Schizophrenia is a chronic and disabling psychiatric illness that is often refractory to treatment. Psychotic symptoms (e.g. hallucinations and delusions) in schizophrenia are reliably correlated with excess dopamine levels in the striatum, and have more recently been related to excess metabolic activity in the hippocampus. Multiple lines of evidence suggest that aberrantly high hippocampal activity may, via hippocampal connections with the limbic basal ganglia, drive excessive dopamine release into the striatum. In the present paper, we hypothesize that inhibition or stabilization of neural activity with high-frequency electrical stimulation of the hippocampus or nucleus accumbens, through different mechanisms, would treat the positive symptoms of schizophrenia. Thus, we suggest a direction for further experimentation aimed at developing neurosurgical therapeutic approaches for this devastating disease.

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Autism Spectrum Disorder (ASD) is a neurodevelopmental disorder characterized by deficits in social cognition and disordered communication. Furthermore, abnormalities in basic motor control and motor learning, are common in ASD. These have been attributed to a possible defect in the pre‐ and postnatal development of specific neural networks including the dentate‐thalamo‐cortical pathway, involved in motor learning, automaticity of movements, and higher cognitive functions.The most consistent neurochemical finding reported in autism is an observed 50‐70% increase in platelet serotonin. Occurring in 30% of autistic subjects, developmental hyperserotonemia (DHS) has been implicated in the pathophysiology of ASD. Prior to its role as a neurotransmitter, serotonin functions as a developmental signal, promoting dendritic elaboration, synaptogenesis, cortical organization and autoregulation of the serotonergic system. Accordingly, it has been hypothesized that during the early stages of neural development, the diffusion of abnormally increased amounts of serotonin into the central nervous system, could induce changes in various neural networks relevant to ASD.In the present study, rat pups were exposed to high levels of the serotonergic agonist 5‐methyloxytryptamine both pre‐and postnatally. This exposure produced changes in the dendritic architecture and synaptic connectivity of neurons in the dentate nucleus of the cerebellum. We observed changes in dendritic branching morphology such that DHS groups presented with short reaching, elaborately branched segments, expressing significantly fewer dendritic spines compared with controls. These alterations may be implicated in the neuropathological and behavioral changes observed in ASD.