Neuroscience of Early-Life Learning in C. elegans

Scientists identify the brain circuits with which newly hatched nematodes form and retrieve a lifelong aversive olfactory memory.

By | February 11, 2016

WIKIMEDIA, BOB GOLDSTEINEarly-life exposure to pathogenic bacteria can induce a lifelong imprinted olfactory memory in C. elegans through two distinct neural circuits, according to a study published today (February 11) in Cell. Researchers from Rockefeller University in New York City have shown that early-life pathogen exposure leads the nematode to have a lifelong aversion to the specific associated bacterial odors, whereas later-in-life exposure spurs only transient aversion.

“This study is very exciting,” said Yun Zhang of Harvard who studies learning in C. elegans but was not involved in the present work. “Imprinting is a form of learning widely observed in many animals [but] finding this in C. elegans is very meaningful because this nematode is genetically tractable, and its small nervous system is well described.”

A classic example of imprinting is how geese form attachments to the first moving object they see after birth; Nobel laureate Konrad Lorenz famously showed that the “moving object” could be himself instead of a mother goose. During the critical period at the start of life, animals often have unusual abilities to create and maintain long-term memories.

For the present study, Rockefeller’s Xin Jin and colleagues described a form of aversive imprinting in their C. elegans: newly hatched nematodes exposed to Pseudomonas aeruginosa PA14 or toxin-emitting Escherichia coli BL21 established a long-term olfactory aversion to it.  Animals that experienced the pathogen immediately after hatching were able to synthesize and maintain the aversive memory for the whole of their four-day lifespans, while animals trained in adulthood only retained the aversive memory for up to 24 hours.

C. elegans has an exceedingly compact nervous system with only 302 neurons (compared with 250,000 in the fruit fly Drosophila and 86 billion in humans). To understand which specific neurons were involved in the different stages of aversive imprinting, the researchers selectively and reversibly deactivated individual brain cells. Silencing the neurons AIB or RIM during the memory-formation phase prevented learning in the newly hatched nematodes, but silencing these same cells during memory retrieval showed no effect. The opposite was true of the neurons AIY and RIA: these cells could be silenced during memory formation with no effect, but were indispensable during memory retrieval.

The principle of separate neural circuits for memory formation and retrieval is far from unique to C. elegans. It was shown in humans through cases such as the famous patient “H.M.” who, following surgery that removed his medial temporal lobe, was able to retrieve old declarative memories but unable to form new ones.

“[The] idea that the transient learning signal would later be dispensable at the time of memory goes back as far as Pavlov. We’re just developing the idea at a different level of resolution to map it onto a physical site and not just a conceptual site,” said study coauthor Cori Bargmann. “It’s a surprise all over again that you can actually implement this in such a compact, little brain.”

Of course, memory formation and retrieval circuits must communicate with each other for learning to occur. The researchers found one molecular bridge between the circuits in the neurotransmitter tyramine, a homologue of adrenaline in mammals. Tyramine was released by the memory-formation neuron RIM and detected by the memory-retrieval neuron AIY; the neurotransmitter alone could replace the requirement for RIM activity in the C. elegans learning process.

“We often describe phenomenology and then speculate about the underlying machinery, but research in C. elegans—and especially this particular group—have really taken it to a different level, describing behaviors in great mechanistic detail,” said Harvard neurobiologist Bence Ölveczky, who was not involved in the research.

The present work is “really just the tip of the iceberg,” Jin told The Scientist. “Thanks to rapidly evolving modern genetics, neuromanipulation and imaging tools, we’re able to study causal effects of animal behaviors at a new level of precision. It’s an exciting time.”

X. Jin et al., “Distinct circuits for the formation and retrieval of an imprinted olfactory memory,” Cell, doi:10.1016/j.cell.2016.01.007, 2016.

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Avatar of: James V. Kohl

James V. Kohl

Posts: 481

February 13, 2016

See also:  Pan-neuronal imaging in roaming Caenorhabditis elegans

Reported as: Watching sensory information translate into behavior

"We have long been recording behavior in worms, but we and others have concluded that, if you want to get physiologically relevant neural activity patterns, you have to look at neurons inside a behaving animal," Samuel explained. "Only in that context are all feedback loops intact, where behavioral output modulates neural activity which, in turn, shapes behavior."

As all serious scientists continue to link ecological variation to ecological speciation via nutrient-dependent pheromone-controlled reproduction in species from microbes to humans, my antagonists have all but disappeared.

Clearly, it is time to finally begin discussion of how virus-driven energy theft links hydrogen-atom transfer in DNA base pairs in solution from mutations to pathology instead of from nutrient-dependent RNA-mediated DNA repair via amino acid substitutions to supercoiled DNA, which protects organized genomes from virus-driven entropy.

Avatar of: Roy Niles

Roy Niles

Posts: 113

Replied to a comment from James V. Kohl made on February 13, 2016

February 16, 2016

Clearly, since viruses weren't discussed in this article, it is not time to begin discussion of how Kohl supposes that virus-driven energy theft "links" hydrogen-atom transfer in DNA base pairs in solution from mutations to pathology, although I suppose if anyone could figure out exactly what "links" are in Kohl's imagination, we might find that he has mistaken the interconnectness of all universal systems as directed or directional links.

And I presume he knows that pathology is the science of the causes and effects of diseases, in which case he seems to be assuming that all virus-driven systems are diseased.  But hey, this kind of thing is what he does.


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