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April 6, 2010
Songbirds, Genes, and Neurons
I just read a New York Times article, From a Songbird, New Insights Into the Brain by Nicholas Wade, and it reminded me of a number of machine understanding issues. So I am going to take a break from my series on the Hierarchical Temporal Memory (HTM) model and muse on intelligence, understanding and song.
The article gives a minimum of information on how genes actually affect the ability of a bird to learn and sing a song. The key revelations of the article are that the zebra finch (Taeniopygia guttata), has had its genome decoded and that about 800 genes change their activity levels in neurons when the finch sings. The article implies that defects in these genes might interrupt singing ability, just as mutated FOXP2 genes in humans cause speech defects. In particular the bird version of FOXP2, if defective, prevents songbirds from singing.
This would seem to go against my basic understanding of how systems of neurons work, which I like to think I is up with the current scientific consensus. Once a basically functioning neural network is in place, I thought genetic activity becomes background activity. Of course the genes would function just like they do in any cell, releasing instructions for making proteins that regulate cell activity. And maybe some of the 800 genes mentioned in Wade's article are ones that would up-regulate or down-regulate any neural activity, not just songs, or learning. But according to David F. Clayton, "these transcripts don't result in the cells producing proteins in the usual way. Instead they seem to modulate the activity of other genes involved in listening."
My (learned from textbooks) model is: genes have blueprints for several types of neurons with varying synapses and neurotransmitters and receptor. Signals are conducted by reasonably well understood mechanisms involving membrane potentials along the neurons and either chemical or electrical transmission at synapses. Genes in the neuron are just caretakers once a system is set up. Learning results from a strengthening or weakening of synaptic thresholds. This is called Hebbian learning, and while there are some theories about how Hebbian learning works at the molecular level, at this point I don't take them as proven.
If the article is true as presented, then individual neurons are more complex than I thought. It is implied that many neurons can function just fine with a mutated FOXP2 genes (every gene would be in every neuron, in fact in every cell), but not neurons that are involved in learning songs. But other neurons learn just fine.
What would distinguish a song-learning neuron from a muscle-coordination learning neuron? I don't know.
As is typical with the New York Times, they want to keep you in their ad ghetto, so they provide no link to the research report, but they say it is in the current issue of Nature. Here is the link: The genome of a songbird