China, Egypt sign deals to boost lunar exploration, spacecraft launching

China and Egypt have signed cooperation documents in space exploration in Beijing on Wednesday to boost deep space exploration, spacecraft development and construction of space infrastructure, which is of great significance to foster a comprehensive strategic partnership between the two countries.

Zhang Kejian, administrator of the China National Space Administration (CNSA) and Sherif Sedky, Chief Operating Officer of the Egyptian Space Agency (EGSA), signed a memorandum of understanding between the governments of the two countries on space cooperation and peaceful use of outer space and a cooperation agreement between the CNSA and the EGSA on the International Lunar Research Station (ILRS).

According to the cooperation documents, both sides will encourage joint researches and development cooperation in a variety of areas including lunar and deep space exploration, development and launch of spacecraft, construction of space infrastructure, satellite data reception and application, the BRICS Remote Sensing Satellite Constellation, space science and astronomical observation.

They will also collaborate on the joint demonstration and research of the ILRS, space missions, space systems and subsystems, space equipment, ground segments and applications, education and training and capacity building.

China and Egypt have achieved fruitful results in space cooperation. The China-assisted Egyptian Satellite Assembly, Integration and Test Center completed the acceptance checks in June this year. The China-funded MisrSat-2 satellite completed its assembly and testing at the center and was launched on Monday.

The satellite MisrSat-2, launched by a Long March-2C carrier rocket from the Jiuquan Satellite Launch Center in Northwest China's Gansu Province, will be used in Egypt's land and resource utilization, water conservancy, agriculture, and other fields. It is a landmark project of deep cooperation between China and Egypt in the field of aerospace high-tech, and is of milestone significance in aerospace cooperation between the two countries, according to the CNSA.

The signing of these space agreements between China and Egypt will guide future collaboration and play a significant role in advancing space technology and fostering comprehensive strategic partnerships between the two countries, said CNSA in a press release on Wednesday.

Italy: The Week of Italian Cuisine in the World kicks off in Beijing, Tianjin and Qingdao

The Week of Italian Cuisine in the World kicked off on Monday, with the aim to promote exquisite Italian cooking, the Mediterranean diet, Italian agri-food products and wine. In the 2023 edition, as in past years, the week will be further enhanced by activities organized by the Italian Embassy in China together with the Italian business community operating in China. 

Several Italian restaurants in Beijing, Tianjin, and Qingdao have been preparing special menus and typical dishes for Chinese friends and expatriates residing in China to enjoy throughout the Italian cuisine week that is set to run until November 19. Beijing's ABBOCCA restaurant, for instance, has provided a special selection for homemade fresh cheeses called "TRILOGY," which includes mozzarella, stracciatella, and ricotta, and has been dubbed a tasty journey through salty and sweet to stimulate all senses complete with fresh basil leaves, cherry tomatoes.

A new map exhibit documents evolving views of Earth’s interior

Much of what happens on the Earth’s surface is connected to activity far below. “Beneath Our Feet,” a temporary exhibit at the Norman B. Leventhal Map Center in the Boston Public Library, explores the ways people have envisioned, explored and exploited what lies underground.

“We’re trying to visualize those places that humans don’t naturally go to,” says associate curator Stephanie Cyr. “Everybody gets to see what’s in the sky, but not everyone gets to see what’s underneath.”
“Beneath Our Feet” displays 70 maps, drawings and archaeological artifacts in a bright, narrow exhibit space. (In total, the library holds a collection of 200,000 maps and 5,000 atlases.) Many objects have two sets of labels: one for adults and one for kids, who are guided by a cartoon rat mascot called Digger Burrows.

The layout puts the planet’s long history front and center. Visitors enter by walking over a U.S. Geological Survey map of North America that is color-coded to show how topography has changed over geologic time.
Beyond that, the exhibit is split into two main themes, Cyr says: the natural world, and how people have put their fingerprints on it. Historical and modern maps hang side by side, illustrating how ways of thinking about the Earth developed as the tools for exploring it improved.

For instance, a 1665 illustration drawn by Jesuit scholar Athanasius Kircher depicts Earth’s water systems as an underground network that churned with guidance from a large ball of fire in the planet’s center, Cyr says. “He wasn’t that far off.” Under Kircher’s drawing is an early sonar map of the seafloor in the Pacific Ocean, made by geologists Marie Tharp and Bruce Heezen in 1969 (SN: 10/6/12, p. 30). Their maps revealed the Mid-Atlantic Ridge. Finding that rift helped to prove the existence of plate tectonics and that Earth’s surface is shaped by the motion of vast subsurface forces.

On another wall, a 1794 topological-relief drawing of Mount Vesuvius — which erupted and destroyed the Roman city of Pompeii in A.D. 79 — is embellished by a cartouche of Greek mythological characters, including one representing death. The drawing hangs above a NASA satellite image of the same region, showing how the cities around Mount Vesuvius have grown since the eruption that buried Pompeii, and how volcano monitoring has improved.

The tone turns serious in the latter half of the exhibit. Maps of coal deposits in 1880s Pennsylvania sit near modern schematics explaining how fracking works (SN: 9/8/12, p. 20). Reproductions of maps of the Dakotas from 1886 may remind visitors of ongoing controversies with the Dakota Access Pipeline, proposed to run near the Standing Rock Sioux Reservation, and maps from the U.S. Environmental Protection Agency mark sites in Flint, Mich., with lead-tainted water.

Maps in the exhibit are presented dispassionately and without overt political commentary. Cyr hopes the zoomed-out perspectives that maps provide will allow people to approach controversial topics with cool heads.

“The library is a safe place to have civil discourse,” she says. “It’s also a place where you have access to factual materials and factual resources.”

A key virus fighter is implicated in pregnancy woes

An immune system mainstay in the fight against viruses may harm rather than help a pregnancy. In Zika-infected mice, this betrayal appears to contribute to fetal abnormalities linked to the virus, researchers report online January 5 in Science Immunology. And it could explain pregnancy complications that arise from infections with other pathogens and from autoimmune disorders.

In pregnant mice infected with Zika virus, those fetuses with a docking station, or receptor, for immune system proteins called type I interferons either died or grew more poorly compared with fetuses lacking the receptor. “The type I interferon system is one of the key mechanisms for stopping viral infections,” says Helen Lazear, a virologist at the University of North Carolina at Chapel Hill, who coauthored an editorial accompanying the study. “That same [immune] process is actually causing fetal damage, and that’s unexpected.”
Cells infected by viruses begin the fight against the intruder by producing type I interferons. These proteins latch onto their receptor on the surfaces of neighboring cells and kick-start the production of hundreds of other antiviral proteins.

Akiko Iwasaki, a Howard Hughes Medical Institute investigator and immunologist at Yale School of Medicine, and her colleagues were interested in studying what happens to fetuses when moms are sexually infected with Zika virus. The researchers mated female mice unable to make the receptor for type I interferons to males with one copy of the gene needed to make the receptor. This meant that moms would carry some pups with the receptor and some without in the same pregnancy.

Pregnant mice were infected vaginally with Zika at one of two times — one corresponding to mid‒first trimester in humans, the other to late first trimester. Of the fetuses exposed to infection earlier, those that had the interferon receptor died, while those without the receptor continued to develop. For fetuses exposed to infection a bit later in the pregnancy, those with the receptor were much smaller than their receptor-lacking counterparts.

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The fetuses without the receptor still grew poorly due to the Zika infection, which is expected given their inability to fight the infection. What was striking, Iwasaki says, is that the fetuses able to fight the infection were more damaged, and were the only fetuses that died.

It’s unclear how this antiviral immune response causes fetal damage. But the placentas—which, like their fetuses, had the receptor — didn’t appear to provide those fetuses with enough oxygen, Iwasaki says.

The researchers also infected pregnant mice that had the receptor for type I interferons with a viral mimic — a bit of genetic material that goads the body to begin its antiviral immune response — to see if the damage happened only during a Zika infection. These fetuses also died early in the pregnancy, an indication that perhaps the immune system could cause fetal damage during other viral infections, Iwasaki notes.

Iwasaki and colleagues next added type I interferon to samples of human placental tissue in dishes. After 16 to 20 hours, the placental tissues developed structures that resembled syncytial knots. These knots are widespread in the placentas of pregnancies with such complications as preeclampsia and restricted fetal growth.

Figuring out which of the hundreds of antiviral proteins made when type I interferon ignites the immune system can trigger placental and fetal damage is the next step, says Iwasaki. That could provide more understanding of miscarriage generally; other infections that cause congenital diseases, like toxoplasmosis and rubella; and autoimmune disorders that feature excessive type I interferon production, such as lupus, she says.

The great Pacific garbage patch may be 16 times as massive as we thought

We’re going to need a bigger trash can.

A pooling of plastic waste floating in the ocean between California and Hawaii contains at least 79,000 tons of material spread over 1.6 million square kilometers, researchers report March 22 in Scientific Reports. That’s the equivalent to the mass of more than 6,500 school buses. Known as the great Pacific garbage patch, the hoard is four to 16 times as heavy as past estimates.

About 1.8 trillion plastic pieces make up the garbage patch, the scientists estimate. Particles smaller than half a centimeter, called microplastics, account for 94 percent of the pieces, but only 8 percent of the overall mass. In contrast, large (5 to 50 centimeters) and extra-large (bigger than 50 centimeters) pieces made up 25 percent and 53 percent of the estimated patch mass.
Much of the plastic in the patch comes from humans’ ocean activities, such as fishing and shipping, the researchers found. Almost half of the total mass, for example, is from discarded fishing nets. A lot of that litter contains especially durable plastics, such as polyethylene and polypropylene, which are designed to survive in marine environments.
To get the new size and mass estimates, Laurent Lebreton of the Ocean Cleanup, a nonprofit foundation in Delft, the Netherlands, and his colleagues trawled samples from the ocean surface, took aerial images and simulated particle pathways based on plastic sources and ocean circulation.
Aerial images provided more accurate tallies and measurements of the larger plastic pieces, the researchers write. That could account for the increase in mass over past estimates, which relied on trawling data and images taken from boats, in addition to computer simulations. Another possible explanation: The patch grew — perhaps driven by an influx of debris from the 2011 tsunami that hit Japan and washed trash out to sea (SN: 10/28/17, p. 32).

Hayabusa2 has blasted the surface of asteroid Ryugu to make a crater

Hayabusa2 has blasted the asteroid Ryugu with a projectile, probably adding a crater to the small world’s surface and stirring up dust that scientists hope to snag.

The projectile, a two-kilogram copper cylinder, separated from the Hayabusa2 spacecraft at 9:56 p.m. EDT on April 4, JAXA, Japan’s space agency, reports.

Hayabusa2 flew to the other side of the asteroid to hide from debris that would have been ejected when the projectile hit (SN: 1/19/19, p. 20). Scientists won’t know for sure whether the object successfully made a crater, and, if so, how big it is, until the craft circles back. But by 10:36 p.m. EDT, Hayabusa2’s cameras had captured a blurry shot of a dust plume spurting up from Ryugu, so the team thinks the attempt worked.
“This is the world’s first collision experiment with an asteroid!” JAXA tweeted.

Hayabusa2 plans to briefly touch down inside the crater to pick up a pinch of asteroid dust. The spacecraft has already grabbed one sample of Ryugu’s surface (SN Online: 2/22/19). But dust exposed by the impact will give researchers a look at the asteroid’s subsurface, which has not been exposed to sunlight or other types of space radiation for up to billions of years.

If all goes as planned, Hayabusa2 will return to Earth with both samples in late 2020. A third planned sample pickup has been scrapped because Ryugu’s boulder-strewn surface is so hazardous for the spacecraft.
Comparing the two samples will reveal details of how being exposed to space changes the appearance and composition of rocky asteroids, and will help scientists figure out how Ryugu formed (SN Online: 3/20/19). Scientists hope that the asteroid contains water and organic material that might help explain how life got started in the solar system.

A Greek skull may belong to the oldest human found outside of Africa

A skull found in a cliffside cave on Greece’s southern coast in 1978 represents the oldest Homo sapiens fossil outside Africa, scientists say.

That skull, from an individual who lived at least 210,000 years ago, was encased in rock that also held a Neandertal skull dating to at least 170,000 years ago, contends a team led by paleoanthropologist Katerina Harvati of the University of Tübingen in Germany.

If these findings, reported online July 10 in Nature, hold up, the ancient Greek H. sapiens skull is more than 160,000 years older than the next oldest European H. sapiens fossils (SN Online: 11/2/11). It’s also older than a proposed H. sapiens jaw found at Israel’s Misliya Cave that dates to between around 177,000 and 194,000 years ago (SN: 2/17/18, p. 6).

“Multiple Homo sapiens populations dispersed out of Africa starting much earlier, and reaching much farther into Europe, than previously thought,” Harvati said at a July 8 news conference. African H. sapiens originated roughly 300,000 years ago (SN: 7/8/17, p. 6).
A small group of humans may have reached what’s now Greece more than 200,000 years ago, she suggested. Neandertals who settled in southeastern Europe not long after that may have replaced those first H. sapiens. Then humans arriving in Mediterranean Europe tens of thousands of years later would eventually have replaced resident Neandertals, who died out around 40,000 years ago (SN Online: 6/26/19).

But Harvati’s group can’t exclude the possibility that H. sapiens and Neandertals simultaneously inhabited southeastern Europe more than 200,000 years ago and sometimes interbred. A 2017 analysis of ancient and modern DNA concluded that humans likely mated with European Neandertals at that time.

The two skulls were held in a small section of wall that had washed into Greece’s Apidima Cave from higher cliff sediment and then solidified roughly 150,000 years ago. Since one skull is older than the other, each must originally have been deposited in different sediment layers before ending up about 30 centimeters apart on the cave wall, the researchers say.
Earlier studies indicated that one Apidima skull, which retains the face and much of the braincase, was a Neandertal that lived at least 160,000 years ago. But fossilization and sediment pressures had distorted the skull’s shape. Based on four 3-D digital reconstructions of the specimen, Harvati’s team concluded that its heavy brow ridges, sloping face and other features resembled Neandertal skulls more than ancient and modern human skulls. An analysis of the decay rate of radioactive forms of uranium in skull bone fragments produced an age estimate of at least 170,000 years.

A second Apidima fossil, also dated using uranium analyses, consists of the back of a slightly distorted braincase. Its rounded shape in a digital reconstruction characterizes H. sapiens, not Neandertals, the researchers say. A bunlike bulge often protrudes from the back of Neandertals’ skulls.
But without any facial remains to confirm the species identity of the partial braincase, “it is still possible that both Apidima skulls are Neandertals,” says paleoanthropologist Israel Hershkovitz of Tel Aviv University. Hershkovitz led the team that discovered the Misliya jaw and assigned it to H. sapiens.

Harvati and her colleagues will try to extract DNA and species-distinguishing proteins (SN: 6/8/19, p. 6) from the Greek skulls to determine their evolutionary identities and to look for signs of interbreeding between humans and Neandertals.

The find does little to resolve competing explanations of how ancient humans made their way out of Africa. Harvati’s suggestion that humans trekked from Africa to Eurasia several times starting more than 200,000 years ago is plausible, says paleoanthropologist Eric Delson of City University of New York’s Lehman College in an accompanying commentary. And the idea that some H. sapiens newcomers gave way to Neandertals probably also applied to humans who reached Misliya Cave and nearby Middle Eastern sites as late as around 90,000 years ago, before Neandertals occupied the area by 60,000 years ago, Delson says.

Hershkovitz disagrees. Ancient humans and Neandertals lived side-by-side in the Middle East for 100,000 years or more and occasionally interbred, he contends. Misliya Cave sediment bearing stone tools dates to as early as 274,000 years ago, Hershkovitz says. Since only H. sapiens remains have been found in the Israeli cave, ancient humans probably made those stone artifacts and could have been forerunners of Greek H. sapiens.

How meningitis-causing bacteria invade the brain

Bacteria can slip into the brain by commandeering cells in the brain’s protective layers, a new study finds. The results hint at how a deadly infection called bacterial meningitis takes hold.

In mice infected with meningitis-causing bacteria, the microbes exploit previously unknown communication between pain-sensing nerve cells and immune cells to slip by the brain’s defenses, researchers report March 1 in Nature. The results also hint at a new way to possibly delay the invasion — using migraine medicines to interrupt those cell-to-cell conversations.
Bacterial meningitis is an infection of the protective layers, or meninges, of the brain that affects 2.5 million people globally per year. It can cause severe headaches and sometimes lasting neurological injury or death.

“Unexpectedly, pain fibers are actually hijacked by the bacteria as they’re trying to invade the brain,” says Isaac Chiu, an immunologist at Harvard Medical School in Boston. Normally, one might expect pain to be a warning system for us to shut down the bacteria in some way, he says. “We found the opposite…. This [pain] signal is being used by the bacteria for an advantage.”

It’s known that pain-sensing neurons and immune cells coexist in the meninges, particularly in the outermost layer called the dura mater (SN: 11/11/20). So to see what role the pain and immune cells play in bacterial meningitis, Chiu’s team infected mice with two of the bacteria known to cause the infection in humans: Streptococcus pneumoniae and S. agalactiae. The researchers then observed where that bacteria ended up in mice genetically tweaked to lack pain-sensing nerve cells and compared those resting spots to those in mice with the nerve cells intact.

Mice without pain-sensing neurons had fewer bacteria in the meninges and brain than those with the nerve cells, the team found. This contradicts the idea that pain in meningitis serves as a warning signal to the body’s immune system, mobilizing it for action.

Further tests showed that the bacteria triggered a chain of immune-suppressing events, starting with the microbes secreting toxins in the dura mater.

The toxins hitched onto the pain neurons, which in turn released a molecule called CGRP. This molecule is already known to bind to a receptor on immune cells, where it helps control the dura mater’s immune responses. Injecting infected mice with more CGRP lowered the number of dural immune cells and helped the infection along, the researchers found.

The team also looked more closely at the receptor that CGRP binds to. In infected mice bred without the receptor, fewer bacteria made it into the brain. But in ones with the receptor, immune cells that would otherwise engulf bacteria and recruit reinforcements were disabled.
The findings suggest that either preventing the release of CGRP or preventing it from binding to immune cells might help delay infection.

In humans, neuroscientists know that CGRP is a driver of headaches — it’s already a target of migraine medications (SN: 6/5/18). So the researchers gave five mice the migraine medication olcegepant, which blocks CGRP’s effects, and infected them with S. pneumoniae. After infection, the medicated mice had less bacteria in the meninges and brain, took longer to show symptoms, didn’t lose as much weight and survived longer than mice that were not given the medication.

The finding suggests olcegepant slowed the infection. Even though it only bought mice a few extra hours, that’s crucial in meningitis, which can develop just as quickly. Were olcegepant to work the same way in humans, it might give doctors more time to treat meningitis. But the effect is probably not as dramatic in people, cautions Michael Wilson, a neurologist at the University of California, San Francisco who wasn’t involved with the work.

Scientists still need to determine whether pain-sensing nerve cells and immune cells have the same rapport in human dura mater, and whether migraine drugs could help treat bacterial meningitis in people.

Neurologist Avindra Nath has doubts. Clinicians think the immune response and inflammation damage the brain during meningitis, says Nath, who heads the team investigating nervous system infections at the National Institute of Neurological Disorders and Stroke in Bethesda, Md. So treatment involves drugs that suppress the immune response, rather than enhance it as migraine medications might.

Chiu acknowledges this but notes there might be room for both approaches. If dural mater immune cells could head the infection off at the pass, it may keep some bacteria from penetrating the defenses, minimizing brain inflammation.

This study might not ultimately change how clinicians treat patients, Wilson says. But it still reveals something new about one of the first lines of defense for the brain.

The Milky Way may be spawning many more stars than astronomers had thought

The Milky Way is churning out far more stars than previously thought, according to a new estimate of its star formation rate.

Gamma rays from aluminum-26, a radioactive isotope that arises primarily from massive stars, reveal that the Milky Way converts four to eight solar masses of interstellar gas and dust into new stars each year, researchers report in work submitted to arXiv.org on January 24. That range is two to four times the conventional estimate and corresponds to an annual birthrate in our galaxy of about 10 to 20 stars, because most stars are less massive than the sun.
At this rate, every million years — a blink of the eye in astronomical terms — our galaxy spawns 10 million to 20 million new stars. That’s enough to fill roughly 10,000 star clusters like the beautiful Pleiades cluster in the constellation Taurus. In contrast, many galaxies, including most of the ones that orbit the Milky Way, make no new stars at all.

“The star formation rate is very important to understand for galaxy evolution,” says Thomas Siegert, an astrophysicist at the University of Würzburg in Germany. The more stars a galaxy makes, the faster it enriches itself with oxygen, iron and the other elements that stars create. Those elements then alter star-making gas clouds and can change the relative number of large and small stars that the gas clouds form.

Siegert and his colleagues studied the observed intensity and spatial distribution of emission from aluminum-26 in our galaxy. A massive star creates this isotope during both life and death. During its life, the star blows the aluminum into space via a strong wind. If the star explodes when it dies, the resulting supernova forges more. The isotope, with a half-life of 700,000 years, decays and gives off gamma rays.

Like X-rays, and unlike visible light, gamma rays penetrate the dust that cloaks the youngest stars. “We’re looking through the entire galaxy,” Siegert says. “We’re not X-raying it; here we’re gamma-raying it.”

The more stars our galaxy spawns, the more gamma rays emerge. The best match with the observations, the researchers find, is a star formation rate of four to eight solar masses a year. That is much higher than the standard estimate for the Milky Way of about two solar masses a year.

The revised rate is very realistic, says Pavel Kroupa, an astronomer at the University of Bonn in Germany who was not involved in the work. “I’m very impressed by the detailed modeling of how they account for the star formation process,” he says. “It’s a very beautiful work. I can see some ways of improving it, but this is really a major step in the absolutely correct direction.”

Siegert cautions that it is difficult to tell how far the gamma rays have traveled before reaching us. In particular, if some of the observed emission arises nearby — within just a few hundred light-years of us — then the galaxy has less aluminum-26 than the researchers have calculated, which means the star formation rate is on the lower side of the new estimate. Still, he says it’s unlikely to be as low as the standard two solar masses per year.
In any event, the Milky Way is the most vigorous star creator in a collection of more than 100 nearby galaxies called the Local Group. The largest Local Group galaxy, Andromeda, converts only a fraction of a solar mass of gas and dust into new stars a year. Among Local Group galaxies, the Milky Way ranks second in size, but its high star formation rate means that we definitely try a lot harder.

Psychedelics may improve mental health by getting inside nerve cells

Psychedelics go beneath the cell surface to unleash their potentially therapeutic effects.

These drugs are showing promise in clinical trials as treatments for mental health disorders (SN: 12/3/21). Now, scientists might know why. These substances can get inside nerve cells in the cortex — the brain region important for consciousness — and tell the neurons to grow, researchers report in the Feb. 17 Science.

Several mental health conditions, including depression and post-traumatic stress disorder, are tied to chronic stress, which degrades neurons in the cortex over time. Scientists have long thought that repairing the cells could provide therapeutic benefits, like lowered anxiety and improved mood.
Psychedelics — including psilocin, which comes from magic mushrooms, and LSD — do that repairing by promoting the growth of nerve cell branches that receive information, called dendrites (SN: 11/17/20). The behavior might explain the drugs’ positive outcomes in research. But how they trigger cell growth was a mystery.

It was already known that, in cortical neurons, psychedelics activate a certain protein that receives signals and gives instructions to cells. This protein, called the 5-HT2A receptor, is also stimulated by serotonin, a chemical made by the body and implicated in mood. But a study in 2018 determined that serotonin doesn’t make these neurons grow. That finding “was really leaving us scratching our heads,” says chemical neuroscientist David Olson, director of the Institute for Psychedelics and Neurotherapeutics at the University of California, Davis.

To figure out why these two types of chemicals affect neurons differently, Olson and colleagues tweaked some substances to change how well they activated the receptor. But those better equipped to turn it on didn’t make neurons grow. Instead, the team noticed that “greasy” substances, like LSD, that easily pass through cells’ fatty outer layers resulted in neurons branching out.

Polar chemicals such as serotonin, which have unevenly distributed electrical charges and therefore can’t get into cells, didn’t induce growth. Further experiments showed that most cortical neurons’ 5-HT2A receptors are located inside the cell, not at the surface where scientists have mainly studied them.

But once serotonin gained access to the cortical neurons’ interior — via artificially added gateways in the cell surface — it too led to growth. It also induced antidepressant-like effects in mice. A day after receiving a surge in serotonin, animals whose brain cells contained unnatural entry points didn’t give up as quickly as normal mice when forced to swim. In this test, the longer the mice tread water, the more effective an antidepressant is predicted to be, showing that inside access to 5-HT2A receptors is key for possible therapeutic effects.

“It seems to overturn a lot about what we think should be true about how these drugs work,” says neuroscientist Alex Kwan of Cornell University, who was not involved in the study. “Everybody, including myself, thought that [psychedelics] act on receptors that are on the cell surface.”
That’s where most receptors that function like 5-HT2A are found, says biochemist Javier González-Maeso of the Virginia Commonwealth University in Richmond, who was also not involved in the work.

Because serotonin can’t reach 5-HT2A receptors inside typical cortical neurons, Olson proposes that the receptors might respond to a different chemical made by the body. “If it’s there, it must have some kind of role,” he says. DMT, for example, is a naturally occurring psychedelic made by plants and animals, including humans, and can reach a cell’s interior.

Kwan disagrees. “It’s interesting that psychedelics can act on them, but I don’t know if the brain necessarily needs to use them when performing its normal function.” Instead, he suggests that the internal receptors might be a reserve pool, ready to replace those that get degraded on the cell surface.

Either way, understanding the cellular mechanisms behind psychedelics’ potential therapeutic effects could help scientists develop safer and more effective treatments for mental health disorders.

“Ultimately, I hope this leads to better medicines,” Olson says.