#gabaergic-interneurons

#gabaergic-interneurons

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.

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.

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.

Rumination activates the default mode network (DMN) - the brain's self-referential processing system. This is the neural circuitry that fires when you're thinking about yourself in relation to others: your identity, your social standing, your mistakes. It's the brain asking, over and over, What does this say about me?

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.

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.

At the Winter Olympics, skiers, bobsledders, speedskaters, and many other athletes all have to master one critical moment: when to start. That split second is paramount during competition because when everyone is strong and skilled, a moment of hesitation can separate gold from silver. A competitor who hesitates too much will be left behind -but moving too early will get them disqualified.

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.

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.

There was a group of neurons that predicted the wrong answer, yet they kept getting stronger as the model learned. So we went back to the original macaque data, and the same signal was there, hiding in plain sight. It wasn't a quirk of the model - the monkeys' brains were doing it too. Even as their performance improved, both the real and simulated brains maintained a reserve of neurons that continued to predict the incorrect answer.

The team, which is being led by Jülich neurophysics professor Markus Diesmann, will leverage the Joint Undertaking Pioneer for Innovative and Transformative Exascale Research (JUPITER) supercomputer for their simulation. JUPITER is currently the fourth most powerful supercomputer in the world according to the TOP500 list, and features thousands of graphical processing units. The team demonstrated last month that a " spiking neural network " could be scaled up and run on JUPITER, effectively matching the cerebral cortex's 20 billion neurons and 100 trillion connections.