(Web Desk): The study sheds light on the brain’s response to temporary oxygen deprivation, known as anoxia-induced long-term potentiation (aLTP). In a new study published in iScience, researchers from the Okinawa Institute of Science and Technology (OIST) and their collaborators have uncovered a crucial mechanism that could explain memory loss observed in conditions like stroke. The study sheds light on the brain’s response to temporary oxygen deprivation, known as anoxia-induced long-term potentiation (aLTP).
When the brain experiences a lack of oxygen, neurons release excessive amounts of the neurotransmitter glutamate. This increased glutamate triggers the production of nitric oxide (NO) in both neurons and brain blood vessels. Remarkably, the researchers discovered that this NO then boosts further glutamate release from neurons, forming a self-sustaining glutamate-NO-glutamate feedback loop.
“We wanted to know how oxygen depletion affects the brain and how these changes occur,” said Dr. Han-Ying Wang, the lead author of the study. “It’s been known that nitric oxide is involved in releasing glutamate in the brain when there is a shortage of oxygen, but the mechanism was unclear.
” Hijacking Memory Processes The cellular processes that support aLTP are shared by those involved in memory strengthening and learning, known as long-term potentiation (LTP). When aLTP is present, it hijacks the molecular activities required for LTP, potentially obstructing memory for.
