Brain Stimulation? - Olfactory Map - Genes & Memory - Food Noise

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Marc Breedlove

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May 2, 2026, 6:34:06 AMMay 2

https://www.nytimes.com/2026/04/28/health/depression-at-home-brain-stimulation-fda.html

Could At-Home Brain Stimulation Reduce Psychiatry’s Reliance on S.S.R.I.s?

By Rachel E. Gross

The first question Sophie Davies had was: Will it affect my memory?

In the three weeks since giving birth, Ms. Davies had been in a downward spiral. She checked herself into the mother-and-baby unit of her hospital in East Anglia, England, where doctors ratcheted up the dose of Prozac she took to manage her obsessive-compulsive disorder.

But every morning she woke up in tears, and every time she looked at her baby boy, she felt hollow with guilt. “I’m never going to be able to be a mom,” she recalled thinking, “or if I am, I’m not going to be able to be a good one.”

A month in, a hospital worker suggested she try a headset that used an electric current to treat depression. The word “electric” gave Ms. Davies, then 34, pause. It sounded like electroconvulsive therapy, or ECT, the scary-sounding treatment that triggers seizures and can result in memory loss.

This therapy was different. Transcranial direct-current stimulation, or tDCS, uses a weak electric current to shock the brain and does not produce seizures.

“This is as far from ECT as a jet engine is from my bicycle,” Dr. Mark George, of the Medical University of South Carolina, where he is a leading expert in neuromodulation, a term that encompasses all therapies that use electricity to modify brain function.

Ms. Davies did an internet search and confirmed that the side effects of tDCS — ringing in the ears, headaches and mild burns or irritation where the electrode pads touched the forehead — were generally transient and didn’t include amnesia. She decided to give it a try.

In England, the brain stimulation device has been approved for treating depression since 2019. It can be prescribed by a doctor or purchased over the counter, where it sells for around $530.

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https://www.nature.com/articles/d41586-026-00894-1

First detailed ‘smell maps’ reveal how noses track odours

Chris Simms

Olfactory receptors in the mouse nose have been mapped out in unprecedented detail — overturning researchers’ understanding of how noses build a sense of smell.

The research, published today in Cell1, shows how around 1,100 olfactory receptors expressed on sensory neurons are organized in tightly regulated spatial locations in the epithelial tissue that lines the nasal cavity. A second study2 provides a complementary atlas of olfactory receptor expression in the olfactory epithelium and their neural connections to the olfactory bulb in the brain.

“For 30 years, we’ve taught students that the mouse olfactory epithelium is divided into a handful of broad zones, within which receptor choice is essentially random,” says Johan Lundström, a psychologist and experimental neuroscientist at the Karolinska Institute in Stockholm.

In the study, researchers examined about five million neurons from hundreds of individual mice. They first used single-cell sequencing to identify which smell receptors were expressed by neurons in the nose, and then used spatial transcriptomics to map out where key genes were being expressed. This allowed them to pinpoint where the receptors are and show that they are always arranged in horizontal stripes running from the top of the nose to the bottom.

“Each receptor adopts a particular position in the nose. Since there are a thousand positions in the nose, each receptor is expressed basically in a stripe that overlaps with other receptor stripes, in a thousand overlapping stripes,” says study co-author Sandeep Robert Datta, a neurobiologist at Harvard Medical School in Boston, Massachusetts.

Datta and his colleagues propose that this spatial mapping is organized during development and is controlled by sets of genes. The authors found that a molecule called retinoic acid had a key role in this process. They discovered a gradient in the amount of retinoic acid present at different points in the nose. By tweaking how much this molecule was expressed, they showed that it helps to control gene activity, guiding each neuron to express the correct type of smell receptor for its location.

https://www.thetransmitter.org/memory/new-study-questions-role-of-persistent-gene-activity-in-memory-maintenance/

New study questions role of persistent gene activity in memory maintenance

By Siddhant Pusdekar

Transcriptional changes are essential for converting new experiences into memories but may not be required to make memories last, a new study suggests.

The findings, published in eNeuro in March, conflict with a model proposing that positive feedback loops of transcription can help maintain long-term memories, says study investigator Irina Calin-Jageman, professor of biological sciences at Dominican University. But they open up a set of hypotheses about how transcription maintains long-term memories and indicate that the handful of genes whose regulation persists for up to two weeks could be “really key,” she adds.

The results, obtained in the sea slug Aplysia californica, are “one small step on our way to understanding this very important question of: What is the role of transcription in forming long-term memories?” says Wayne Sossin, distinguished James McGill professor of neurology and neurosurgery at McGill University, who is listed as a reviewer for the paper. Disproving models doesn’t “get the attention it deserves, I think, from the scientific community,” he says, but science is built on overturning theory.

Irina Calin-Jageman and her colleagues focused on the transcriptional traces of a partially faded memory in the sea slug. When the animal feels threatened, it retracts a breathing apparatus on its back called a siphon. After traumatic experiences—such as induced shocks—the slug retracts its siphon for longer than usual, previous work showed. Also, sensory neurons in the pleural ganglia change their gene expression patterns and remain more excitable for up to 24 hours, and synaptic changes can last for several days to weeks, depending on the training.

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https://knowablemagazine.org/content/article/mind/2026/what-addiction-does-to-synapses-in-brain

What addiction does to the brain

By Emma Yasinski

“Relapse is a part of recovery”: That’s a common refrain among professionals who treat substance use disorders. Many people who have completed treatment programs return to substance use and reenter treatment multiple times, after days, weeks or even years of sobriety.

Marina Wolf, a behavioral neuroscientist at the Oregon Health & Science University, studies how cells in the brain respond to drug exposure in ways that can lead people to develop powerful cravings even months after they stop using drugs such as cocaine, opioids or alcohol. Specifically, she has focused on an aspect of this problem called cue-induced craving, in which people’s brains come to associate a cue — such as seeing a certain location where they previously used drugs — with the desire to use that drug. These learned associations, as she described in the 2025 Annual Review of Pharmacology and Toxicology, are caused by structural changes to the brain — neuroplasticity — as a result of drug use, including the strengthening of connections, called synapses, between specific nerve cells.

These changes don’t disappear as soon as a person, or animal, stops using a drug. Cravings, in fact, can strengthen after abstinence, leaving a person vulnerable to resume using.

How did you become interested in neuroplasticity and addiction?

I never had any formal training in synaptic plasticity or addiction. As a graduate student and then a postdoctoral fellow, I worked on how neurons are regulated by the neurotransmitter dopamine, but we studied dopamine’s role in antipsychotic drug effects, not addiction. But when I was setting up my own lab in the early 1990s, I had a friend from graduate school who was involved in groundbreaking studies to work out synaptic plasticity mechanisms in the brain’s hippocampus, a region of the brain responsible for encoding memories. This was fascinating work that helped demonstrate a critical role for a neurotransmitter called glutamate in synaptic plasticity, so I followed it closely.

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https://www.nytimes.com/2026/04/27/health/food-noise-obesity-drugs-glp-1.html

The Day the Food Noise Died

By Gina Kolata

Before the new obesity drugs came on the market, almost no one used the term food noise.

Researchers studying and developing drugs like Ozempic, Wegovy, Mounjaro and Zepbound analyzed doses, side effects, weight loss and improvements in conditions such as diabetes, heart disease and sleep apnea. Incessant thoughts about food and internal dialogues about what to eat, what not to eat, when to eat, how to resist eating — these were not on the research agenda.

But if the obesity-drug researchers weren’t talking about food noise, people taking GLP-1s had a lot to say about it. For as long as they could remember, users of the drugs said, they had been plagued by food noise. But they thought it was just a normal part of life. They thought everyone had it.

Until they took one of the new drugs.

Suddenly, food noise was silenced.

And that effect is leading to new questions about the drugs. If researchers can clarify the source of this inner buzz and what makes it go away, that could lead to a clearer understanding of what causes obesity in the first place.
‘You Don’t Want the Salad’

People who struggle with their weight describe relentless thoughts of food.

Lena Smith Parker, 53, of Hamden, Conn., spent decades dieting and regaining weight. All the while, she said, she was plagued by internal voices urging her to eat and shaming her for eating.
© 2026 The New York Times Company

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https://www.theguardian.com/science/2026/apr/29/dogs-brains-shrink-5000-years-ago

Dogs’ brains began to shrink at least 5,000 years ago

Nicola Davis Science correspondent

It has long been known that dogs have less between their ears than wolves, but now research has suggested their brains started to get smaller at least 5,000 years ago.

Experts say the results offer fresh insights into the domestication of our canine companions. However, the findings are unlikely to explain why your spaniel will only drink from a muddy puddle: the researchers say a reduction in brain size does not mean dogs are dafter than their wolf-like ancestors.

“The way our dogs live nowadays doesn’t give them the opportunity to always express most of their intelligence,” said Dr Thomas Cucchi, first author of the study from the French National Centre for Scientific Research.

“But they are extremely clever and domestication didn’t make them stupid, but made them really capable of reading us and communicating with us.”

The relationship between humans and canines is ancient, with research revealing the oldest direct genetic evidence for domestic dogs dates back more than 15,000 years.

But while a reduction in brain size is typically considered a hallmark of domestication, there has long been debate over exactly when dogs ended up with smaller brains than wolves, with some experts suggesting this may have occurred early in the dog-human relationship.

However, others argue smaller brain size is not a hallmark of domestication but instead reflects the emergence of pedigree breeds in the last 200 years.

Writing in the journal Royal Society Open Science, Cucchi and colleagues studied CT scans of the skulls of 22 prehistoric wolves and dogs, dating from 35,000 to 5,000 years ago, as well as CT scans from the skulls of 59 modern wolves and 104 modern dogs. The latter included different modern breeds as well as stray or “village” dogs, and dingoes.

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