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פרופ' יוסי זוהר נבחר לתפקיד הנכבד של נשיא נבחר (PRESIDENT ELECT) | ד"ר אריקה טוט ממכון ויצמן זכתה בפרס על הפוסטר שהציגה

15.11.2010, 18:14

The effect of subconvulsive electrical stimulation of the nucleus accumbens on depressive behavior

Citation: European Neuropsychopharmacology The Journal of the European College of Neuropsychopharmacology, Volume 17 Supplement 4, Page S334

E. Toth, R. Gersner, M. Shabat-Simon, A. Zangen

Weizmann Institute of Science, Department of Neurobiology, Rehovot, Israel

Objective: Electroconvulsive therapy (ECT) is the most effective treatment for major depression. Our aim was to test whether sub-convulsive electrical stimulation (SCES) of specific reward-related brain regions such as the nucleus accumbens (NAc) can induce a similar antidepressant effects and alter levels of brain-derived neurotrophic factor (BDNF) in specific brain regions.

Methods: Animals intended for the SCES experiments (real or sham) underwent surgeries to implant electrodes (left NAc) before the initiation of the CMS protocol (Willner, 2005). After completion of the 4-week CMS protocol, SCES treatment was performed for 10 days using frequencies and patterns parallel to those in human transcranial magnetic stimulation studies. Subsequently, animals underwent all behavioral tests during a 3-weeks period.

The behavioral tests included sucrose preference (a measure for anhedonia), exploration (using locomotion boxes equipped with photobeams), sexual behavior and Morris water maze. 24 hours after completion of all behavioral tests, brain were removed and punches were extracted from the caudal part of the dorsal striatum (Str), as well as from dorsal (dHc) and ventral hippocampus (vHc) for further BDNF ELISA measurements.

Results: CMS induced a significant reduction in sucrose preference relative to the control group (p = 0.007), which was normalized after SCES treatment of the NAc (p = 0.02). The number of mounts in CMS sham animals was significantly lower than control sham animals (p = 0.04) and SCES treatment of the NAc normalized the reduction in sexual drive (p = 0.004). Two-way mixed ANOVA with group as a between-subjects factor and different stimulus female (existing and new) as a within-subjects factor revealed a significant main effect of the stimulus females [F(1,2) = 9.98, p = 0.006]. In addition control animals preferred to mount more often the new female compared to their previous partner while CMS sham and SCES treated animal did not show such preference. In the exploration test SCES of the NAc induced an increase in rearing behavior (p = 0.004) relative to that of CMS sham animals. In addition CMS sham animals visited the central portion of the exploration box significantly less often than control sham animals (p = 0.006). Learning in the Morris water maze was not affected by the SCES treatment. BDNF levels in the dorsal hippocampus [F(2,21) = 3.92, p = 0.036] and in the striatum [F(2,13) = 4.06, p = 0.04] was significantly altered by the treatments as indicated by one-way ANOVA. In the dorsal hippocampus the levels of BDNF decreased in CMS animals relative to controls (p = 0.02) and normalized by the SCES treatment (p = 0.03). The SCES treatment also increased BDNF levels in the striatum relative to the CMS sham group (p = 0.014).

Discussion: BDNF levels in the dorsal dentate gyrus, previously found to be decreased in depression (Smith et al. 1995; Toth et al., in preparation) and increased after chronic antidepressant treatment (Smith et al. 1995), are increased following SCES treatment of the NAc, suggesting a potential therapeutic mechanism. In conclusion these results suggest that SCES of the NAc is an effective approach for treating depression without induction of cognitive side effects, and point to the important role of the NaC in the pathology of depression.

References:

1. Willner P, 2005, Chronic Mild Stress (CMS) revisited: consistency and behavioural–neurobiological concordance in the effects of CMS. Neuropsychobiology 52, 90–110.

2. Smith MA, Makino S, Kvernansky R, et al, 1995, Stress alters the expression of brain-derived neurotrophic factor and neurotrophin-3 mRNAs in the hippocampus. J Neurosci 15, 1768–1777.

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