garcia, Alexandre Kanashiro, Alline Cristina de Campos, Norberto Cysne Coimbra","doi":"10.1159/000521184","DOIUrl":"https://doi.org/10.1159/000521184","url":null,"abstract":"<p><strong>Introduction: </strong>Environmental enrichment (EE) is a useful and sophisticated tool that improves rodents' well-being by stimulating social behaviour and cognitive, motor, and sensory functions. Exposure to EE induces neuroplasticity in different brain areas, including the limbic system, which has been implicated in the control of anxiety and fear. However, the effects of EE on ethologically relevant naturalistic behaviours, such as those displayed by prey in the presence of predators, remain largely unexplored.</p><p><strong>Material and methods: </strong>In the present study, we investigated anxiety- and panic attack-like behaviours in a predator (cat)-prey confrontation paradigm and compared them with those in classical assays, such as the elevated plus-maze (EPM), marble-burying, and open field tests (OFTs), using C57BL/6J male mice housed in enriched or standard environments for 6 weeks.</p><p><strong>Results: </strong>We observed that EE exposure caused enhancement of the levels of anxiety-like behaviours in the EPM and OFTs, increasing risk assessment (an anxiety-related response), and decreasing escape (a panic attack-like response) behaviours during exposure to the predator versus prey confrontation paradigm.</p><p><strong>Conclusion: </strong>Taken together, our findings suggest that enriched external environments can modify the processing of fear- and anxiety-related stimuli in dangerous situations, changing the decision-making defensive strategy.</p>","PeriodicalId":19239,"journal":{"name":"Neuropsychobiology","volume":null,"pages":null},"PeriodicalIF":3.2,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39908597","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"心理学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}