Media, Poetics and the Narrativization of War

https://digitalcommons.lasalle.edu/vietnam_papers/1002/thumbnail.jp

Imagining Vietnam: Tim O\u27Brien\u27s The Things They Carried

https://digitalcommons.lasalle.edu/vietnam_papers/1001/thumbnail.jp

Cellular Correlates of Enhanced Anxiety Caused by Acute Treatment with the Selective Serotonin Reuptake Inhibitor Fluoxetine in Rats

Selective serotonin reuptake inhibitors (SSRIs) are used extensively in the treatment of depression and anxiety disorders. The therapeutic benefits of SSRIs typically require several weeks of continuous treatment. Intriguingly, according to clinical reports, symptoms of anxiety may actually increase during the early stages of treatment although more prolonged treatment alleviates affective symptoms. Consistent with earlier studies that have used animal models to capture this paradoxical effect of SSRIs, we find that rats exhibit enhanced anxiety-like behavior on the elevated plus-maze 1 h after a single injection of the SSRI fluoxetine. Next we investigated the potential neural substrates underlying the acute anxiogenic effects by analyzing the morphological and physiological impact of acute fluoxetine treatment on principal neurons of the basolateral amygdala (BLA), a brain area that plays a pivotal role in fear and anxiety. Although earlier studies have shown that behavioral or genetic perturbations that are anxiogenic for rodents also increase dendritic spine density in the BLA, we find that a single injection of fluoxetine does not cause spinogenesis on proximal apical dendritic segments on BLA principal neurons an hour later. However, at the same time point when a single dose of fluoxetine caused enhanced anxiety, it also enhanced action potential firing in BLA neurons in ex vivo slices. Consistent with this finding, in vitro bath application of fluoxetine caused higher spiking frequency and this increase in excitability was correlated with an increase in the input resistance of these neurons. Our results suggest that enhanced excitability of amygdala neurons may contribute to the increase in anxiety-like behavior observed following acute fluoxetine treatment

“Writing about War”: Dương Thu Hương’s Representations of the Vietnam-American War

While 30 April 1975 represented the end of hostilities between North and South Vietnam, it was not the end of internecine conflicts. The victorious communists treated Southerners with contempt and subjected them to humiliation and violence, including incarceration in so-called re-education camps. Dương Thu Hương served in the Women’s Youth Brigade during the war and hoped that victory would lead to the establishment of a more egalitarian and democratic society. Dương was appalled when the communist party clamped down on all freedoms and she expressed her dissent in public and through her fiction. This essay analyses two of her novels in English translation, Novel Without a Name (1995) and Memories of a Pure Spring (2000), focusing on recurrent thematics that are central to these works, including the paradoxes of remembrance, critiques of war, the idea of fiction as testimony, and indictments of communist orthodoxy and double standards

A sex difference in the response of the rodent postsynaptic density to synGAP haploinsufficiency

SynGAP is a postsynaptic density (PSD) protein that binds to PDZ domains of the scaffold protein PSD-95. We previously reported that heterozygous deletion of Syngap1 in mice is correlated with increased steady-state levels of other key PSD proteins that bind PSD-95, although the level of PSD-95 remains constant (Walkup et al., 2016). For example, the ratio to PSD-95 of Transmembrane AMPA-Receptor-associated Proteins (TARPs), which mediate binding of AMPA-type glutamate receptors to PSD-95, was increased in young Syngap1+/- mice. Here we show that only females and not males show a highly significant correlation between an increase in TARP and a decrease in synGAP in the PSDs of Syngap1+/- rodents. The data reveal a sex difference in the adaptation of the PSD scaffold to synGAP haploinsufficiency