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When we experience a new event, our brain records a memory of not only what happened, but also the context, including the time and location of the event. A new study from MIT neuroscientists sheds light on how the timing of memory is encoded in the hippocampus and suggests that time and space are encoded separately.

In a study of mice, the researchers identified a hippocampal circuit that the animals used to store information about the timing of when they should turn left or right in a maze. When this circuit was blocked, the mice were unable to remember which way they were supposed to turn next. However, disrupting the circuit did not appear to impair their memory of where they were in space.

The findings add to a growing body of evidence suggesting that when we form new memories, different populations of neurons in the brain encode time and place information, the researchers say.

The attentional control that organisms need to succeed in their goals comes from two abilities: the focus to ignore distractions and the discipline to curb impulses. A new study by MIT neuroscientists shows that these abilities are independent, but that the activity of norepinephrine-producing neurons in a single brain region, the locus coeruleus, controls both by targeting two distinct areas of the prefrontal cortex.

“Our results demonstrate a fundamental causal role of LC neuronal activation in the implementation of attentional control by the selective modulation of neural activity in its target areas,” wrote the authors of the study from the research group of Susumu Tonegawa, Picower Professor of Biology and Neuroscience at RIKEN-MIT Laboratory of Neural Circuit Genetics at The Picower Institute for Learning and Memory and Howard Hughes Medical Institute.

Imagine you are meeting a friend for dinner at a new restaurant. You may try dishes you haven’t had before, and your surroundings will be completely new to you. However, your brain knows that you have had similar experiences — perusing a menu, ordering appetizers, and splurging on dessert are all things that you have probably done when dining out.

MIT neuroscientists have now identified populations of cells that encode each of these distinctive segments of an overall experience. These chunks of memory, stored in the hippocampus, are activated whenever a similar type of experience takes place, and are distinct from the neural code that stores detailed memories of a specific location.

The researchers believe that this kind of “event code,” which they discovered in a study of mice, may help the brain interpret novel situations and learn new information by using the same cells to represent similar experiences.

When you expect a really bad experience to happen and then it doesn’t, it’s a distinctly positive feeling. A new study of fear extinction training in mice may suggest why: The findings not only identify the exact population of brain cells that are key for learning not to feel afraid anymore, but also show these neurons are the same ones that help encode feelings of reward.

The study, published Jan. 14 in Neuron by scientists at MIT’s Picower Institute for Learning and Memory, specifically shows that fear extinction memories and feelings of reward alike are stored by neurons that express the gene Ppp1r1b in the posterior of the basolateral amygdala (pBLA), a region known to assign associations of aversive or rewarding feelings, or “valence,” with memories. The study was conducted by Xiangyu Zhang, a graduate student, Joshua Kim, a former graduate student, and Susumu Tonegawa, Professor of Biology and Neuroscience at RIKEN-MIT Laboratory of Neural Circuit Genetics at the Picower Institute for Learning and Memory at MIT and Howard Hughes Medical Institute.

Neuroscientists identify a circuit that helps the brain record memories of new locations.

When you enter a room, your brain is bombarded with sensory information. If the room is a place you know well, most of this information is already stored in long-term memory. However, if the room is unfamiliar to you, your brain creates a new memory of it almost immediately.

MIT neuroscientists have now discovered how this occurs. A small region of the brainstem, known as the locus coeruleus, is activated in response to novel sensory stimuli, and this activity triggers the release of a flood of dopamine into a certain region of the hippocampus to store a memory of the new location.

Existence of “silent engrams” suggests that existing models of memory formation should be revised.

Neuroscientists discover a brain circuit dedicated to retrieving memories.

When we have a new experience, the memory of that event is stored in a neural circuit that connects several parts of the hippocampus and other brain structures. Each cluster of neurons may store different aspects of the memory, such as the location where the event occurred or the emotions associated with it.

Neuroscientists who study memory have long believed that when we recall these memories, our brains turn on the same hippocampal circuit that was activated when the memory was originally formed. However, MIT neuroscientists have now shown, for the first time, that recalling a memory requires a “detour” circuit that branches off from the original memory circuit.

New findings challenge standard model of memory consolidation.

When we visit a friend or go to the beach, our brain stores a short-term memory of the experience in a part of the brain called the hippocampus. Those memories are later “consolidated” — that is, transferred to another part of the brain for longer-term storage.

A new MIT study of the neural circuits that underlie this process reveals, for the first time, that memories are actually formed simultaneously in the hippocampus and the long-term storage location in the brain’s cortex. However, the long-term memories remain “silent” for about two weeks before reaching a mature state.

Surprisingly, the neurons are located in a brain region thought to be linked with fear.

Scientists have long believed that the central amygdala, a structure located deep within the brain, is linked with fear and responses to unpleasant events.

However, a team of MIT neuroscientists has now discovered a circuit in the central amygdala that responds to rewarding events. In a study of mice, activating this circuit with certain stimuli made the animals seek those stimuli further. The researchers also found a circuit that controls responses to fearful events, but most of the neurons in the central amygdala are involved in the reward circuit, they report.

A delicate balance between positive and negative emotion

Our emotional state is governed partly by a tiny brain structure known as the amygdala, which is responsible for processing positive emotions such as happiness, and negative ones such as fear and anxiety.

A new study from MIT finds that these emotions are controlled by two populations of neurons that are genetically programmed to encode memories of either fearful or pleasurable events. Furthermore, these sets of cells inhibit each other, suggesting that an imbalance between these populations may be responsible for disorders such as depression and post-traumatic stress disorder.

Cells in the hippocampus store memories of acquaintances, a new study reports.

Mice have brain cells that are dedicated to storing memories of other mice, according to a new study from MIT neuroscientists. These cells, found in a region of the hippocampus known as the ventral CA1, store “social memories” that help shape the mice’s behavior toward each other.

The researchers also showed that they can suppress or stimulate these memories by using a technique known as optogenetics to manipulate the cells that carry these memory traces, or engrams.

“You can change the perception and the behavior of the test mouse by either inhibiting or activating the ventral CA1 cells,” says Susumu Tonegawa, the Picower Professor of Biology and Neuroscience and director of the RIKEN-MIT Center for Neural Circuit Genetics at the Picower Institute for Learning and Memory.

Tonegawa is the senior author of the study, which appears in the Sept. 29 online edition of Science. MIT postdoc Teruhiro Okuyama is the paper’s lead author.

Neuroscientists retrieve missing memories in mice with early Alzheimer’s symptoms.

In the early stages of Alzheimer’s disease, patients are often unable to remember recent experiences. However, a new study from MIT suggests that those memories are still stored in the brain — they just can’t be easily accessed.

The MIT neuroscientists report in Nature that mice in the early stages of Alzheimer’s can form new memories just as well as normal mice but cannot recall them a few days later.

Furthermore, the researchers were able to artificially stimulate those memories using a technique known as optogenetics, suggesting that those memories can still be retrieved with a little help. Although optogenetics cannot currently be used in humans, the findings raise the possibility of developing future treatments that might reverse some of the memory loss seen in early-stage Alzheimer’s, the researchers say.

Neuroscientists identify a brain circuit that is critical for forming episodic memories.

When you remember a particular experience, that memory has three critical elements — what, when, and where. MIT neuroscientists have now identified a brain circuit that processes the “when” and “where” components of memory.

This circuit, which connects the hippocampus and a region of the cortex known as entorhinal cortex, separates location and timing into two streams of information. The researchers also identified two populations of neurons in the entorhinal cortex that convey this information, dubbed “ocean cells” and “island cells.”

Previous models of memory had suggested that the hippocampus, a brain structure critical for memory formation, separates timing and context information. However, the new study shows that this information is split even before it reaches the hippocampus…

Artificially reactivating positive memories could offer an alternative to traditional antidepressants.

MIT neuroscientists have shown that they can cure the symptoms of depression in mice by artificially reactivating happy memories that were formed before the onset of depression.

The findings, described in the June 18 issue of Nature, offer a possible explanation for the success of psychotherapies in which depression patients are encouraged to recall pleasant experiences. They also suggest new ways to treat depression by manipulating the brain cells where memories are stored. The researchers believe this kind of targeted approach could have fewer side effects than most existing antidepressant drugs, which bathe the entire brain…

Scientists use optogenetics to reactivate memories that could not otherwise be retrieved.

Memories that have been “lost” as a result of amnesia can be recalled by activating brain cells with light.

In a paper published today in the journal Science, researchers at MIT reveal that they were able to reactivate memories that could not otherwise be retrieved, using a technology known as optogenetics.

The finding answers a fiercely debated question in neuroscience as to the nature of amnesia, according to Susumu Tonegawa, the Picower Professor in MIT’s Department of Biology and director of the RIKEN-MIT Center at the Picower Institute for Learning and Memory, who directed the research by lead authors Tomas Ryan, Dheeraj Roy, and Michelle Pignatelli…