JNeurosci: Highlights From the October 12 Issue
Check out these newsworthy studies from the October 12, 2016, issue of JNeurosci. Media interested in obtaining the full text of the studies should contact email@example.com.
The HIV virus can cause problems with memory, motor function, and behavior, and HIV patients with Type 2 diabetes may be at an increased risk of developing these neurocognitive disorders. The virus may exert these effects by infecting and activating the central nervous system’s primary immune cells, microglia. In a new study, researchers find insulin treatment blocks the expression of inflammatory genes, inhibits HIV replication, and prevents neurotoxicity in microglia from people with HIV. They also find insulin treatment delivered intranasally improves neurocognitive function in cats with feline immunodeficiency virus.
Corresponding author: Christopher Power, firstname.lastname@example.org
Ischemic stroke kills brain cells and perturbs neural networks. It also impairs the ability of glial cells to remove excess levels of the excitatory neurotransmitter glutamate, exacerbating neurotoxicity. In a new study, researchers transplant neural precursor cells into the brains of mice after ischemic stroke and find the treatment enhances glial cells’ ability to clear excess glutamate and promotes regenerative plasticity in the brain. The results show how stem cell transplantation can promote recovery from stroke.
Corresponding author: Marco Bacigaluppi, email@example.com
The brainstem’s respiratory control center drives automatic breathing. This network of neurons monitors levels of oxygen and carbon dioxide in the blood and adjusts respiration accordingly. In people, a dip in carbon dioxide — hypocapnia — reduces the drive to breathe because there is less carbon dioxide to expel. But this only happens during sleep and when under anesthesia. When we’re awake, we continue breathing in spite of the dip in carbon dioxide. In a new study, researchers measure participants’ brain activity using electroencephalography during normal and hypocapnic breathing and find activity in the cerebral cortex drives hypocapnic breathing, similar to the brain activity that drives volitional breathing. Human speech depends on our ability to override the brainstem’s automatic control of breathing, and the results of this study could aid in the study of speech disorders.
Corresponding author: Thomas Similowski, firstname.lastname@example.org
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.