While a patient is fully anesthetized and unresponsive, neurons in the hippocampus continue to process language, distinguish different types of words, and generate neural activity consistent with predicting upcoming words.

Researchers at Baylor College of Medicine directly recorded this neural activity, offering new insight into how unconsciousness works at the cellular level. Their findings, published in Nature, show that hippocampal neurons continue to process aspects of language even when the brain is unconscious.

“Our findings show that the brain is far more active and capable during unconsciousness than previously thought,” said Dr. Sameer Sheth, professor and Cullen Foundation Endowed Chair of neurosurgery and a McNair Scholar at Baylor. “Even when patients are fully anesthetized, their brains continue to analyze the world around them.”

a Rare Look Inside the Anesthetized Hippocampus

Sheth’s team recorded from hundreds of individual neurons in the hippocampus, a region of the brain essential for memory formation. Researchers collected data during epilepsy surgeries, specifically anterior temporal lobectomies, when patients were under general anesthesia and the hippocampus was temporarily accessible. This rare opportunity allowed researchers to directly record hippocampal activity, something scalp EEG cannot.

The researchers used Neuropixels probes, high-density recording devices that can monitor hundreds of neurons simultaneously. This study represents the first use of this technology in the human hippocampus during anesthesia. Seven patients participated, all under propofol anesthesia with consistent sedation levels maintained throughout the recordings.

The Unconscious Brain Still Learns

In the initial test, researchers played patients a repeating tone with occasional unexpected pitches. Hippocampal neurons consistently detected these outlier tones, and their sensitivity increased over approximately ten minutes. Researchers usually observe this kind of adaptive neural response during wakefulness.

To dig deeper, the researchers built a computer model of a recurrent neural network, trained to perform the same tone discrimination task. The model showed the same pattern as the human brain recordings, suggesting that this increased sensitivity to outlier tones can arise from local brain circuits alone, without the need for higher-level conscious processing.

Predicting Words Before They’re Spoken

The researchers also played short stories to anesthetized patients while recording from the same neurons. Hippocampal activity tracked language in real time, distinguishing between nouns, verbs, and adjectives. Neural activity reflected both the current word and prediction of the upcoming word in the sequence. “The brain appears to anticipate what comes next in a story, even without conscious awareness,” Sheth said.

“This kind of predictive coding is something we associate with being awake and attentive, yet it’s happening here in an unconscious state,” added Baylor neurosurgery professor Benjamin Hayden.

What This Means for the Science of Consciousness

The results show that the hippocampus can support neural computations associated with complex cognition even during unconsciousness. This suggests that at least some components of language processing and prediction may not require conscious awareness. Sheth’s team proposes that consciousness does not arise from a single brain region but rather emerges from interactions among multiple brain regions. The hippocampus may process information that later becomes part of awareness.

The researchers noted a parallel with artificial intelligence. Large language models generate text by predicting the next word in a sequence; the anesthetized hippocampus showed a similar pattern of prediction. This similarity may provide neuroscientists and AI researchers with a shared framework for studying language prediction based on biological circuitry.

“Can we use these signals to deploy and run a speech prosthetic for some of the parts of the brain that are damaged by stroke or injury? These are questions that we can now consider in relation to this part of the brain,” said study author and Baylor neurosurgery resident Kalman Katlowitz.

While these results are promising, the team acknowledged the study’s limitations. The research focused only on propofol-based general anesthesia, so the results may not apply to other unconscious states such as natural sleep or coma. Additionally, the researchers examined only the hippocampus, so they cannot yet determine how broadly this type of unconscious processing occurs in other brain regions.

“This work pushes us to rethink what it means to be conscious,” Sheth concluded. “The brain is doing much more behind the scenes than we fully understand.”

Austin Burgess is a writer and researcher with a background in sales, marketing, and data analytics. He holds an MBA, a Bachelor of Science in Business Administration, and a data analytics certification. His work focuses on breaking scientific developments, with an emphasis on emerging biology, cognitive neuroscience, and archaeological discoveries.

Schistosoma mansoni is a parasitic worm that infects millions of people worldwide, entering the body through the skin. Unlike bacterial infections that often cause pain and inflammation, S. mansoni usually slips in unnoticed, rarely causing discomfort. Scientists have long wondered why our skin’s defenses don’t react more strongly to this invader.

Researchers from the University of Pennsylvania and Tulane University explored whether a specialized group of pain-sensing neurons, called TRPV1+, plays a role in detecting and fighting off S. mansoni during its invasion. TRPV1+ neurons are nerve cells in the skin that respond to heat, spicy foods, and certain bacteria and fungi. When activated, they can trigger pain and release molecules that alert the immune system. Previous researchers have shown that these neurons help defend against bacterial and fungal skin infections, but their role in fighting off parasites was unclear. 

To examine how S. mansoni infects its hosts, the team conducted experiments using groups of 4 to 8 mice, matched for age and sex. They repeated each experiment 2 to 3 times to ensure their data was reproducible. They anesthetized the mice, exposed their ears to a solution containing 100 to 150 live S. mansoni larvae, and covered the area with vaseline to keep the solution in place. After 20 to 30 minutes, they counted the number of larvae remaining in the mice’s ears to assess how many had successfully penetrated their skin. 

Next, the team measured pain sensitivity in the mice exposed to the parasite by placing them in chambers and applying an infrared heat source to their paws. They recorded how long it took each mouse to withdraw its paw as a sign of pain. They repeated this test 3 times per paw on each mouse, waited at least 5 minutes between each measurement, and calculated an average withdrawal time. They found that mice infected with S. mansoni were approximately half as sensitive to heat-induced pain as an uninfected control group, suggesting that the parasite could be suppressing the mice’s TRPV1+ neurons.

To investigate this further, the team isolated nerve cells that transmit sensory signals from the mice’s skin, known as dorsal root ganglia, and grew them in the lab. They stimulated these neurons by adding a spicy compound in chili peppers, known as capsaicin. Then they measured calcium influx, a sign the neurons were active, using a special dye that glows differently under a microscope depending on calcium levels. This allowed them to see how active the neurons were and how many molecules they released in response to infection and stimulation. They found that 68% of neurons from uninfected mice responded to capsaicin, but only 26% of neurons from infected mice did so, confirming that the parasite dampened their sensory neuron responses.

To test whether restoring the mice’s neuron activity could help their bodies resist parasite invasion, the researchers genetically engineered the mice to produce a light-sensitive protein in their TRPV1+ neurons, called channelrhodopsin. They “turned on” these neurons by stimulating them with blue light for 30 minutes every day for 5 days before infecting the mice with parasites. Six days later, they assessed the mice’s immune response by using a laser to count immune cells in samples of ear tissue. They also determined how far the parasites had spread by counting larvae in lung samples. They saw that mice with the artificially activated TRPV1+ neurons had nearly double the immune response, blocked roughly twice as many larvae at the skin, and had about 20% fewer parasites in their lungs.

Next, the researchers selectively destroyed TRPV1+ neurons in a new set of mice using a compound known as resiniferatoxin. Three weeks later, they confirmed the treatment had worked by testing the mice’s pain sensitivity using the same heat assay as before. After confirming the mice had lost their pain sensitivity, the team exposed the mice to the parasites. They found that the reinfected mice had 1% to 3% weaker skin immune responses and approximately 25% to 30% more parasites in their lungs than a control group, further confirming that TRPV1+ neurons play a protective role during early infection.

The team concluded that S. mansoni has evolved ways to silence pain-sensing neurons, like TRPV1+. Their discovery suggests that future scientists could boost skin immunity against parasites by targeting sensory neurons. For example, they could develop topical creams or therapies that activate these neurons to help our bodies fight off S. mansoni and similar parasitic invaders.

The post A parasite that numbs your pain appeared first on Sciworthy.

Before the prefrontal cortex evolved, another system in the brain may already have been directing attention, scientists have now revealed. 

In a recent study published in Nature Communications, researchers at Johns Hopkins University have identified a small group of brainstem neurons that act as an internal attention filter.

When these neurons were deactivated in mice, the animals became highly distractible, mirroring one of the hallmark features of ADHD. Restoring activity in these neurons allowed the mice to regain normal focus.

An Old Problem With No Modern Answer

Selective spatial attention is the brain’s ability to focus on relevant information while ignoring distractions. This process allows a person to follow a conversation in a noisy environment or recognize a familiar face in a crowd. Conditions such as ADHD and autism also often involve disruptions in selective attention. For many years, scientists believed the prefrontal cortex was primarily responsible for this function.

However, this view does not fully explain how attention works across different species. Primates have a well-developed prefrontal cortex, while other vertebrates have a less pronounced version, yet birds, fish, and turtles still effectively focus their attention.

“If we really go back in evolution, for hundreds of millions of years, birds have had this ability, fish have had this ability. And they do not typically have a highly developed prefrontal cortex, so how does the brain solve this problem?” said lead author Ninad Kothari, a postdoctoral fellow in Johns Hopkins’ Department of Psychological and Brain Sciences. “We were able to identify an evolutionarily old region in the brainstem which affords this ability.”

A Filter Hiding in Plain Sight

The researchers traced this behavior to a network of inhibitory neurons located deep within the brainstem, a region found in all vertebrates. Mysore’s laboratory had previously studied this area in birds, frogs, and turtles before examining it in mice.

The team created an attention task, similar to those used in human studies, to test the role of these neurons. Mice viewed visual cues on a screen and earned rewards for responding to a target in front of them while ignoring a distracting signal off to the side. This test measured how well the mice could pick out important information and ignore distractions. The mice successfully performed the task until researchers deactivated the brainstem neurons, at which point they became easily distracted.

Ruling Out the Obvious Explanations

Before concluding that these neurons controlled attention, the researchers tested for other possible explanations, such as vision or motor problems, that might account for the mice’s behavior. However, the researchers ruled out these alternative explanations.

“The only thing impaired was their ability to take the competing pieces of information, compare them, and pay attention to the location with the most important information,” said senior author Shreesh Mysore, a neuroscientist who studies neural circuits tied to behavior. “This part of the brain is like an attentional selection engine. It helps solve the question: ‘What is most important information I should pay attention to right now?'”

The attention deficit was not permanent. When the neurons were reactivated, the same mice that had previously been unable to ignore faint distractions were once again able to ignore even strong distractors.

“A hallmark of ADHD is that even faint distractors draw attention away — and that’s exactly what we see here when these neurons are silenced,” Mysore said. “But the very next day, when the neurons are turned back on, the same animal can ignore distractors again, even very strong ones.”

What This Could Mean for Human Brains

“All the evidence to date suggests that these neurons exist in humans too,” Mysore said. “But are they responsible for selective spatial attention in humans? An exciting hypothesis is that they play a crucial role.”

If researchers find that these neurons function differently in people with attention disorders, the circuit could become a target for future therapies.

Austin Burgess is a writer and researcher with a background in sales, marketing, and data analytics. He holds an MBA, a Bachelor of Science in Business Administration, and a data analytics certification. His work focuses on breaking scientific developments, with an emphasis on emerging biology, cognitive neuroscience, and archaeological discoveries.