#nmda-receptor

#nmda-receptor

To characterize CREs and TFs for neocortical ExNs, we used Arpp21-Gfp or Fezf2-Gfp transgenic mice and enriched GFP-expressing neocortical upper layer (L2-4) intratelencephalic (IT) neurons or deep layer (L5-6) predominantly extratelencephalic (ET) neurons, respectively, from neonatal mice (postnatal day (PD) 0), an age at which neocortical ExN identity and connectivity are established.

DNA damage can originate from internal sources like metabolic by-products or normal cellular activities, as well as external factors such as cosmic radiation, diet, and pollution.

This could open up some interesting possibilities for therapeutic interventions for depression-like behaviors or maladaptive changes in motivational behaviors down the road where microglia are known to play a really important role.

Dopamine is one of the most extensively studied neurotransmitters, chemicals that convey signals from cell to cell. It's the one with the highest profile outside neuroscience: often known as the 'pleasure chemical', it's depicted as the hit of reward that people get from recreational drugs or scrolling through social media. That's a gross simplification of what dopamine does; on that, researchers agree.

Young, two-month-old lab mice housed with older, 18-month-old mice showed really impaired cognition. Researchers exposed young mice raised in a sterile, microbe-free environment to gut bacteria from old mice, causing the younger animals to perform worse on cognitive tests, as if they had prematurely aged, just like the cohoused mice.

Anyone living with schizophrenia understands the true limitations of current treatment options. Antipsychotics remain the single leading treatment for the disorder, and they are riddled with undesirable side effects. Weight gain, tardive dyskinesia, and excessive drowsiness are a few. Much research is devoted to expanding the range of medication options, and few academics have pursued other avenues. However, there is a possibility that treatment for schizophrenia can be approached through cellular methods if long-term research validates early signs of hope.

The human brain is engineered to ignore most of what it sees and hears, according to the neuroscientists I interviewed for the audio original Viral Voices. If that's the case, how are you supposed to make a memorable impression? The empowering news is that if you understand how the brain works, what it discards, and what it pays attention to, you'll be far more persuasive than you've ever imagined. Persuasive people have influence in their personal and professional lives.

Neuroscientists have a name for the brain network that fires up when you're not focused on an external task: the default mode network, or DMN. It's the constellation of regions - the medial prefrontal cortex, posterior cingulate cortex, and angular gyrus among them - that hums to life when you daydream, reflect on yourself, or think about other people's mental states.

Our results are highly promising, especially since currently there are no approved treatments that address the underlying cause of Dravet syndrome. Since this gene regulation product targets the actual root cause of Dravet syndrome, we observed improvements in other developmental and cognitive symptoms, in addition to seizure control. This is unprecedented.

A groundbreaking study found that adults who sit for 10 or more hours daily face a significantly higher risk of dementia compared to those who sit less. The research, which tracked over 50,000 adults using wearable devices, revealed that the risk increases dramatically after crossing that 10-hour threshold.

We've always said that SuperAgers show that the aging brain can be biologically active, adaptable, flexible, but we didn't know why. This is biological proof that their brains are more plastic, and a real discovery that shows that neurogenesis of young neurons in the hippocampus may be a contributing factor.

A recent study published in Biological Psychiatry identified a distinct subtype of psychiatric illness marked by brain inflammation, one that cuts across traditional diagnoses and may explain why standard treatments fail for some people (Tang et al., 2025).This new brain imaging study offers an interesting clue. It turns out that across different psychiatric disorders, some people show clear signs of brain inflammation, visible on scans and confirmed through immune system tests.

N-methyl-d-aspartate receptors (NMDARs) are glutamate-gated ion channels that mediate excitatory neurotransmission throughout the brain1. As obligate heterotetramers, their activation requires the binding of both glycine and glutamate2. Although recent structural studies have provided insights into endogenous receptors from select brain regions3, most previous work has relied on recombinant receptors and engineered constructs, which limits our understanding of native NMDARs across the whole brain.

But questions remain about the accuracy and uncertainty of these tests, and experts caution that the assays aren't ready for prime time. While the results here are encouraging, they are not yet at the level of having significant clinical benefit for individual patients, says Corey Bolton, a clinical neuropsychologist and an assistant professor of medicine at Vanderbilt University Medical Center, who was not involved in the new study.

Tumours lure and then hijack nearby sensory neurons to boost their own growth. The cancer cells use these neurons to send a signal to the brain that subdues the activity of immune cells around the tumour, which allows it to grow unchecked. When researchers deactivated these neurons in mice with lung cancer, they saw "a huge, dramatic reduction" in tumour growth - more than 50% - says cancer immunologist and study co-author Chengcheng Jin.

Haavik was surprised to hear this because the scientific data do not suggest an unequivocal link between low levels of the neurotransmitter dopamine and ADHD. But the idea that low dopamine is a direct cause of ADHD is a common misconception, one that's amplified on social media and even in popular books about the condition. The reality, Haavik and other researchers say, is that the causes of ADHD are more diverse and nuanced than a simple deficit in one chemical cue in the brain.

If you get migraines, you already know they don't just stay in your head. The pounding pain might be the headline symptom, but the real story is how an attack can throw your entire body out of whack - making light feel blinding, everyday sounds unbearable, and even simple texts impossible to answer. That's because a migraine isn't just about sore neck muscles or scalp tension. It's a full-body neurological event, driven by a cascade of changes in the brain.

You know that moment when you walk into a room and completely forget why you went there? Or when someone you've known for years walks up to you at the grocery store and their name just... vanishes from your brain? Last week, I spent ten minutes searching for my reading glasses while they were sitting on top of my head. My first thought wasn't "oh, silly me." It was "Is this how it starts?"

New therapies for Alzheimer's disease should target a particular gene linked to the condition, according to researchers who said most cases would never arise if its harmful effects were neutralised. The call to action follows the arrival of the first wave of drugs that aim to treat Alzheimer's patients by removing toxic proteins from the brain. While the drugs slow the disease down, the benefits are minor,

Researchers used data from two health studies to track the caffeine-drinking habits of more than 130,000 people over four decades. They found that drinking 2-3 cups of coffee or 1-2 cups of tea a day was associated with the greatest reductions in rate of cognitive decline, a result that held true even in people with a genetic variant called APOE4, which is associated with Alzheimer's disease.