A possible mechanism for odors processing in a neural network that includes the olfactory bulb, the piriform cortex, the olfactory tubercle, which is the part of the ventral striatum, the ventral pallidum, the mediodorsal thalamic nucleus, and the orbitofrontal cortex, has been proposed. According to this mechanism, dopamine released by midbrain neurons in response to odor and reinforcement, as well as adenosine receptor antagonists, modulate in a certain way the efficacy of excitatory synaptic inputs to spiny cells of the olfactory tubercle projecting into the ventral pallidum. As a result, the neurons of the olfactory bulb are disinhibited by the ventral pallidum and contrasted odor representations are formed on them, as well as on their target cells in the piriform cortex. Simultaneously, there is a disinhibition of neurons of the mediodorsal nucleus and their target cells in the orbitofrontal cortex, which excites the neurons of the piriform cortex. This promotes the induction of LTP at the inputs from the olfactory bulb to the piriform cortex and the memorization of odor representations. For the first time it is pointed out that the mechanism for odor processing is similar to those we earlier proposed for processing of auditory and visual information in topographically organized cortico-basal ganglia-thalamocortical loops, which include the primary and higher areas of the auditory and visual cortex, as well as the prefrontal cortex. It is proposed that mechanism for olfactory processing is similar in vertebrates at different stages of evolution, including lampreys, due to the similarity of the functional organization of the basal ganglia and their interactions with other structures. It follows from the proposed mechanism that in cases when dopamine drugs are not effective in restoring the odor perception, it is desirable to use adenosine A2A receptor antagonists. Supporting this prediction is evidence of improved sense of smell in patients with COVID-19 when treated with A2A receptor antagonists.
