Activating Memories of Depression Alters the Experience of Voluntary Action.

Activating memories of depression alters the experience of voluntary action.

Filed under: Depression Treatment

Exp Brain Res. 2012 Dec 18;
Obhi SS, Swiderski KM, Farquhar R

The sense of agency is a profoundly important human experience and is strongly linked to volitional action. The importance of this experience is underscored by the fact that many neurological and psychiatric disorders are partially characterized by an abnormal sense of agency (e.g., schizophrenia, anxiety disorders, depression). Healthy participants perceive the temporal interval between a voluntary action and its effect to be shorter than it actually is, and this illusion has been suggested as an implicit index of agency. Here, we investigated whether activating memories of depression alters perception of this action-effect interval, compared to activating memories of the previous day, or a baseline condition in which specific memories were not activated. Results showed that action-effect interval estimates were significantly longer after remembering a depressing episode than after remembering the previous day, or in the baseline condition. Thus, activating memories of depression alters the experience of voluntary actions and effects. We suggest that interval estimation measures could be useful in clinical settings, to implicitly assess the sense of agency in patients with disorders affecting their sense of control. In this way, obtaining action-effect interval estimates, pre-, during, and post-treatment, could aid in tracking treatment-induced changes in the sense of agency.
HubMed – depression

 

[Establishment and evaluation of animal model for studying the effect of traumatic brain injury on bone fracture healing].

Filed under: Depression Treatment

Beijing Da Xue Xue Bao. 2012 Dec 18; 44(6): 831-7
Chen XH, Bai L, Gu HY, Chen B, Li QT, An S, Wang ZY, Deng JX, Kou YH, Zhang PX, Yin XF, Han N, Jiang BG

To establish a stable animal model for studying the effect of traumatic brain injury on bone fracture healing.Eighty adult male Sprague-Dawley rats were randomly divided into fracture combined brain injury group (A) and simple fracture group (B). Animals of the two groups were killed 6 hours, 1 week, 2 weeks, 1 month and 2 months after trauma, respectively. Their brain histopathology changes were observed and neurological severity scores (NSS, 0 through 25 from no injury to severe injury) determined to measure the brain injury after head trauma, and fracture-healing was assessed by measuring callus volume and X ray examination at the scheduled time points after trauma. The callus volumes were compared between the groups using independent-samples t test 1 week, 2 weeks, 1 month and 2 months after trauma respectively. A value of P<0.05 was considered statistically significant.Ninety percent of the rats of group A presented with hemiplegia and the mortality rate was 10% (4/40) . The survived rats developed decorticated flexion deformity of the forelimbs, with behavioral depression, and lost some reflexes and muscle tone. The NSS were 10.83±1.94, 9.33±0.82, 8.17±1.17, 7.83±0.75 and 8.07±0.82 with 6 hours, 1 week, 2 weeks, 1 month and 2 months after trauma, respectively. It showed that the animals received moderate head injury, which tended to be stable from 2 weeks after trauma. Brain pathology showed that blood brain barrier was destroyed, and neurons were degenerative and necrotic at and around the trauma sites. The callus volumes(unit: mm(3)) of the two groups 1 week, 2 weeks, 1 month and 2 months after trauma were 60.03±28.05 and 32.80±11.04, 78.54±15.16 and 51.36±23.02, 93.01±10.65 and 72.38±20.38, 115.26±40.00 and 60.30±13.34, respectively. The callus volumes of the two groups 2 weeks, 1 month and 2 months after trauma were statistically and significantly different (P values were 0.036, 0.006 and 0.01 respectively), and there was no difference 1 week after trauma (P=0.065).This model is capable of producing accurately quantified brain injury. The animal model is credible, stable and reproducible, so it is an effective platform for studying the effect of traumatic brain injury on fracture. HubMed – depression

 

Tetrahydrobiopterin Improves Diastolic Dysfunction by Reversing Changes in Myofilament Properties.

Filed under: Depression Treatment

J Mol Cell Cardiol. 2012 Dec 13;
Jeong EM, Monasky MM, Gu L, Taglieri DM, Patel BG, Liu H, Wang Q, Greener I, Dudley SC, Solaro RJ

Despite the increasing prevalence of heart failure with preserved left ventricular function, there are no specific treatments, partially because the mechanism of impaired relaxation is incompletely understood. Evidence indicates that cardiac relaxation may depend on nitric oxide (NO), generated by NO synthase (NOS) requiring the co-factor tetrahydrobiopterin (BH(4)). Recently, we reported that hypertension-induced diastolic dysfunction was accompanied by cardiac BH(4) depletion, NOS uncoupling, a depression in myofilament cross-bridge kinetics, and S-glutathionylation of myosin binding protein C (MyBP-C). We hypothesized that the mechanism by which BH(4) ameliorates diastolic dysfunction is by preventing glutathionylation of MyBP-C and thus reversing changes of myofilament properties that occur during diastolic dysfunction. We used the deoxycorticosterone acetate (DOCA)-salt mouse model, which demonstrates mild hypertension, myocardial oxidative stress, and diastolic dysfunction. Mice were divided into two groups that received control diet and two groups that received BH(4) supplement for 7days after developing diastolic dysfunction at post-operative day 11. Mice were assessed by echocardiography. Left ventricular papillary detergent-extracted fiber bundles were isolated for simultaneous determination of force and ATPase activity. Sarcomeric protein glutathionylation was assessed by immunoblotting. DOCA-salt mice exhibited diastolic dysfunction that was reversed after BH(4) treatment. Diastolic sarcomere length (DOCA-salt 1.70 ± 0.01 vs. DOCA-salt+BH(4) 1.77 ± 0.01 ?m, P<0.001) and relengthening (relaxation constant, ?, DOCA-salt 0.28 ± 0.02 vs. DOCA-salt+BH(4) 0.08 ± 0.01, P<0.001) were also restored to control by BH(4) treatment. pCa(50) for tension increased in DOCA-salt compared to sham but reverted to sham levels after BH(4) treatment. Maximum ATPase rate and tension cost (?ATPase/?Tension) decreased in DOCA-salt compared to sham, but increased after BH(4) treatment. Cardiac MyBP-C glutathionylation increased in DOCA-salt compared to sham, but decreased with BH(4) treatment. MyBP-C glutathionylation correlated with the presence of diastolic dysfunction. Our results suggest that by depressing S-glutathionylation of MyBP-C, BH(4) ameliorates diastolic dysfunction by reversing a decrease in cross-bridge turnover kinetics. These data provide evidence for modulation of cardiac relaxation by post-translational modification of myofilament proteins. HubMed – depression

 

Treatment Plans and Interventions for Depression and Anxiety Disorders
Includes CD-ROM with Reproducible Forms!This one-of-a-kind resource provides the busy practitioner with empirically supported trea…

Overcoming Depression in Teens and Pre-Teens: A Parent’s Guide (Dr. T’s Living Well Series)
The treatment modalities for pre-teen and teenager depression require a multi-factorial approach. Cognitive-behavioral therapy in …

Psychodynamic Treatment of Depression
The advent of multiple effective psychopharmacologic interventions and targeted psychotherapeutic treatments has led to remarkable…

More Depression Treatment Information…