Slashdot Mirror
Memory Molecule Identified
Reader Ostracus informs us of research led by Michael Ehlers of Duke University that has identified a molecule, myosin Vb (five-b), that seems to be a critical component in the formation of memory. "A major puzzle for neurobiologists is how the brain can modify one... synapse at a time in a brain cell and not affect the thousands of other connections nearby. Plasticity, the ability of the brain to precisely rearrange the connections between its nerve cells, is the framework for learning and forming memories ... The discovery of a molecule that moves new receptors to the synapse so that the neuron... can respond more strongly helps to explain several observations about [brain] plasticity ... [The researchers] found that the myosin Vb molecule in hippocampal neurons responded to a flow of calcium ions from the synaptic space by popping up and into action. One end of the myosin is attached to meshlike actin filaments so it can 'walk' to the end of the nerve cells where receptors are. On its other end, it tows an endosome, a packet that contains new receptors. 'These endosomes are like little memories waiting to happen,' Ehlers said."
I'm not sure they can call this a "memory molecule" so much as a "molecule responsible for changing the receptors at the synapse to make a memory." The molecule itself is not what memories are actually made of, which is what I would think of. The changed activity of the neuron is more akin to that. And it's also not specific to memories. The process of myosin Vb bringing endosomes to the surface is not unique to neurons, that's been known for a while (http://www.ncbi.nlm.nih.gov/pubmed/11408590).
That said, it's really interesting that they've identified this, as it not only tells you how the change is made, but also tells you the stimulus to change it.
The closer we are to immortal memory. That would be both good and bad. We would forever despair of our failures. We would always remember where we left our keys.
Since all the other parts of a Man are capable of being restored through regressing any cell into a T-cell and then culturing it into the desired part, if this gets us to where we can keep the mind functional as well, then we've found Ponce deLeon's fountain of youth.
That would be great, because there are only 6 billion of us, and that number was not growing nearly fast enough.
Help stamp out iliturcy.
I'm taking actin and will soon kick your ass. I will crush you with my contractile system and force feed you ATP with my sliding filaments as I hurl you in toward my M line.
myosin Vb molecule in hippocampal neurons responded to a flow of calcium ions
"So remember to drink your milk, boys and girls, or you will forget how to."
That's what everyone said last time we discovered this, back in 1925, 1903, and 1871. Somehow, after discovering these molecules, everyone forgets to follow up.
Death is a part of the natural renewal of things. It is a short life span and the continual and restarting of youth that allows humanity to not only change its education but its social attitudes.
Mourn the ones we lose, for sure, but ultimately, death is necessary. Without death, young people could never remake the world with each generation, and we'd be stuck forever with the weirdness of the old. Sometimes we old people, instead of clinging to life, just need accept that we're going to die.
This is my sig.
I see here a possible method of improving AI. If we can indeed model synthetic neurons to perform in a similar way, we might have the key to designing more efficient captcha breaking systems.
Views expressed do not necessarily reflect those of the author.
At least now we know why it's so unstable
Google on "artificial neural network" and read a few of the 600,000 hits that you will find. ANN theory is as old as digital computers. Commercial ANN applications have been growing in number and sophistication for over 10 years, e.g,, Dragon NaturallySpeaking and other speech recognition software, Caere OmniPage and other OCR packages.
What TFA is about is reporting the discovery of a key part of the mechanism that changes the weighting factors in a neuron in a biological neural net. Of itself, I doubt that this will trigger any insights on how to improve ANNs: the frankenmeisters already know how to do that with the neurones they work with. But this does open the door for further research by biologists into wetware neural net mechanisms, and that could lead to some interesting things.