“I’m Not the Same,but I’m Not Sorry”: Exploring Dialogical Positioning in the Self-Transformation of a Former Politically Violent Militant

This article traces the personal and cultural voices expressed in the life-story interview of a former politically violent militant regarding her engagement with and disengagement from the armed struggle. Rather than looking at the macro and meso aspects related to politically motivated violence, we examine micro-narratives which express individual arguments, sociocultural discourses, and negotiations within and between them, These are voiced in the dynamics that take place within the self-system at times of key identity transitions (e.g., from being a committed militant to becoming a former militant). In this vein, we highlight how the embodied emotional chords of personal positions, the development of meta-positions, and the positioning and repositioning movements within the dialogical self, facilitate the emergence of new and more adaptive meanings in the personal meaning system of former militants.     

A link between role of two prefrontal areas in immediate memory and in long-term memory consolidation

The dorsolateral and medial prefrontal cortex are critical for immediate memory processing. The possibility has been raised that those two areas may also contribute to long-term memory formation. Here, we studied the role of specific receptors in dorsolateral and medial prefrontal cortex in immediate and in long-term memory formation of one-trial inhibitory avoidance. Four different specific receptor ligands were infused into these two areas: the dopamine D1 receptor antagonist, SCH23390, the GABA(A) receptor agonist, muscimol, the AMPA glutamatergic receptor antagonist, ciano-nitro-quinoxaline-dione (CNQX), and the NMDA glutamatergic receptor antagonist, aminophosphonovaleric acid (AP5). In all cases the doses used had been previously shown to affect immediate or long-term memory. In the experiments on immediate memory the drugs were given 5 min before training and the animals were tested 3s post-training. These animals were then also tested 24h later for long-term memory. The effect of the treatments on long-term memory was studied by their infusion 0, 90, 180 or 270 min post-training, testing the animals 24h after training. Immediate memory was inhibited by SCH23390, muscimol and CNQX, but not by AP5, given into any of the two subregions. Long-term memory formation was inhibited by SCH23390, muscimol and CNQX, but not by AP5, given pre-training or 0, 90 or 180 but not 270 min post-training into the dorsolateral region; or 90 but not 0 or 180 min post-training into the medial region. Thus, there is a time- and receptor-dependent correlation in the two areas between their role in immediate and in long-term memory processing. Both roles require intact glutamate AMPA and dopamine D1 receptors, are inhibited by GABAergic synapses, and are unaffected by AP5. In the dorsolateral prefrontal cortex the link between immediate and long-term memory appears to be direct; in the medial area the link suffers a 90 min delay.     

Na+,K(+)-ATPase activity is reduced in hippocampus of rats submitted to an experimental model of depression: effect of chronic lithium treatment and possible involvement in learning deficits

This study was undertaken to verify the effects of chronic stress and lithium treatments on the hippocampal Na+,K(+)-ATPase activity of rats, as well as to investigate the effects of stress interruption and post-stress lithium treatment on this enzyme activity and on spatial memory. Two experiments were carried out; in the first experiment, adult male Wistar rats were divided into two groups: control and submitted to a chronic variate stress paradigm, and subdivided into treated or not with LiCl. After 40 days of treatment, rats were killed, and Na+,K(+)-ATPase activity was determined. In the second experiment, rats were stressed during 40 days, and their performance was evaluated in the Water Maze task. The stressed group was then subdivided into four groups, with continued or interrupted stress treatment and treated or not with lithium for 30 additional days. After a second evaluation of performance in the Water Maze, rats were killed and Na+,K(+)-ATPase activity was also measured. Results showed an impairment in Na+,K(+)-ATPase activity and in Water Maze performance of chronically stressed rats, which were prevented by lithium treatment and reversed by lithium treatment and by stress interruption. These results suggest that the modulation of Na+,K(+)-ATPase activity may be one of the mechanisms of action of lithium in the treatment of mood disorders.