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JNeurosci: Highlights From the December 7 Issue
08 December 2016
Society for Neuroscience (SfN)
Check out these newsworthy studies from the December 7, 2016, issue of JNeurosci.
Impaired Sound Processing May Explain Persistent Hearing Deficits in People With Cochlear Implants
Cochlear implants have restored hearing in hundreds of thousands of people around the world, but many users still have hearing difficulties — they may have trouble recognizing musical melodies or struggle to comprehend speech in noisy environments. But how cochlear implants affect the brain to enable hearing — and how they fall short — is still a mystery. In a new study in marmosets, researchers compare how individual neurons in the brain’s auditory cortex respond to sound and cochlear implant stimulation. The scientists identify neurons that don’t respond to cochlear implant stimulation and find those neurons are sharply tuned to frequency and sound level, revealing a potential mechanism of hearing deficits in those with cochlear implants.
Corresponding author: Xiaoqin Wang, email@example.com
Breathing May Coordinate Brain’s Rhythmic Activity to Influence Cognitive Function
Brain activity fluctuates, producing rhythms or oscillations, and previous studies in animals indicate oscillations in the brain’s smell-processing centers are synchronized to the rate of breathing. In a new study, researchers discover the same phenomenon occurs in people and supports cognitive function. Using intracranial electroencephalographic (iEEG) recordings, they find nasal breathing drives oscillatory activity in smell-processing areas of the cortex, as well as in the amygdala and hippocampus, regions critical for emotion and memory. Breathing rhythm and whether you breathe through your nose or mouth may also influence cognitive performance: Subjects were better at recognizing fearful faces and recalling objects if they saw them while inhaling rather than exhaling, but only if they breathed through their nose.
Blocking Enzyme Improves Motor Function in Parkinson’s Mouse Model
In the brains of people with Parkinson’s disease, misfolded alpha-synuclein proteins accumulate and clump together, and these protein aggregates are believed to be toxic to neurons. Previous studies found a specific enzyme in the brain — prolyl oligopeptidase, or PREP — boosts protein aggregation and may be involved in Parkinson’s pathology. In a new study, researchers find blocking the PREP enzyme with a small molecule inhibitor reduced alpha-synuclein clumping and improved motor function in a mouse model of Parkinson’s disease, suggesting drugs targeting the enzyme may be a therapeutic strategy.
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.