Recent “connectionist” models provide a new explanatory alternative to the digital computer as a model for brain function. Evidence from our EEG research on the olfactory bulb suggests that the brain may indeed use computational mechanisms like those found in connectionist models. In the present paper we discuss our data and develop a model to describe the neural dynamics responsible for odor recognition and discrimination. The results indicate the existence of sensory- and motor-specific information in the spatial dimension of EEG activity and call for new physiological metaphors and techniques of analysis. Special emphasis is placed in our model on chaotic neural activity. We hypothesize that chaotic behavior serves as the essential ground state for the neural perceptual apparatus, and we propose a mechanism for acquiring new forms of patterned activity corresponding to new learned odors. Finally, some of the implications of our neural model for behavioral theories are briefly discussed. Our research, in concert with the connectionist work, encourages a reevaluation of explanatory models that are based only on the digital computer metaphor.

Considerable evidence from preclinical and clinical investigations implicates disturbances of brain dopamine (DA) function in the pathophysiology of several psychiatric and neurologic disorders. We describe a neural model that may help organize theseindependent experimental observations. Cortical regions classically associated with the limbic system interact with infracortical structures, including the nucleus accumbens, ventral pallidum, and dorsomedial nucleus of the thalamus. In our model, overactivity in forebrain DA systems results in the loss of lateral inhibitory interactions in the nucleus accumbens, causing disinhibition of pallidothalamic efferents; this in turn causes rapid changes and a loss of focused corticothalamic activity in cortical regions controlling cognitive and emotional processes. These effects might be manifested clinically by some symptoms of psychoses. Underactivity of forebrain DA results in excess lateral inhibition in the nucleus accumbens, causing tonic inhibition of pallidothalamic efferents; this perpetuates tonic corticothalamic activity and prevents the initiation of new activity in other critical cortical regions. These effects might be manifested clinically by some symptoms of depression. This model parallels existing explanations for the etiology of several movement disorders, and may lead to testable inferences regarding the neural substrates of specific psychopathologies.