Catálogo de publicaciones - revistas

<jats:title>Theory Drives Understanding</jats:title> <jats:p> The role of theory and simulation in neuroscience has been hotly debated over the past few years, in particular in the context of the recent launch of several big projects aimed at creating artificial or virtual brains. <jats:bold> Gerstner <jats:italic>et al.</jats:italic> </jats:bold> (p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" page="60" related-article-type="in-this-issue" vol="338" xlink:href="10.1126/science.1227356">60</jats:related-article> ) review how theory and simulations have interacted over the years and how they have contributed to our present view of how the brain works. </jats:p>

<jats:p> Basic and clinical studies demonstrate that depression is associated with reduced size of brain regions that regulate mood and cognition, including the prefrontal cortex and the hippocampus, and decreased neuronal synapses in these areas. Antidepressants can block or reverse these neuronal deficits, although typical antidepressants have limited efficacy and delayed response times of weeks to months. A notable recent discovery shows that ketamine, a <jats:italic>N</jats:italic> -methyl- <jats:sc>d</jats:sc> -aspartate receptor antagonist, produces rapid (within hours) antidepressant responses in patients who are resistant to typical antidepressants. Basic studies show that ketamine rapidly induces synaptogenesis and reverses the synaptic deficits caused by chronic stress. These findings highlight the central importance of homeostatic control of mood circuit connections and form the basis of a synaptogenic hypothesis of depression and treatment response. </jats:p>

<jats:p>Adult-generated hippocampal neurons are required for mood control and antidepressant efficacy, raising hopes that someday we can harness the power of new neurons to treat mood disorders such as depression. However, conflicting findings from preclinical research—involving stress, depression, and neurogenesis—highlight the complexity of considering neurogenesis as a road to remission from depression. To reconcile differences in the literature, we introduce the “neurogenic interactome,” a platform from which to consider the diverse and dynamic factors regulating neurogenesis. We propose consideration of the varying perspectives—system, region, and local regulation of neurogenesis—offered by the interactome and exchange of ideas between the fields of learning and memory and mood disorder research to clarify the role of neurogenesis in the etiology and treatment of depression.</jats:p>

<jats:p>Advances in characterizing the neuropathology and functional dysconnectivity of depression and promising trials with emerging circuit-targeted and fast-onset therapeutics are providing unprecedented opportunities to gain deeper insight into the neurobiology of this devastating and pervasive disorder. Because of practical and ethical limitations to dissecting these mechanisms in humans, continued progress will critically depend on our ability to emulate aspects of depressive symptomatology and treatment response in nonhuman organisms. Although various experimental models are currently available, they often draw skepticism from both clinicians and basic research scientists. We review recent progress and highlight some of the best leads to diversify and improve discovery end points for preclinical depression research.</jats:p>

<jats:p>Human responses to stress and trauma vary widely. Some people develop trauma-related psychological disorders, such as posttraumatic stress disorder (PTSD) and depression; others develop mild to moderate psychological symptoms that resolve rapidly; still others report no new psychological symptoms in response to traumatic stress. Individual variability in how animals and humans respond to stress and trauma depends on numerous genetic, developmental, cognitive, psychological, and neurobiological risk and protective factors.</jats:p>

<jats:title>Close to a Black Hole</jats:title> <jats:p> At the center of our Galaxy, there is a black hole that is 4 million times as massive as the Sun. Using data from the Keck Observatory, <jats:bold> Meyer <jats:italic>et al.</jats:italic> </jats:bold> (p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" page="84" related-article-type="in-this-issue" vol="338" xlink:href="10.1126/science.1225506">84</jats:related-article> ) detected a star orbiting this black hole with a period of 11.5 years, the shortest period among the stars orbiting it. The star is the second well-sampled star with an orbital period under 20 years. Having detailed knowledge about two stars with short periods and full orbit coverage will be crucial in testing Einstein's theory of general relativity in the gravitational field close to a massive black hole. </jats:p>

<jats:title>Homogeneous Melting</jats:title> <jats:p> The nucleation and melting of crystals are primarily driven by surfaces and defects, which can lower the thermodynamic barrier to a phase transition. A harder problem to study is when the transition occurs uniformly. <jats:bold> Wang <jats:italic>et al.</jats:italic> </jats:bold> (p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" page="87" related-article-type="in-this-issue" vol="338" xlink:href="10.1126/science.1224763">87</jats:related-article> ; see the Perspective by <jats:bold> <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6103" page="55" related-article-type="in-this-issue" vol="338" xlink:href="10.1126/science.1228952">Weeks</jats:related-article> </jats:bold> ) imaged the homogeneous melting of superheated colloidal crystals using a laser to initiate the melting at the interior of the crystal. The authors were then able to track nucleation precursors and nucleus evolution and to find where defects and instabilities limited the homogeneous melting process. </jats:p>