(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 formation.
“Long-term maintenance of aLTP requires continuous synthesis of nitric oxide. NO synthesis is self-sustaining, supported by the NO-glutamate loop, but blocking molecular steps for NO-synthesis or those that trigger glutamate release eventually disrupt the loop and stop aLTP,” explained Prof. Tomoyuki Takahashi, leader of the former Cellular and Molecular Synaptic Function Unit at OIST.
During a stroke, when the brain is deprived of oxygen, amnesia – the loss of recent memories – can be one of the symptoms.
The researchers suggest that the continuous presence of aLTP could potentially hinder the brain’s memory strengthening processes, potentially explaining the memory loss observed in certain patients after experiencing a stroke.
“If we can work out what’s going wrong in those neurons when they have no oxygen, it may point in the direction of how to treat stroke patients,” said Dr. Patrick Stoney, a scientist in OIST’s Sensory and Behavioral Neuroscience Unit.
Prof. Takahashi emphasised that the formation of a positive feedback loop between glutamate and NO when the brain is temporarily deprived of oxygen is an important finding. It explains the long-lasting nature of aLTP and may offer a solution for memory loss caused by a lack of oxygen.
This research not only sheds light on the brain’s response to oxygen deprivation but also opens up new avenues for potential therapeutic interventions to address memory loss associated with conditions like stroke.
