Summary: Blocking DNA methylation alters how honeybees form and refine long-term memories, a new study reports.
Source: Frontiers
Researchers identify a molecular mechanism that shapes memory specificity over time and suggest that studying honeybee memory could inform approaches to degenerative brain disorders.
Memory dysfunction in humans contributes to conditions such as Alzheimer’s disease and other dementias. Investigating the simpler nervous system of the honeybee can reveal fundamental processes of long-term memory formation. New research published in Frontiers in Molecular Neuroscience reports that DNA methylation, an epigenetic modification, plays a key role in adjusting memory specificity and promoting relearning in honeybees.
“We show that DNA methylation is one molecular mechanism that regulates memory specificity and re-learning, and through which experiences of the organism could be accumulated and integrated over their lifetime,” says Dr. Stephanie Biergans, first author of the study and a researcher at the University of Queensland, Australia.
Honeybees display remarkable learning and memory abilities. They can count small quantities, recognize visual patterns and landmarks, and learn the locations and quality of food sources. As social insects, they also communicate and learn from one another, which makes their foraging strategies highly adaptable. These complex behaviors depend on memory processes that share similarities with those in mammalian brains, yet the honeybee brain is much smaller and genetically simpler, making it an attractive model to study the cellular and molecular basis of long-term memory.
When memories form, molecular events can lead to physical changes in the brain—altered neural activity, strengthened or new connections between neurons, and persistent changes in how genes are expressed. Epigenetic mechanisms, such as DNA methylation, modify gene activity without changing the DNA sequence itself and can be influenced by experience and the environment.
“We knew that DNA methylation is an epigenetic process that occurs in the brain and is related to memory formation,” Biergans explains. “When we block this process in honeybees it affects how they remember.”
In the study, researchers trained two groups of honeybees to associate a specific odor with a sugar reward. One group received many paired exposures to the odor and sugar, representing repeated learning; the other group experienced the pairing only once, representing a single-trial learning event. In both groups, some bees were treated with a pharmacological inhibitor that blocks DNA methyltransferase enzymes, preventing DNA methylation, while control bees were left untreated. The team then tested memory formation, memory specificity, and the bees’ ability to relearn associations when odor cues changed.
Results showed that DNA methylation modulates memory specificity depending on training context. After multiple training trials, DNA methylation increased memory specificity: bees were less likely to respond to a novel odor and more likely to respond selectively to the trained odor. In contrast, after a single training trial, DNA methylation reduced memory specificity, producing more generalized responses. In reversal and relearning paradigms, the activity of DNA methylation machinery contributed to both re-acquisition of an association and to the suppression or forgetting of a previous association, facilitating flexible updating of learned information.
Ecologically, these findings make good sense. A single rewarding encounter with a flower does not produce a reliable signal about its long-term value, so a forager benefits from a more general memory that encourages further exploration. Repeated rewarding experiences reinforce the value of a particular odor or location, and increased memory specificity helps the bee reliably return to rich food sources.
DNA methylation is present in mammalian brains as well, and the mechanisms identified in honeybees could inform how experience-dependent epigenetic changes accumulate to influence memory across a lifetime. Understanding how epigenetic modifications contribute to both forming and updating memories may ultimately provide new insights into age-related or degenerative brain diseases where lifetime accumulation of molecular changes alters neural function.
“By understanding how changes to the epi-genome accumulate, manifest and influence brain function, we may, in the future, be able to develop treatments for brain diseases that also develop over a lifetime,” Biergans concludes. “There is thought to be a genetic predisposition for some conditions, such as Alzheimer’s and dementia, but in many cases environmental factors determine whether the disease will manifest.”
Funding: The research received support from the Australian Research Council, the National Health and Medical Research Council of Australia, the Deutsche Forschungsgemeinschaft (DFG), an Australian Research Council Future Fellowship, and the University of Queensland Postgraduate Research Scholarship and Travel Award.
Source: Monica Favre – Frontiers
Image Source: This image is stated to be in the public domain.
Original Research: The study is titled “DNA Methylation Adjusts the Specificity of Memories Depending on the Learning Context and Promotes Relearning in Honeybees” by Stephanie D. Biergans, Charles Claudianos, Judith Reinhard and C. G. Galizia, published in Frontiers in Molecular Neuroscience, 2016. DOI: 10.3389/fnmol.2016.00082.
Frontiers. “Honeybee Memories Could Unlock Another Piece of Alzheimer’s Puzzle.” Neuroscience News, December 1, 2016.
Abstract
DNA Methylation Adjusts the Specificity of Memories Depending on the Learning Context and Promotes Relearning in Honeybees
The activity of the epigenetic writers DNA methyltransferases (Dnmts) after olfactory reward conditioning is important for stimulus-specific long-term memory (LTM) formation and for extinction. This study asked which memory components Dnmts regulate (for example, associative versus non-associative processes) and how different training contexts influence that regulation. Using a pharmacological Dnmt inhibitor and classical appetitive conditioning in the honeybee Apis mellifera, the authors quantified effects on naïve odor and sugar responses and on responses following olfactory reward conditioning. The results show that (1) Dnmts do not influence naïve odor or sugar responsiveness, (2) Dnmts do not affect initial learning of new stimuli, but (3) Dnmts influence odor coding and stimulus-specific LTM: they reduce memory specificity after single-trial training while increasing specificity after multiple-trial training, producing ecologically adaptive behavior, and (4) during reversal learning Dnmts regulate both excitatory (re-acquisition) and inhibitory (forgetting) processes.
Reference: Stephanie D. Biergans, Charles Claudianos, Judith Reinhard and C. G. Galizia. Frontiers in Molecular Neuroscience, published online September 12, 2016. DOI: 10.3389/fnmol.2016.00082.