Cells have a trick called splicing. They can cut a gene’s message into pieces and decide which fragments to keep. By mixing and matching these fragments, a single gene can produce many different proteins, giving tissues and organs more options to thrive and evolve. Out of all tissues, splicing is most prevalent in the brain.

Researchers at the Center for Genomic Regulation (CRG) have discovered that one such fragment, a “microexon” just nine amino acids long, is inserted into the DAAM1 protein exclusively in neurons and nowhere else in the body. The inclusion of the microexon is critical for healthy neuronal development, with effects rippling all the way up to memory function. The findings are published in Nature Communications.

DAAM1 makes a protein that helps cells maintain their shape and enables their movement. When the team deleted the nine-letter microexon in mice, the animals were healthy at birth, but their adult brain cells had half of the usual “learning spines,” protrusions known to be important for learning and retrieval of memories.

The ability to detect imminent threats and execute behaviors aimed at protecting oneself, such as hiding, running away or defending oneself, is central to the survival of most animal species. A region of the mammalian brain known to play a key role in threat response is the hypothalamus, which also regulates the release of hormones and other vital bodily functions.

Researchers at California Institute of Technology (Caltech) and Howard Hughes Medical Institute recently carried out a study aimed at better understanding how a specific group of neurons in the mouse ventromedial hypothalamus dorsomedial subdivision (VMHdm), which are identified by the presence of the steroidogenic factor 1 (SF1) gene, contribute to the coding of predator imminence.

Their findings, published in Neuron, show that distinct subsets of VMHdm^SF1 neurons encode multiple internal states that are evoked by the imminence of predators.

At the level of molecules and cells, ketamine and dexmedetomidine work very differently, but in the operating room they do the same exact thing: anesthetize the patient. By demonstrating how these distinct drugs achieve the same result, a new study in animals by neuroscientists at The Picower Institute for Learning and Memory at MIT identifies a potential signature of unconsciousness that is readily measurable to improve anesthesiology care.

What the two drugs have in common, the researchers discovered, is the way they push around brain waves, which are produced by the collective electrical activity of neurons.

When brain waves are in phase, meaning the peaks and valleys of the waves are aligned, local groups of neurons in the brain’s cortex can share information to produce conscious cognitive functions such as attention, perception and reasoning, said Picower Professor Earl K. Miller, senior author of the new study in Cell Reports. When brain waves fall out of phase, local communications, and therefore functions, fall apart, producing unconsciousness.

A phenomenon largely ignored since its discovery 100 years ago appears to be a crucial component of diabetic pain, according to new research from The University of Texas at Dallas’s Center for Advanced Pain Studies (CAPS).

Findings from a new study published in Nature Communications suggest that cell clusters called Nageotte nodules are a strong indicator of nerve cell death in human sensory ganglia. These could prove to be a target for drugs that would protect these nerves or help manage diabetic neuropathy.

“The key finding of our study is really a new view of diabetic neuropathic pain,” said Dr. Ted Price, Ashbel Smith Professor of neuroscience in the School of Behavioral and Brain Sciences, CAPS director and co-corresponding author of the study. “We believe our data demonstrate that neurodegeneration in the dorsal root ganglion is a critical facet of the disease—which should really force us to think about the disease in a new and urgent way.”