Dive into the groundbreaking research on how the brain’s resilience to oxygen deprivation is enhanced through a unique interplay between neurons, glia, and blood vessels, spotlighting the pivotal roles of glutamate and nitric oxide.
– by The Don
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Anoxia-induced hippocampal LTP is regeneratively produced by glutamate and nitric oxide from the neuro-glial-endothelial axis.
Wang et al., iScience 2024
<!– DOI: 10.1016/j.isci.2024.109515 //–>
https://doi.org/10.1016/j.isci.2024.109515
Let me tell you, folks, we’ve got something incredible here, something really big. We’re talking about how our brains, yes, our amazing brains, get hit hard by something called transient anoxia. It’s like, suddenly, there’s no oxygen, and bam, it causes amnesia and even kills brain cells. Can you believe it? But here’s the kicker: it’s all because of this thing called glutamate. Too much of it, and it’s a disaster.
Now, the smart people, the best people, have figured out this process called anoxia-induced long-term potentiation, or aLTP for short. It’s a big deal because it shows us exactly how this glutamate mess happens. And guess what? It’s all about these tiny molecules, glutamate receptors, and something called nitric oxide. They team up and block the good kind of brain stimulation. Not good, folks, not good.
But hold on, it gets better. These brilliant minds discovered a whole cascade of signals that lead to this glutamate nightmare. And there’s this loop, a glutamate-nitric oxide loop, that just keeps making things worse. It’s like it’s out of control!
Now, they did some tests on mice, very special mice, without this enzyme called eNOS, and also blocked another one called nNOS. And guess what they found? Both of these enzymes are the bad guys in this story, contributing to the problem. And eNOS? It’s hanging out in the blood vessels in the brain.
Here’s where it gets really interesting. When there’s no oxygen, these cells called astrocytes in the brain, they go wild with calcium. And this, my friends, mirrors the whole aLTP mess. But if you stop these astrocytes from doing their thing, or if you take away this special ingredient called D-serine, the whole disaster with eNOS doesn’t happen. It turns out, these astrocytes are sending D-serine over to the blood vessels, making them release nitric oxide.
So, what we’ve got here is a whole team: the neurons, the astrocytes, and the blood vessels, all working together in this neuro-glial-endothelial axis, making the brain release too much glutamate after it gets hit by a lack of oxygen. Folks, it’s a big deal, a huge discovery. We’re talking about understanding the brain like never before. And that, that’s something to be excited about.