The neural mechanisms underlying schizophrenic behavior are unknown and very difficult to investigateexperimentally, although a few experimental and modeling studies suggested possible causes for someof the typical psychotic symptoms related to this disease. The brain region most involved in theseprocesses seems to be the hippocampus, because of its critical role in establishing memories for objectsor events in the context in which they occur. In particular, a hypofunction of the N-methyl-D-aspartate(NMDA) component of the synaptic input on the distal dendrites of CA1 pyramidal neurons has beensuggested to play an important role for the emergence of schizophrenic behavior. Modeling studies haveinvestigated this issue at the network and cellular level. Here, starting from the experimentally supportedassumption that hippocampal neurons are very specific, sparse, and invariant in their firing, we explorean experimentally testable prediction at the single neuron level. The model shows how and to whatextent a pathological hypofunction of a context-dependent distal input on a CA1 neuron can generatehallucinations by altering the normal recall of objects on which the neuron has been previously tuned.The results suggest that a change in the context during the recall phase may cause an occasional butvery significant change in the set of active dendrites used for feature recognition, leading to a distortedperception of objects.
|Numero di pagine||8|
|Stato di pubblicazione||Published - 2011|
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