How groups of neurons support the formation of memories

Amazing stuff! Too bad, the study is limited to fear memory acquisition/formation!

"... Engrams are essentially permanent physical and/or chemical changes in the brain associated with the assimilation of specific information or with the formation of new memory associations. A brain region that is known to play a key role in the learning of links between stimuli and outcomes is the CA1 area in the hippocampus.

Researchers ... carried out a study involving mice that was aimed at better understanding how groups of CA1 neurons contribute to the formation of memories. Their findings ... suggest that different groups of cells are active at different phases of learning and encode distinct aspects of experiences. ..."

"... In this study, researchers show that during the formation of a fear memory in mice, not all activated neurons play the same role. Only certain groups appear to form the core of the memory trace, known as the engram.

The team focused on the hippocampus, a key brain region for memory. Using a highly precise optogenetic tool able to label active neurons within very short time windows, they distinguished several groups of cells recruited at different moments of learning: before the shock, during the shock, during episodes of fear-related immobility (“freezing”), and outside these episodes. This temporal precision changes the scale of observation. Instead of treating all neurons activated during the experience as a single population, it becomes possible to break memory down into finer sequences.

The main result is clear. Artificially reactivating the neurons active during the shock or during freezing was enough to trigger a fear response in a different context.
By contrast, reactivating neurons recruited before the shock, or outside freezing periods, did not produce this effect.

Even more strikingly, inhibiting these same “shock” or “freezing” neurons later disrupted natural memory recall. In other words, not every cell engaged during learning becomes a memory cell. The brain appears to make a selection, as if it retained above all the neurons linked to the most salient moments of the experience. ..."

From the abstract:

"The mechanisms of associative memory formation, including which cells encode a memory and the timing of their engagement, remain poorly understood. By visualizing and tagging cells based on their calcium influx with unparalleled temporal precision, we identified nonoverlapping dorsal CA1 neuronal ensembles that are differentially active during associative fear memory acquisition. We dissected the acquisition experience into periods during which salient stimuli were presented, or certain mouse behaviors occurred, and found that cells associated with specific acquisition periods are sufficient alone to drive memory expression and contribute to fear engram formation. This study delineated the distinct identities of the cell ensembles active during learning and revealed which ones form the core engram and are essential for memory formation and recall."

How groups of neurons support the formation of memories

How the hippocampus builds memory piece by piece (original news release)

Deconstruction of a memory engram reveals distinct ensembles recruited at learning (no public access)

Histological sections of the mouse hippocampus showing labeled neurons

Scholars Discover a Universal Law of Memory

Amazing stuff! A unification of human memory and mathematics?

Human memory as a random tree with multiple key points along the way when a story is retrieved from memory. 

"... a team of IAS scholars to a surprising discovery about the individualized content and organization of our memories: they are united by a common mathematical structure.

In a study investigating how people recall stories, the team discovered a general law that governs the way we store and compress meaningful memories. Although memories align with an individualized sense of what matters, our brains use a common architecture to organize our recollections, nesting information in a hierarchical structure that helps us navigate them efficiently.

Even more striking is the team’s finding that these hierarchical structures give rise to a universal pattern in the way people encode and communicate what they remember. For the first time, scientists are offering evidence that humans compress information into a limited number of “building blocks” that represent detailed stories. 

These units of information are capacious, able to summarize ever greater swaths of information as a narrative grows. But no matter how long or short the original story—whether it is War and Peace or a quick jolt of horror from Stephen King—people will still use the same finite set of units to relay their memory of the narrative.  ...

Physics meets neuroscience

A specialist in statistical mechanics, he applies methods originating in the probabilistic explanation of complex physical systems to neuroscience. ...

This model, described as a “random tree ensemble,” highlights above all the efficiency of our biology. Our working memory—the system our brains use to hold, sort, and retrieve information for active processing—is, by nature, limited. The model displays how our brains optimize for this limitation, using hierarchical networks that cascade downward in a tree-like formation to nest details inside meaningful events.

To recall a story or a series of autobiographical events, we travel down this tree, which accounts for the complex nature of narrative memory. ...

The IAS team modeled subjects’ recollections using linguistic clauses as fundamental building blocks (similar to how physics models the collective behavior of atoms) and analyzed their structural organization statistically. 

The resulting model shows that the average length of our recall of a story does not increase in proportion with the length of the story itself. Instead, as a story becomes longer and more detailed, our brains compress the narrative into resourceful summaries. 

The model also makes an important new prediction: as narratives grow longer, a universal, scale-invariant limit emerges. 

“Whether we give people [subjects of study] a novel or a short story, the average distribution of their summarization and compression levels would be exactly the same ... “The chance a clause from the recall will summarize 10% of the story is independent of the story’s length, for example. Our brains seem to have evolved to consolidate information in this universal way to make the most of our physiology’s advantages and limitations.” ..."

From the abstract:

"Traditional studies of memory for meaningful narratives focus on specific stories and their semantic structures but do not address common quantitative features of recall across different narratives.

We introduce a statistical ensemble of random trees to represent narratives as hierarchies of key points, where each node is a compressed representation of its descendant leaves, which are the original narrative segments.

Recall from this hierarchical representation is constrained by working memory capacity. Our analytical solution aligns with observations from large-scale narrative recall experiments.

Specifically, our model explains that

(1) average recall length increases sublinearly with narrative length and

(2) individuals summarize increasingly longer narrative segments in each recall sentence.

Additionally, the theory predicts that for sufficiently long narratives, a universal, scale-invariant limit emerges, where the fraction of a narrative summarized by a single recall sentence follows a distribution independent of narrative length."

IAS Scholars Discover a Universal Law of Memory - Ideas | Institute for Advanced Study

Random Tree Model of Meaningful Memory (open access)

Fig. 1 Ensemble of random trees.

(a) Schematics of memory retrieval from a random hierarchical representation. ...

(b) Mean recalled length 𝐶 as a function of the encoded length 𝑁. ... 

(c) Distribution of the chunk size at the 𝐷th level 𝑛(𝐷) ( 𝐷 =4) given root size 𝑛(1) =𝑁; the range between tick marks in the 𝑦 axis corresponds to [0, 1].

(d) Distribution of compression ratios scaled by 𝑁 as a function of the compression ratios divided by 𝑁. Simulations of different 𝑁’s are shown in different shades of green. The red dashed line is the asymptotic scaling function from Eq. (7).

The random tree of memory, sketched on a blackboard

Pupil size in sleep reveals how memories are processed

Amazing stuff! More on the enigma of longer term memory formation!

"The eyes may be the window to the soul, but the pupil is key to understanding how, and when, the brain forms strong, long-lasting memories ...

By studying mice equipped with brain electrodes and tiny eye-tracking cameras, the researchers determined that new memories are being replayed and consolidated when the pupil is contracted during a substage of non-REM sleep.

When the pupil is dilated, the process repeats for older memories. The brain’s ability to separate these two substages of sleep with a previously unknown micro-structure is what prevents “catastrophic forgetting” in which the consolidation of one memory wipes out another one.  ...

The recordings showed that the temporal structure of sleeping mice is more varied, and more akin to the sleep stages in humans, than previously thought.

By interrupting the mice’s sleep at different moments and later testing how well they recalled their learned tasks, the researchers were able to parse the processes. When a mouse enters a substage of non-REM sleep, its pupil shrinks, and it’s here the recently learned tasks – i.e., the new memories – are being reactivated and consolidated while previous knowledge is not. Conversely, older memories are replayed and integrated when the pupil is dilated. ..."

From the abstract:

"Recently acquired memories are reactivated in the hippocampus during sleep, an initial step for their consolidation. This process is concomitant with the hippocampal reactivation of previous memories posing the problem of how to prevent interference between older and recent, initially labile, memory traces. Theoretical work has suggested that consolidating multiple memories while minimizing interference can be achieved by randomly interleaving their reactivation.

An alternative is that a temporal microstructure of sleep can promote the reactivation of different types of memories during specific substates.

Here, to test these two hypotheses, we developed a method to simultaneously record large hippocampal ensembles and monitor sleep dynamics through pupillometry in naturally sleeping mice. Oscillatory pupil fluctuations revealed a previously unknown microstructure of non-REM sleep-associated memory processes. We found that memory replay of recent experiences dominated in sharp-wave ripples during contracted pupil substates of non-REM sleep, whereas replay of previous memories preferentially occurred during dilated pupil substates. Selective closed-loop disruption of sharp-wave ripples during contracted pupil non-REM sleep impaired the recall of recent memories, whereas the same manipulation during dilated pupil substates had no behavioural effect. Stronger extrinsic excitatory inputs characterized the contracted pupil substate, whereas higher recruitment of local inhibition was prominent during dilated pupil substates. Thus, the microstructure of non-REM sleep organizes memory replay, with previous versus new memories being temporally segregated in different substates and supported by local and input-driven mechanisms, respectively. Our results suggest that the brain can multiplex distinct cognitive processes during sleep to facilitate continuous learning without interference."

Pupil size in sleep reveals how memories are processed "Cornell University researchers have found that the pupil is key to understanding how, and when, the brain forms strong, long-lasting memories."

Pupil size in sleep reveals how memories are sorted and preserved (original news release)

Sleep microstructure organizes memory replay (no public access)

Neuroscientists discover a new pathway to forming long-term memories without the formation of short term memory

Amazing stuff!

"... Their work, published in Nature Neuroscience, suggests that long-term memory can form independently of short-term memory, a finding that opens exciting possibilities for understanding memory-related conditions. ...

"The prevailing theory suggested a single pathway, where short-term memories were consolidated into long-term memories. However, we now have strong evidence of at least two distinct pathways to memory formation—one dedicated to short-term memories and another to long-term memories. This could mean our brains are more resilient than previously thought." ...

The key finding: Disrupting short-term memory formation did not block long-term memory

The research team focused on a specific enzyme in neurons called CaMKII, which is critical for short-term memory formation. Previously, they developed an optogenetic approach that uses light to temporarily deactivate CaMKII. With this tool in hand, the team set out to use light to block short-term memory formation in a mouse. ...

When the research team used their tool to disrupt memory formation, even those mice that had a frightening experience an hour earlier entered the dark space, suggesting they had no memory of the experience. The scientists had successfully blocked short-term memory formation.

What happened next was surprising to the research team. A day, week, or even a month later, these mice were altering their behavior to avoid where they were previously frightened.

Mice that didn't seem to remember the frightening experience an hour after it occurred, showed clear evidence of remembering at later times. In other words, blocking short-term memory of the event did not disrupt long-term memory. ..."

From the abstract:

"Long-term memory (LTM) consolidation is thought to require the prior establishment of short-term memory (STM). Here we show that optogenetic or genetic CaMKII inhibition impairs STM for an inhibitory avoidance task at 1 h but not LTM at 1 day in mice. Similarly, cortico-amygdala synaptic potentiation was more sensitive to CaMKII inhibition at 1 h than at 1 day after training. Thus, LTM does not require the formation of STM, and CaMKII-dependent plasticity specifically regulates STM for avoidance memory."

Neuroscientists discover a new pathway to forming long-term memories in the brain

New Pathways to Long-Term Memory Formation (original news release) "Researchers from Max Planck Florida Institute for Neuroscience have discovered a new pathway to forming long-term memories in the brain. Their work suggests that long-term memory can form independently of short-term memory, a finding that opens exciting possibilities for understanding memory-related conditions."

Formation of long-term memory without short-term memory revealed by CaMKII inhibition (no public access)

Formation of long-term memory without short-term memory by CaMKII inhibition (preprint, open access)

Astrocytes make long-term fear memories fade before they form

Amazing stuff!

"Manipulating important non-neuronal brain cells called astrocytes using light prevented fear memories from being retained long-term, according to new research. The findings add to growing evidence about astrocytes’ role in memory and open the door to potential treatments for conditions like PTSD, which is characterized by abnormal fear memory.

Astrocytes, the long-tailed, star-shaped cells that make up the majority of cells in the central nervous system, are known to perform metabolic, structural, and neuroprotective tasks in the brain. But scientists have started discovering that these cells play an important role in memory, too. ..."

"... Researchers ... discovered that part of the memory selection process depends on the function of astrocytes, a special type of cell that surrounds neurons in the brain. They showed that artificially acidifying the astrocytes did not affect short-term memory but prevented memories from being remembered long-term. ...

A mild electrical shock was delivered to mice in an experiment chamber. When placed back in the same chamber, the mice remembered the shock and froze as a natural response. In comparison, the mice who had their astrocytes acidified immediately after the mild shock were able to temporarily hold onto the fear memory, but they forgot it by the next day. This shows that acidifying the astrocytes did not affect short-term memory but prevented the memories from being remembered long-term.

A different effect was seen for mice who had their astrocytes alkalinized. When tested three weeks later, control mice typically showed signs of forgetting, demonstrated by a decrease in freezing responses. However, mice whose astrocytes were alkalinized immediately after a strong shock still displayed strong fear responses even after three weeks. This suggests that astrocytes play a key role in determining whether memories are erased or preserved for a long time, immediately after a traumatic event. ..."

From the abstract:

"While some vivid memories are unyielding and unforgettable, others fade with time. Astrocytes are recognized for their role in modulating the brain's environment and have recently been considered integral to the brain's information processing and memory formation. This suggests their potential roles in emotional perception and memory formation. In this study, we delve into the impact of amygdala astrocytes on fear behaviors and memory, employing astrocyte-specific optogenetic manipulations in mice. Our findings reveal that astrocytic photoactivation with channelrhodopsin-2 (ChR2) provokes aversive behavioral responses, while archaerhodopsin-T (ArchT) photoactivation diminishes fear perception. ChR2 photoactivation amplifies fear perception and fear memory encoding but obstructs its consolidation. On the other hand, ArchT photoactivation inhibits memory formation during intense aversive stimuli, possibly due to weakened fear perception. However, it prevents the decay of remote fear memory over three weeks. Crucially, these memory effects were observed when optogenetic manipulations coincided with the aversive experience, indicating a deterministic role of astrocytic states at the exact moment of fear experiences in shaping long-term memory. This research underscores the significant and multifaceted role of astrocytes in emotional perception, fear memory formation, and modulation, suggesting a sophisticated astrocyte-neuron communication mechanism underlying basic emotional state transitions of information processing in the brain."

'Star cells' make long-term fear memories fade before they form

Saying Goodbye to Traumatic Memories: Astrocytic Manipulation of the Fate of Memory (original news release)

Astrocytic determinant of the fate of long-term memory (open access)

Selective suppression of long-term memory formation through ChR2 photoactivation of amygdala astrocytes. The experiments suggest the presence of parallel processes governing short-term and long-term memory formation, respectively.

Mice inherently possess a selective filtering mechanism that enhances the memory of intense experiences; however, this filtering function was inhibited by ArchT photoactivation of astrocytes in the amygdala. Additionally, the natural forgetting process over three weeks was suppressed by the light stimulation of ArchT-expressing astrocytes.

Non-brain cells can form memories, too

Amazing stuff! Imagine your entire body full of memories?

"Non-brain cells exposed to chemical pulses similar to the ones that brain cells are exposed to when presented with new information caused the non-brain cells to switch on a gene critical for memory formation. ...

The researchers wanted to see whether non-brain cells reacted similarly, so they developed two separate lines of generic human cells, one from nerve tissue and one from kidney tissue, to test it. They replicated the massed-spaced effect, exposing the non-brain cells to different pulses of chemical signals to mimic the way neurons are exposed to chemical neurotransmitters when new information is learned.

The researchers found that the non-brain cells switched on a memory gene, the same one neurons do when they form memories. The cells could also tell when the chemical pulses were repeated rather than simply prolonged, in the same way neurons can tell the difference between learning with breaks versus cramming. When the pulses were spaced out, the memory gene was activated more strongly and for a longer time than when the pulses were delivered all at once. ..."

From the abstract:

"The massed-spaced effect is a hallmark feature of memory formation. We now demonstrate this effect in two separate non-neural, immortalized cell lines stably expressing a short-lived luciferase reporter controlled by a CREB-dependent promoter. We emulate training using repeated pulses of forskolin and/or phorbol ester, and, as a proxy for memory, measure luciferase expression at various points after training. Four spaced pulses of either agonist elicit stronger and more sustained luciferase expression than a single “massed” pulse. Spaced pulses also result in stronger and more sustained activation of molecular factors critical for memory formation, ERK and CREB, and inhibition of ERK or CREB blocks the massed-spaced effect. Our findings show that canonical features of memory do not necessarily depend on neural circuitry, but can be embedded in the dynamics of signaling cascades conserved across different cell types."

Non-brain cells can form memories, too

Memories Are Not Only in the Brain (original news release) Study shows kidney and nerve tissue cells learn and make memories in ways similar to neurons

The massed-spaced learning effect in non-neural human cells (open access)

Fig. 1: Levels of neural computation.

Fig. 3: Massed-spaced effect in CRE-luc cells.

When will my brain be extended by a biological memory?

We can attach any number of hard drives to a computer!

Given that today two of the pioneers of machine learning and AI were honored with a Noble prize in physics, I am still waiting for my brain to be extended by a biological drive to help me to better and faster remember what I already learnt.

Quick fact checking and debunking would be one of many benefits!

Or as they say those who do not remember the blunders of history are doomed to repeat them!

Patience is the name of the game! 😊

Brain found to store three copies of every memory and their memory dynamics

Amazing stuff!

"... the rodent brains called three different sets of neurons into action to record the memory. The first are known as early-born neurons and are the earliest to develop as a fetus is growing. At the other end of the spectrum are the late-born neurons, which show up late in embryonic development. Between these are neurons that form somewhere right in the middle of growth in the womb.

The imaging study revealed that when the new memory is stored in the early-born neurons, it is initially hard to retrieve, but it becomes stronger as time goes on.

The copy of the memory stored in the late-born neurons, on the other hand, was very strong to start, but faded over time to the point that it eventually became inaccessible by the brain. In the middle, the memory copy showed a higher degree of stability than with either of the other neuronal groups. ..."

"... that in the hippocampus, a brain region responsible for learning from experience, a single event is stored in parallel memory copies among at least three different groups of neurons, which emerge at different stages during embryonic development. ..."

From the editor's summary, abstract and structured abstract:

"Editor’s summary

... the mechanisms that govern the reorganization of neuronal ensembles linked to a specific memory and how these dynamic changes affect memory persistence over time. They found that in the hippocampal network, learning resulted in the parallel establishment of two distinct memory traces. These traces were represented in distinct neurogenesis-defined subpopulations of early- and late-born neurons. Even though temporally restricted, the transient recruitment of late-born neurons was necessary for a memory’s long-term permanence, whereas shifts in the recruitment of early- and late-born neurons had a strong impact on the plasticity of a recently acquired memory. ...

Abstract

... By targeting developmentally distinct subpopulations of principal neurons, we discovered that memory encoding resulted in the concurrent establishment of multiple memory traces in the mouse hippocampus. Two of these traces were instantiated in subpopulations of early- and late-born neurons and followed distinct reactivation trajectories after encoding. The divergent recruitment of these subpopulations underpinned gradual reorganization of memory ensembles and modulated memory persistence and plasticity across multiple learning episodes. Thus, our findings reveal profound and intricate relationships between ensemble dynamics and the progression of memories over time.

Structured abstract

...

RATIONALE

Hippocampal neurons born at different times during embryonic development segregate into subpopulations that preferentially connect across subdivisions and are endowed with distinct genetic, anatomical, and functional properties. We hypothesized that the activation of developmentally and functionally distinct neuronal subpopulations at specific stages of a memory’s lifetime might confer dynamic properties to a memory and underpin its long-term permanence. We thus exploited multiple methods to record and manipulate the activity of hippocampal neurons with specific birth dates—in combination with hippocampus-dependent associative learning paradigms—to dissect the contribution of birth-dated subpopulations to the encoding, persistence, and evolution of a memory over time.

... Late-born neurons were preferentially recruited for retrieval at short latency after acquisition, whereas early-born neurons were preferentially recruited at later times. These divergent trajectories recapitulated reactivation dynamics recorded through longitudinal calcium imaging experiments, which further revealed distinct network-wide responses between subpopulations. Whereas in the late-born subnetwork, learning was associated with a plastic reorganization of coactivity dynamics and functional connectivity, activity patterns among early-born neurons were more rigidly structured and unaffected by learning-induced activity changes. Targeted manipulation experiments indicated that each subpopulation’s activation supported memory expression at specific times after encoding, with late-born neurons supporting recall shortly after acquisition and early-born neurons becoming necessary at later times. Even though temporally restricted, activation of late-born neurons was necessary for a memory’s long-term permanence because silencing their activity at acquisition or during a specific window of consolidation impaired remote-memory expression. Moreover, the systematic shift in recruitment from late- to early-born neurons happened concomitantly to a transient plasticity window occurring shortly after memory encoding, during which mice could combine information acquired across multiple learning episodes to reinforce previously learned associations or make inferences. Manipulating the recruitment of early- or late-born neurons around the closure of such windows had the potential to modulate memory plasticity in opposite ways.

CONCLUSION

We discovered that an underlying logic driving the reorganization of hippocampal memory ensembles over time is anchored in the divergent recruitment of populations of neurons defined by neurogenesis, which is necessary for memory retrieval. Ensemble reorganization is thus not disruptive of memory processes; conversely, the timely recruitment of distinct neuronal subpopulations modulates a memory’s properties at different stages of its lifetime. Our study therefore sheds light on the complex interplay between ensemble activity dynamics, memory encoding, consolidation, and retrieval and the processes governing memory evolution over time. Specifically, we reveal that within the hippocampal network, the divergent recruitment of distinct memory traces emerging in parallel at encoding underpins memory persistence and modulates the plasticity of recently acquired memories."

Brain found to store three copies of every memory

The brain creates three copies for a single memory (original news release) "A new study ... reveals that the memory for a specific experience is stored in multiple parallel “copies”. These are preserved for varying durations, modified to certain degrees, and sometimes deleted over time ..."

Divergent recruitment of developmentally defined neuronal ensembles supports memory dynamics

Parallel-emerging memory traces encoded in developmentally defined hippocampal subpopulations underpin memory dynamics.

Research uncovers kidney and brain expressed KIBRA protein that helps ensure memory formation and stabilization

Amazing stuff! When will humans have a better memory?

They say love goes through the stomach. Perhaps memory goes through the kidney? 😊

"... A study ... has uncovered a biological explanation for long-term memories. It centers on the discovery of the role of a molecule, KIBRA, that serves as a "glue" to other molecules, thereby solidifying memory formation. ..."

"... In a study using laboratory mice, the scientists focused on the role of KIBRA, or kidney and brain expressed protein, the human genetic variants of which are associated with both good and poor memory. They focused on KIBRA’s interactions with other molecules crucial to memory formation—in this case, protein kinase Mzeta (PKMzeta). This enzyme is the most crucial molecule for strengthening normal mammalian synapses that is known, but it degrades after a few days.

Their experiments reveal that KIBRA is the “missing link” in long-term memories, serving as a “persistent synaptic tag,” or glue, that sticks to strong synapses and to PKMzeta while also avoiding weak synapses. ..."

From the abstract:

"How can short-lived molecules selectively maintain the potentiation of activated synapses to sustain long-term memory? Here, we find kidney and brain expressed adaptor protein (KIBRA), a postsynaptic scaffolding protein genetically linked to human memory performance, complexes with protein kinase Mzeta (PKMζ), anchoring the kinase’s potentiating action to maintain late-phase long-term potentiation (late-LTP) at activated synapses. Two structurally distinct antagonists of KIBRA-PKMζ dimerization disrupt established late-LTP and long-term spatial memory, yet neither measurably affects basal synaptic transmission. Neither antagonist affects PKMζ-independent LTP or memory that are maintained by compensating PKCs in ζ-knockout mice; thus, both agents require PKMζ for their effect. KIBRA-PKMζ complexes maintain 1-month-old memory despite PKMζ turnover. Therefore, it is not PKMζ alone, nor KIBRA alone, but the continual interaction between the two that maintains late-LTP and long-term memory."

Research uncovers 'molecular glue' that helps ensure memory formation and stabilization

How Do Our Memories Last a Lifetime? New Study Offers a Biological Explanation (original news release) Ground-breaking research uncovers “molecular glue” that helps ensure memory formation and stabilization

KIBRA anchoring the action of PKMζ maintains the persistence of memory (open access)

Fig. 1. Strong synaptic stimulation facilitates formation of persistent KIBRA-PKMζ complexes in late-LTP maintenance.

Memories are stored by the interaction of two proteins: a structural protein, KIBRA (green), that acts as a persistent synaptic tag, and a synapse-strengthening enzyme, protein kinase Mzeta (red). Drugs that disrupt the memory-perpetuating interaction (other colors) erase pre-established long-term and remote memories. 

Brain Waves Travel in One Direction When Memories Are Made and the Opposite When Recalled

Sounds almost too neat! The subjects of this study were also special!

Memory and travelling brain waves! Wow!

"... By carefully monitoring neural activity of people who were recalling memories or forming new ones, the researchers managed to detect how a newly appreciated type of brainwave — traveling waves — influences the storage and retrieval of memories. ...

The researchers say these findings advance fundamental neuroscience research and point toward diagnostic and therapeutic approaches for memory-related disorders. ...

Brain waves are patterns of electrical oscillations that reflect the state of hundreds or thousands of individual neurons at a particular moment. One major question, which remains unsettled, is whether brain waves drive activity or simply occur as a byproduct of neural activity that was already happening. Researchers who study brain waves have tended to treat them as a stationary phenomenon that occurs in a particular region, noting when oscillations in multiple regions seem synchronized.

In this study, ... contribute to a growing understanding of these oscillations differently, as “traveling waves” that spread across the brain’s cortex, the outermost layer that supports higher cognitive processing. ...

This study drew on data from participants who were being treated for drug-resistant epilepsy at hospitals across the United States. The experiments occurred while the participants had grids or strips of electrodes temporarily implanted on the surface of the brain, beneath the skull, to determine where the patients’ seizures arise. For the researchers, these electrodes offer the chance to perform experiments that wouldn’t otherwise be feasible.  ..."

From the abstract:

"To support a range of behaviours, the brain must flexibly coordinate neural activity across widespread brain regions. One potential mechanism for this coordination is a travelling wave, in which a neural oscillation propagates across the brain while organizing the order and timing of activity across regions. Although travelling waves are present across the brain in various species, their potential functional relevance has remained unknown. Here, using rare direct human brain recordings, we demonstrate a distinct functional role for travelling waves of theta- and alpha-band (2–13 Hz) oscillations in the cortex. Travelling waves propagate in different directions during separate cognitive processes. In episodic memory, travelling waves tended to propagate in a posterior-to-anterior direction during successful memory encoding and in an anterior-to-posterior direction during recall. Because travelling waves of oscillations correspond to local neuronal spiking, these patterns indicate that rhythmic pulses of activity move across the brain in different directions for separate behaviours. More broadly, our results suggest a fundamental role for travelling waves and oscillations in dynamically coordinating neural connectivity, by flexibly organizing the timing and directionality of network interactions across the cortex to support cognition and behaviour."

Brain Waves Travel in One Direction When Memories Are Made and the Opposite When Recalled | Columbia Engineering

The direction of theta and alpha travelling waves modulates human memory processing (no public access)

Traveling wave propagation directions in the memory task reveal how the brain quickly coordinates activity and shares information across multiple regions.

Bacteria Can Store Memories And Pass Them on For Generations

Amazing stuff!

"... The ubiquitous bacterium, Escherichia coli, is one of the most well-studied life forms on Earth, and yet scientists are still discovering unexpected ways that it survives and spreads. ..."

"... Researchers ... found that E. coli bacteria use iron levels as a way to store information about different behaviors that can then be activated in response to certain stimuli. ..."

From the significance and abstract:

"Significance

... We report here a multigenerational memory in Escherichia coli swarming motility, where bacteria “remember” their swarming experience for several generations. We show unambiguously that the molecular basis of this memory is the levels of available cellular iron. The act of swarming “conditions” the cells with this memory. Given the central role of iron in cellular metabolism, an iron-based memory might offer the advantage of providing a hub connecting various stress responses such as antibiotic survival and biofilms.

Abstract

The importance of memory in bacterial decision-making is relatively unexplored. We show here that a prior experience of swarming is remembered when Escherichia coli encounters a new surface, improving its future swarming efficiency. We conducted >10,000 single-cell swarm assays to discover that cells store memory in the form of cellular iron levels. This “iron” memory preexists in planktonic cells, but the act of swarming reinforces it. A cell with low iron initiates swarming early and is a better swarmer, while the opposite is true for a cell with high iron. The swarming potential of a mother cell, which tracks with its iron memory, is passed down to its fourth-generation daughter cells. This memory is naturally lost by the seventh generation, but artificially manipulating iron levels allows it to persist much longer. A mathematical model with a time-delay component faithfully recreates the observed dynamic interconversions between different swarming potentials. We demonstrate that cellular iron levels also track with biofilm formation and antibiotic tolerance, suggesting that iron memory may impact other physiologies."

Bacteria Can Store Memories And Pass Them on For Generations : ScienceAlert

Bacteria Store Memories and Pass Them on for Generations

A heritable iron memory enables decision-making in Escherichia coli (no public access)

Bacterial swarm on a laboratory plate