Researchers at Vall d'Hebron Research Institute (VHIR) have discovered that ion cannel Kir6.2 is overexpressed on brain bruises, especially in astrocytes. This type of glial cells act as supportive cells in the central nervous system.The cranioencephalic traumatism affects mainly the population below 40-45 years old, and means a great cost on matters of healthy, economy and society. The brain bruises are one of the most frequent injuries in patients that suffered from a cranioencephalic trauma mild or serious. In more than 50% of these patients, the size of the bruise increases their volume as an added result of the side injuries such as edema at the area surrounding the injury and/or the bleeding progression.These secondary injuries cause a neurological aggravation, provoking in some patients the need of surgical interventions to avoid a bigger extension of the injury, a brain hernia and lastly, the death of the patient. The main goal of the research, published at https://www.ncbi.nlm.nih.gov/pubmed/29737232 Journal of Neurotrauma, was to achieve a better comprehension on the involved mechanisms in physiopathology of the brain bruises and identify new therapeutic targets to treat this pathology.In previous publications, the appearance of brain edema had been proved and linked to the ion channel named SUR1-TRPM4, in which SUR1 act as a regulator. SUR1 also regulates another ion channel, Kir6.2. http://en.vhir.org/web_vhir/portal1/grup-presentacio.asp?s=recerca&contentid=186903&idrefer= The Neurotraumatology and Neurosurgery Unit (UNINN) of VHIR, led by Dr. Joan Sahuquillo, decided to research on the role of this ion channel (Kir6.2), that up to date had not been studied on cranioencephalic traumas, and no overexpression had been identified before. Therefore, the channel was not considered as a key channel on brain bruises.The researchers discovered that against all believes, Kir6.2 was overexpressed on brain bruises. "From this point on we decided to study all cell types that expressed this channel: blood vessels, microglia, astrocytes, neurons, etc., finding out that the overexpression was mainly happening in astrocytes", explains Lidia Castro, researcher at UNINN and first author of the paper."Now we have finally described in which cells the channel is expressed, and that the channel is overexpressed in brain bruises. Our next goal is to find out what role does Kir6.2 have in this pathology, as to study its location in a ultrastructural level", adds Castro. One of the main hypothesis is that its expression at the astrocytes could be related to the transport of glutamate in these cells. The glutamate released at the extracellular space is neurotoxic in certain concentrations for the neurons. "We want to see if Kir6.2 participates in the glutamate transport to the interior of the astrocytes and to avoid this way the damage produced to the neuronal level. We will study this mechanism by inhibiting Kir6.2 in astrocyte cultures", adds Dr. Sahuquillo.