Neural Darwinism

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Neural Darwinism, a large scale theory of brain function by Gerald Edelman, was initially published in 1978, in a book called The Mindful Brain (MIT Press). It was extended and published in the 1989 book Neural Darwinism – The Theory of Neuronal Group Selection.

Edelman won the Nobel Prize in 1972 for his work in immunology showing how the population of lymphocytes capable of binding to a foreign antigen is increased by differential clonal multiplication following antigen discovery. Essentially, this proved that the human body is capable of creating complex adaptive systems as a result of local events with feedback. Edelman's interest in selective systems expanded into the fields of neurobiology and neurophysiology, and in Neural Darwinism, Edelman puts forth a theory called "neuronal group selection". It contains three major parts:

Contents

Degeneracy

With neuronal heterogeneity (by Edelman called degeneracy), it is possible to test the many circuits (on the order of 30 billion neurons with an estimated one quadrillion connections between them in the human brain) with a diverse set of inputs, to see which neuronal groups respond "appropriately" statistically. Functional "distributed" (widespread) brain circuits thus emerge as a result.

Edelman goes into some detail about how brain development depends on a variety of cell adhesion molecules (CAMs) and substrate adhesion molecules (SAMs) on cell surfaces which allow cells to dynamically control their intercellular binding properties. This surface modulation allows cell collectives to effectively "signal" as the group aggregates, which helps govern morphogenesis. So morphology depends on CAM and SAM function. And CAM and SAM function also depend on developing morphology.

Edelman theorized that cell proliferation, cell migration, cell death, neuron arbor distribution, and neurite branching are also governed by similar selective processes.

Synaptic modification

Once the basic variegated anatomical structure of the brain is laid down during early development, it is more or less fixed. But given the numerous and diverse collection of available circuitry, there are bound to be functionally equivalent albeit anatomically non-isomorphic neuronal groups capable of responding to certain sensory input. This creates a competitive environment where circuit groups proficient in their responses to certain inputs are "chosen" through the enhancement of the synaptic efficacies of the selected network. This leads to an increased probability that the same network will respond to similar or identical signals at a future time. This occurs through the strengthening of neuron-to-neuron synapses. And these adjustments allow for neural plasticity along a fairly quick timetable.

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