Touch sensor of the carnivorous plant Venus flytrap revealed

Saitama University

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The Venus flytrap possesses sensory hairs that detect prey via touch stimuli. Bending of the sensory hair trigger Ca2+ and electrical signals that propagate to the leaf blade.

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Credit: Masatsugu Toyota/Saitama University

Saitama, Japan: Plants lack nerves, yet they can sensitively detect touch from other organisms. In the Venus flytrap, highly sensitive sensory hairs act as tactile sensing organs; when touched twice in quick succession, they initiate the closure cascade that captures prey. However, the molecular identity of the touch sensor has remained unclear.

Assistant Professor Hiraku Suda and Professor Masatsugu Toyota at Saitama University, Saitama, Japan, together with colleagues and in collaboration with the research group of Professor Mitsuyasu Hasebe at the National Institute for Basic Biology (NIBB), Okazaki, Japan, have revealed that an ion channel named DmMSL10, enriched at the base of the sensory hairs, is the key touch sensor that enables the detection of very faint prey touches. The research is scheduled to be published in Nature Communications on September 30, 2025.

To visualize Ca2+ dynamics, the team engineered flytraps expressing the fluorescent Ca2+ indicator protein GCaMP6f and used two-photon microscopy with intracellular electrical recordings. “Our approach enabled us to visualize the moment a physical stimulus is converted into a biological signal in living plants,” says Suda (Figure).

The team observed that a gentle bend produces a local Ca2+ rise and a small local electrical change (receptor potential) that remains localized (Video 1). By contrast, a stronger bend first elicits a larger receptor potential. Once this electrical signal crosses a threshold—like a switch being flipped—it triggers an all-or-none, large electrical spike (action potential) together with a Ca2+ wave (Video 2). Both signals then propagate from the hair base to the leaf blade. These results indicate that a threshold‑regulated, action-potential-triggering mechanism underlies this response, similar in principle to animal nervous systems.

To further analyze the mechanism underlying this tactile sensing system, the team used genetic tools to create DmMSL10 knockout (gene-disabled) plants and demonstrated the role of DmMSL10 in touch sensing. In DmMSL10 knockout plants, stimuli that trigger action potentials and long‑range Ca2+ waves in wild-type plants elicited only subthreshold receptor potentials and local Ca2+ signals (Video 3). These findings show that DmMSL10 acts like an amplifier, boosting the initial small electrical signal until it is strong enough to trigger an action potential.

To test relevance under naturalistic conditions, the team built a small ecosystem in which ants freely walked over traps (Video 4). In wild-type plants, ant touches triggered Ca2+ waves across the trap, followed by trap closure (Video 5). In DmMSL10 knockout plants, these waves were much less frequent, and closures tended to be fewer (Video 6).

“Our findings show that DmMSL10 is a key mechanosensor for the highly sensitive sensory hairs that enable the detection of touch stimuli from even the faintest, barely grazing contacts,” says Suda. “Many plant responses arise from mechanosensing—the plant’s tactile sense—so the underlying molecular mechanisms may be shared beyond the Venus flytrap.”

Video 1: Weak-deflection response in the sensory hair [VIDEO] | EurekAlert! Science News Releases

Video 2: Strong-deflection response in the sensory hair [VIDEO] | EurekAlert! Science News Releases

Video 3: Calcium signal in a DmMSL10 knockout plant [VIDEO] | EurekAlert! Science News Releases

Video 4: A microecosystem for ants and flytraps [VIDEO] | EurekAlert! Science News Releases

Video 5: Interactions between an ant and a trap in a wild-type plant [VIDEO] | EurekAlert! Science News Releases

Video 6: Interactions between an ant and a trap in a DmMSL10 knockout plant [VIDEO] | EurekAlert! Science News Releases

Journal

Nature Communications

DOI

10.1038/s41467-025-63419-w 

Method of Research

Experimental study

Article Title

MSL10 is a high-sensitivity mechanosensor in the tactile sense of the Venus flytrap

Article Publication Date

30-Sep-2025

 

CU Anschutz School of Medicine researchers identify new method for treating alcohol use disorder

Joseph Schacht, PhD, and Drew Winters, PhD, of the Department of Psychiatry, found that the drug tolcapone increases behavioral control by increasing activation of the prefrontal cortex

University of Colorado School of Medicine

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Currently, the treatments for alcohol use disorder (AUD) work in one of two ways, explains Joseph Schacht, PhD, associate professor of psychiatry at the University of Colorado Anschutz School of Medicine — they either make the effects of alcohol less pleasurable, or they reduce cravings for alcohol.

“Those are important things for alcohol and substance use disorders — reducing how good the drug makes you feel or how much you want to use it,” Schacht says.

But is there another mechanism a drug could target to help people with alcohol use disorder? Schacht and his colleague Drew Winters, PhD, research associate in the CU Anschutz Department of Psychiatry, hypothesized that there could be — and their research published recently in the journal Biological Psychiatry: Cognitive Neuroscience and Neuroimaging shows that their theory may be correct. 

Targeting the prefrontal cortex

“The current medications for AUD target the neurotransmitter dopamine in the reward-related parts of the brain,” Schacht says. “But we were interested in understanding how dopamine might act in a different part of the brain — the prefrontal cortex — and how its action there might affect a different behavior, which is behavioral control.”

Because AUD and addiction are diseases of the “gas” — wanting to feel good by using the substance — as well as the “brakes,” or the inability to control one’s behavior when a craving arises, a medication that increases the amount of control one has over their behavior could be another way to treat them, the researchers hypothesized.

Enter tolcapone

To test the theory, they turned to a drug called tolcapone, an FDA-approved medication, originally designed to treat Parkinson’s disease, that increases dopamine in the prefrontal cortex by suppressing the action of an enzyme that degrades dopamine. In the CU randomized study, participants with AUD who took the medication instead of a placebo performed better on a computer-based test called a “stop signal task,” in which they must stop themselves from pressing the space bar when a certain signal comes up on the screen.

“You have a greater number of trials where you just press the space bar,” Winters says. “You're already primed to hit the space bar, then when a different signal comes up, you have to stop yourself and not press anything. We were measuring if they can stop, and we also want to see, when they make an error, are they making corrections afterward?”

Reduction in use

MRI images taken during the stop signal task showed that the drug increased activation in the prefrontal cortex when people were trying to control their behavior, which is consistent with tolcapone increasing dopamine in the prefrontal cortex. The researchers also asked participants about their alcohol use during the seven days they were taking the drug.

“They came in, we gave them the medication, they came back a week later, and we said, ‘How much did you drink during the last week?’” Schacht says. “Greater prefrontal cortex activation was associated with less drinking during that week, suggesting that the mechanism of increased control was having an effect on their behavior in the real world.”

“It was very gratifying to see that this medication is working in the ways that we expected it to, and that there were actually changes in the brain that associate with behavior,” Winters adds. “That connection is really important.”

Next steps

Schacht, who also has conducted research on the effects of GLP-1 agonist drugs like Ozempic on AUD, is now conducting a study on the effects of tolcapone on people with AUD who also have attention-deficit/hyperactivity disorder (ADHD).

“Those patients are the ones who might especially benefit from being able to control their behavior more, because they have not only AUD, which is impairing the ‘brakes,’ but also this disorder related to difficulties with controlling impulsivity,” he says.

Because tolcapone is no longer used to treat Parkinson’s, the researchers say, it’s unlikely that it would be repurposed to treat AUD. But their research sets the stage for a pharmaceutical company to develop a drug that works similarly to treat AUD and substance use disorders.

“I've worked in AUD medication development for a long time, and I’ve tested many medications with different mechanisms of action,” Schacht says. “It was very fulfilling to see that one that works in a different way could also be effective. It suggests that we might be able to broaden the space for what medications might be useful in this condition.”

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Journal

Biological Psychiatry Cognitive Neuroscience and Neuroimaging

DOI

10.1016/j.bpsc.2025.06.003 

 

Psilocybin may present unique risks during the postpartum period

University of California - Davis

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Magic mushrooms may not be the answer to postpartum depression, new research from the University of California, Davis suggests. 

In a first-of-its-kind study appearing in Nature Communications, an interdisciplinary team from the university’s Institute for Psychedelics and Neurotherapeutics (IPN) dosed mouse mothers with psilocybin and found that the drug amplified anxiety and depressive-like symptoms associated with perinatal mood disorders — mental health conditions that can arise during or after pregnancy.  

While psilocybin and its ability to promote neuronal growth have been previously shown to benefit those with mental health conditions, the new research indicates that it’s not a one-size-fits-all therapy.

“The IPN has done a lot of work demonstrating that a single dose of a psychedelic can lead to long-lasting, beneficial effects,” said study co-author David E. Olson, director of the IPN and a professor of chemistry, biochemistry and molecular medicine at UC Davis. “But it’s a little more nuanced than that in terms of who can really benefit and who might be at risk. There are different patient populations.” 

With mental illness being the leading cause of pregnancy-related deaths in the United States, the research lays a critical foundation in the search for a viable therapeutic.

“There is an urgent need for treatments in the postpartum period,” said study co-author and IPN affiliate Danielle Stolzenberg, an associate professor of psychology at UC Davis. “I think most importantly what we’ve learned is that the effects of psychedelics can differ based on the ovarian hormone context and that is a critically important finding.” 

Not only were psylocibin’s negative impacts long-lasting in mouse mothers (persisting for two weeks after a single dose), but the researchers also found that offspring raised by psylocibin-treated mothers also exhibited anxiety and depression-like symptoms long into adulthood. 

The finding suggests that the mothers passed on those negative effects via lactation, permanently stunting the offspring’s neurodevelopment. 

A one-of-a-kind mouse model for postpartum depression

The study was built around Stolzenberg’s innovative mouse model of postpartum depression.

In the model, mouse mothers live with their offspring in a two-cage system that allows them to escape from the demands of motherhood. Stolzenberg found that repeated exposure to a social threat (a male mouse) destabilizes maternal behavior, leading to infant avoidance and triggering other stress responses. These symptoms are hallmarks of postpartum depression in humans. 

“One of the things that’s discussed consistently in the clinical literature is that moms often feel like they have trouble bonding with their infants when they’re experiencing depressive symptoms,” Stolzenberg said. “The mouse moms in the social stress paradigm spend significantly more time in the cage without the pups. They will often run back and forth to check on them but tend to actively avoid their infants for long periods of time.” 

The team initially thought the treatment might help alleviate postpartum depression symptoms. 

“Psilocybin was of such interest for us because it’s been demonstrated to be useful across a whole host of mental disorders, including addressing anxiety and depression,” said study first-author Cassandra Hatzipantelis, a postdoctoral fellow at the IPN. “We thought it could have the ability to address things that go wrong in postpartum depression like parent-infant connection.” 

Instead, psilocybin induced the opposite effect, having both negative behavioral impacts on mothers and their offspring. Mouse mothers continued avoiding their offspring and displaying anxiety and depressive-like symptoms. These symptoms persisted after mice were separated from their offspring. 

“Two weeks after a single dose of psylocibin, the mothers were dramatically impaired,” Hatzipantelis said. “We were shocked.” 

Psilocybin-treated mice, the researchers found, were at higher risk for behavioral impairments and depressive-like symptoms. 

“I was very surprised that we saw the moms getting worse,” Olson said. 

Virgin female mice did not show such effects. The findings indicate that there may be distinct neurochemical differences in the brains of mouse mothers that led to psilocybin producing adverse effects. 

“We know that ovarian hormones regulate serotonergic signaling, but we understand very little about the interaction between ovarian hormones and drugs that impact serotonin,” said Stolzenberg, noting that the latter is critical to how psychedelics affect the brain.

Passing on negative effects to offspring

The team also found that behavioral effects were passed to the offspring. Nine weeks after weaning, both male and female offspring exhibited pronounced measures of anxiety and depression compared to the control groups. Their brains also showcased traces of psilocin — a metabolite of psilocybin. 

“We now know that even low doses of exposure can impact offspring for long periods of time,” Stolzenberg said. 

The study highlights the IPN’s commitment to studying both the positive and negative effects of psychedelics. 

“These could be really important therapeutics, but we also realize they have limitations, and we have to conduct rigorous science to understand what those limitations are,” Olson said. 

Since its launch in 2023, the IPN has attracted nearly 80 UC Davis faculty affiliates spanning diverse fields from anthropology and chemistry to neuropharmacology and genomics. 

“UC Davis has incredible experts across a breadth of fields and in specialized domains,” Olson said. “That’s why we can do this type of high impact, interdisciplinary science. It’s really the people.”

Additional study authors include Min Liu, Adam Love, Sadie J. Leventhal, Hero Maera, Srinidhi Viswanathan, Emily Avetisyan, Liana Belinsky, McKenna M. Rangel, Nina J. Jain, Max Kelly, Claire Copeland, Yara A. Khatib and Oliver Fiehn..

The research reported here was supported by funding from the National Institutes of Health (R01HD087709, R35GM148182), the W. M. Keck Foundation, the University of California at Davis Pilot Project Program Award from the Perinatal Origins of Disparities Center, and the University of California at Davis Academic Senate Large Grant Award. 

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Journal

Nature Communications

DOI

10.1038/s41467-025-64371-5 

Method of Research

Experimental study

Subject of Research

Animals

Article Title

Psilocybin during the postpartum period induces long-lasting adverse effects in both mothers and offspring

Article Publication Date

30-Sep-2025

COI Statement

David Olson is a cofounder of Delix Therapeutics, Inc., serves as the chief innovation officer and head of the scientific advisory board, and has had sponsored research agreements with Delix Therapeutics.