A Review of Evidence Linking Disrupted Neural Plasticity to Schizophrenia. (February 2013)

• Record Type: Journal Article
• Authors: Voineskos, Daphne; Rogasch, Nigel C; Rajji, Tarek K; Fitzgerald, Paul B; Daskalakis, Zafiris J
• Is Part Of: Canadian journal of psychiatry =. Volume 58:Number 2(2013)
• Page Start: 86
• Page End: 92
• Publication Date: 2013-02
• Subjects: plasticity -- schizophrenia -- N-methyl-d-aspartate -- gamma-aminobutyric acid -- dopamine -- transcranial magnetic stimulation -- motor cortex -- dorsolateral prefrontal cortex; Psychiatry -- Periodicals; Psychiatry -- Canada -- Periodicals; 616.8900971
• DOI: 10.1177/070674371305800205
• Languages: English
• ISSNs: 0706-7437

Abstract

The adaptations resulting from neural plasticity lead to changes in cognition and behaviour, which are strengthened through repeated exposure to the novel environment or stimulus. Learning and memory have been hypothesized to occur through modifications of the strength of neural circuits, particularly in the hippocampus and cortex. Cognitive deficits, specifically in executive functioning and negative symptoms, may be a corollary to deficits in neural plasticity. Moreover, the main excitatory and inhibitory neurotransmitters associated with neural plasticity have also been extensively investigated for their role in the cognitive deficits associated with schizophrenia. Transcranial magnetic stimulation (TMS) represents some of the most promising approaches to directly explore the physiological manifestations of neural plasticity in the human brain. Three TMS paradigms (use-dependent plasticity, paired associative stimulation, and repetitive TMS) have been used to evaluate neurophysiological measures of neural plasticity in the healthy brain and in patients with schizophrenia, and to examine the brain's responses to such stimulation. In schizophrenia, deficits in neural plasticity have been consistently shown which parallel the molecular evidence appearing to be entwined with this debilitating disorder. Such pathophysiology may underlie the learning and memory deficits that are key symptoms of this disorder and may even be a key mechanism involved in treatment with antipsychotics.