Recent research suggests a role for GABA receptor in synaptic pruning. Autism (and schizophrenia) are often associated with a lack of synaptic pruning, meaning neurons are more active, with positive feedback dominating.
GABA is associated with negative feedback, meaning the brain slows down to a steady-state. Glutamine is similarly associated with negative feedback. Glutamate is associated with positive feedback. All of these are neurotransmitters. More, they are closely related to each other, and can be biochemically derived from each other.
This suggests a few potential pathways to autism. If there is a problem with the GABA receptor, you would not get enough pruning. But if there is not enough GABA being produced, you would have the same effect. A mutation on either the GABA receptor protein or on one of the enzymes associated with GABA production could have pretty much the same result.
Neurons with unpruned dendritic spines get more input than do those properly pruned. The more input a neuron (or other complex system) has, the more is acts as though there is positive feedback. Indeed, it can result in increasing cycles, driving more input. In essence the brain becomes more hyperactive, at least until a physical limit is reached, at which point the system crashes, cycling down.
The result is a more active brain that may have some difficulty learning new things, but which may at the same time show exceptional abilities because of the higher activity. While the senses themselves won't show increased activity at the source, you would see increased activity in the brain, resulting in the sensory overload associated with autism. One would even expect a certain degree of "phantom" sensory information--as we see with schizophrenia. Indeed, this association between autism and schizophrenia (which I keep coming across in different ways) does suggest that the old categorization of autism with schizophrenia meant that the researchers at the time were on to something.
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