Researchers led by biologists at Tufts University have discovered that the brains of developing frog embryos damaged by nicotine exposure can be repaired by treatment with certain drugs called “ionoceuticals” that drive the recovery of bioelectric patterns in the embryo, followed by repair of normal anatomy, gene expression and brain function in the growing tadpole. The research, published today in Frontiers in Neuroscience, introduces intervention strategies based on restoring the bioelectric “blueprint” for embryonic development, which the researchers suggest could provide a roadmap for the exploration of therapeutic drugs to help repair birth defects.

A molecule commonly produced by gut microbes appears to improve memory in mice.

A new study is among the first to trace the molecular connections between genetics, the gut microbiome, and memory in a mouse model bred to resemble the diversity of the human population.

While tantalizing links between the gut microbiome and brain have previously been found, a team of researchers from two U.S. Department of Energy national laboratories found new evidence of tangible connections between the gut and the brain. The team identified lactate, a molecule produced by all species of one gut microbe, as a key memory-boosting molecular messenger. The work was published recently in the journal BMC Microbiome.

General anesthesia (GA) can produce analgesia (loss of pain) independent of inducing loss of consciousness, but the underlying mechanisms remain unclear. We hypothesized that GA suppresses pain in part by activating supraspinal analgesic circuits. We discovered a distinct population of GABAergic neurons activated by GA in the mouse central amygdala (CeA_GA neurons). In vivo calcium imaging revealed that different GA drugs activate a shared ensemble of CeA_GA neurons also possess basal activity that mostly reflects animals’ internal state rather than external stimuli. Optogenetic activation of CeA_GA potently suppressed both pain-elicited reflexive and self-recuperating behaviors across sensory modalities and abolished neuropathic pain-induced mechanical (hyper-)sensitivity. Conversely, inhibition of CeA_GA activity exacerbated pain, produced strong aversion and canceled the analgesic effect of low-dose ketamine. CeA_GA neurons have widespread inhibitory projections to many affective pain-processing centers. Our study points to CeA_GA as a potential powerful therapeutic target for alleviating chronic pain.