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JNeurosci: Highlights From the Nov. 23 issue

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Check out these newsworthy studies from the November 23, 2016, issue of JNeurosci. Media interested in obtaining the full text of the studies should contact [email protected]

Mental Time and Space Travel Activate Different Brain Networks

As humans, we can envision the future, relive the past, or imagine ourselves in a different place. In a new study, researchers uncover the neural correlates of this mental time and space travel. Using functional magnetic resonance imaging (fMRI), they measured participants' brain activity while they mentally transported themselves to different times and places, and evaluated how close these scenarios were to specific historical events. The researchers find mental time and space travel activate different areas of the brain, except for overlapping activity in a small region of the inferior parietal lobe. They speculate this region may be involved in readjusting our frame of reference during mental time and space travel.

Corresponding author: Baptiste Gauthier, [email protected]

Glucose Transport Pathway Impaired in Insulin Resistance Is Important for Memory in Rats

In healthy individuals, insulin triggers a specific transport protein called GluT4 to move from the interior of muscle or fat cells to the membrane, where it shuttles in glucose for energy. This process is faulty in people with insulin resistance. The same pathway is found in the brain, but its role there is less clear, although the brain is critically dependent on glucose supply. In a new study in rats, researchers find that memory acquisition triggers GluT4 movement to cell membranes in the hippocampus, a region of the brain critical for learning and memory. Blocking GluT4's ability to transport glucose into cells also impairs rats' ability to acquire new memories. The results identify how insulin resistance impacts the brain and may help explain why type 2 diabetes is a risk factor for Alzheimer's disease.

Corresponding author: Jiah Pearson-Leary, [email protected]

Allergic Disorders May Activate Immune Cells to Cause Neuropathic Pain

Allergic disorders like asthma and eczema are becoming more prevalent around the world. They've been linked to neuropsychiatric disorders such as autism as well as neuropathic pain, but the mechanism of this relationship is still a mystery. In a new study, researchers find mice with asthma or eczema have more activated immune cells, or microglia, in the spinal cord and show increased sensitivity to touch, indicative of pain. Blocking a specific receptor on microglia prevented their activation to an inflammatory phenotype and eliminated pain.

Corresponding author: Jun-ichi Kira, [email protected]

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The Journal of Neuroscience is published by the Society for Neuroscience, an organization of nearly 38,000 basic scientists and clinicians who study the brain and nervous system.

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