Myoclonic jumping can be seen in normal mouse strains, possibly as a result of simply being put inside a cage. Like other types, it is also triggered by changes in GABA, 5HT, and dopamine neurotransmission. Implicated brain regions include hippocampus and dorsal striatum, possibly with respect to D-1 dopamine, NMDA, and delta opioid receptors. There is reason to suspect that myoclonic jumping is underreported due to insufficient observations into mouse cages. (c) 2012 Elsevier Ireland Ltd and the Japan Neuroscience Society. All rights reserved.”
“We applied Dactolisib price a covariance-based multivariate analysis

to functional magnetic resonance imaging (fMRI) data to investigate abnormalities in working memory (WM) systems in patients with post-traumatic stress disorder (PTSD). Patients (n = 13) and matched controls (n = 12) were scanned with fMRI while updating or maintaining trauma-neutral verbal stimuli in WM. A multivariate statistical analysis was used to investigate large-scale brain networks associated with these experimental tasks. For the control group, the first network reflected brain activity associated

with WM updating and see more principally involved bilateral prefrontal and bilateral parietal cortex. Controls’ second network was associated with WM maintenance and involved regions typically activated during storage and rehearsal of verbal material, including lateral premotor and inferior parietal cortex. In contrast, PTSD patients appeared to activate a single fronto-parietal network for both updating and maintenance tasks. This is indicative of abnormally elevated activity during WM maintenance and suggests inefficient allocation of resources for differential task demands. A second network in PTSD, which was not activated in controls, showed regions differentially activated between WM tasks, including the anterior cingulate, medial prefrontal cortex, fusiform and supplementary motor area. These activations may be linked to hyperarousal and

abnormal reactivity, which are characteristic of PTSD. (C) 2008 Elsevier Ireland Ltd. All rights reserved.”
“Mitochondria are critical for cell survival and normal development, as they provide find more energy to the cell, buffer intracellular calcium, and regulate apoptosis. They are also major targets of oxidative stress, which causes bioenergetics failure in astrocytes through the activation of different mechanisms and production of oxidative molecules. This review provides an insightful overview of the recent discoveries and strategies for mitochondrial protection in astrocytes. We also discuss the importance of rotenone as an experimental approach for assessing oxidative stress in the brain and delineate some molecular strategies that enhance mitochondrial function in astrocytes as a promising strategy against brain damage. (c) 2012 Elsevier Ireland Ltd and the Japan Neuroscience Society. All rights reserved.