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Archive - Nov 11, 2013

New Studies Outline Different Approaches to Understanding and Perhap Treating Depression—Neuroscience 2013

When treating debilitating mental disorders, researchers look not only to the brain, but also to the body for answers. A new study in mice shows that levels of the inflammatory cytokine interleukin-6 (IL-6), a molecule that is produced and secreted by white blood cells of the immune system, can be used to predict how animals might react to social stress. The findings were presented at Neuroscience 2013, the annual meeting of the Society for Neuroscience and the world’s largest source of emerging news about brain science and health. 30,000 scientists are attending this meeting. More than 350 million people worldwide suffer from clinical depression and between 5 and 25 percent of adults suffer from generalized anxiety, according to the World Health Organization. The resulting emotional and financial costs to people, families, and society are significant. Further, antidepressants are not always effective and often cause severe side effects. Social stress is one of the most significant contributors to depression in humans, yet some individuals experience no adverse effects, while others are vulnerable. Understanding the differences could drastically affect how depression is treated. In the IL-6 study, the researchers found that higher levels of IL-6 released by stimulation of the white blood cells before a defeat experience predicted depression-like behavior, while lower levels predicted stress-resistance. They also showed that reducing IL-6 in the body made mice immune to social stress. Conversely, increasing IL-6 with a bone marrow transplant from a stress-susceptible mouse had the opposite effect, provoking depression-like behavior. The results suggest that measuring stimulated IL-6, a chemical easily found in the blood, could serve as a biomarker for stress sensitivity.

Nobel Prize Winner Says MicroRNAs and piRNAs Influence the Coordinated Regulation of Transcription in the Nucleus, and Translation at the Synapse—Neuroscience 2013

Classic behavioral studies of memory storage in people and animals have defined two temporally distinct phases for memory storage: a short-term memory lasting minutes that can be elicited by one training trial, and a long-term memory lasting days or more that typically requires repeated training trials. In earlier work, Eric Kandel, M.D., Director of the Kavil Institute for Brain Science at Columbia University, Howard Hughes Medical Institute senior investigator, and a co-recipient of the 2000 Nobel Prize in Physiology or Medicine for discoveries concerning signal transduction in the nervous system, together with colleagues, delineated these two behavioral memory phases in studies of learned fear, an implicit form of memory, using the simple gill-withdrawal reflex of Aplysia, which is a marine snail. This work revealed that there is a cellular representation of the learning process. The substrate of learning is the synapse, and learning leads to changes in the strength of synaptic connections. These studies found that short-term memory is mediated by a transient synaptic facilitation of pre-existing connections due to covalent modification of pre-existing proteins, whereas long-term memory results from a persistent facilitation mediated by transcription and synaptic growth. The critical transcriptional switch that converts short-term to long-term facilitation and long-term memory in Aplysia is mediated by the removal of the repressive step of CREB-2 and the activation of CREB-1. Because small RNAs are important in transcriptional control and post-transcriptional regulation of gene expression, Dr. Kandel and his group wondered whether they might also regulate this key transcriptional switch from short-term to long-term memory. Together with collaborators, Dr.

Experiences, Including Learning and Drug Use, Leave Genetic Marks on Brain Behavior—Neuroscience 2013

New human and animal research released today demonstrates how experiences impact genes that influence behavior and health. Today’s studies, presented at a press conference of Neuroscience 2013, the annual meeting of the Society for Neuroscience and the world’s largest source of emerging news about brain science and health, provide new insights into how experience might produce long-term brain changes in behaviors like drug addiction and memory formation. 30,000 scientists are attending this meeting in San Diego. Years of heroin abuse may change how genes are expressed and how the brain functions, according to new human research described today in a news conference organized by the Society of Neuroscience. The studies focus on an area of research called epigenetics, in which the environment and experiences can turn genes “on” or “off,” while keeping underlying DNA intact. These changes affect normal brain processes, such as development or memory, and abnormal brain processes, such as depression, drug dependence, and other psychiatric disease — and can be passed down to subsequent generations. According to the World Health Organization, 9.5 million people abuse heroin around the world, which increases their risk of death by 20 to 30 times compared to that of non-drug users. “Our study addresses a critical gap in our knowledge about heroin addiction because we cannot often directly study the brains of addicted humans,” said senior author Yasmin Hurd, Ph.D., of the Icahn School of Medicine at Mount Sinai in New York. “Our results provide important insights into how human brains change in response to long-term heroin use, and give us to knowledge to help treat this dangerous disease.” Dr.

Absence of Specific Serotonin Receptor During Development Linked to Aggression and Impulsivity in Adults—Neuroscience 2013

Blocking serotonin receptors during development results in highly aggressive and impulsive behavior, according to new animal research. Reintroducing the receptors in adulthood suppresses impulsivity, but not aggression, to normal levels. These and related findings were described during a press conference on Sunday, November 10, at Neuroscience 2013, the annual meeting of the Society for Neuroscience and the world’s largest source of emerging news about brain science and health. 30,000 scientists are attending this convention in San Diego. Previous studies have identified a link between low serotonin levels and impulsive, violent aggression. However, therapeutic treatments that used antidepressants to increase serotonin generally did not reduce the negative behaviors. New research, led by Katherine Nautiyal, Ph.D., from Columbia University, identified a specific serotonin receptor (5-HT1B)(see image) as a key factor in aggressive and impulsive behaviors. Mice lacking this receptor during development exhibited more frequent and intense fighting than did control mice. They were also more impulsive in neutral situations, more vulnerable to abusing drugs, and demonstrated less restraint, even when rewarded to do so. Understanding the impact of changes in specific prefrontal regions during brain development could lead to new treatments and earlier interventions for disorders in which impulsivity plays a key factor. The research may have implications for understanding and dealing with aggressive and troublesome behaviors. The new findings show that: the absence of serotonin receptors during early development leads to highly aggressive and impulsive behaviors in mice.