How much does the SPAUN and the Semantic Pointer Architecture (SPA) that was used to build it take neurotransmitters into account? In the book How to Build a Brain, various inhibitory and excitatory connections are mentioned as supplying a biological foundation for implementing the Basal Ganglia. Additionally, it's mentioned that the learning rule that the SPA uses, hPES, uses dopamine to modulate learning. However, I'm still a bit confused on the details of all this. How do neurotransmitters fit into Nengo? How much detail does Nengo go into in regards to neurotransmitters? Does it take into account the neurotransmitter distribution and consumption as observed in the brain?

Note: For more information on the relation between Nengo, SPA and SPAUN, please see my previous question.


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At this point in time, the difference in neurotransmitter types affect the synaptic time constant (i.e. the filter on the incoming spike train) between neurons in Nengo. See Neural Engineering p.112 and these notes (see the section called "Biologically plausible filter") from a course covering the book.

Neurotransmitters are also leveraged more theoretically. For example, in connection between neurons that involve learning, dopamine is often said to modulate this learning. For example, see Dan Rasmussen's neural hierarchical reinfrocement learning implementation (PHD link pending).

Hypothetically, it would be possible to implement a back-end to Nengo using a more biologically detailed software such as Neuron to take into account neurotransmitter generation, concentration and consumption. Although I can attest anecdotally that this has been attempted with mixed success, there has been no formal release or publication of this approach.


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