Impairments of event-related magnetic fields in schizophrenia patients with predominant negative symptoms.

Recently there is a growing understanding that patients suffering from negative symptoms of schizophrenia represent a distinct patient population. However, despite the abundance of EEG studies characterizing schizophrenia patients in general, only a handful of studies have focused on the electrophysiological correlates of negative symptoms. The current study examined whether the impairments in event-related magnetic fields (ERFs) commonly reported in heterogeneous groups of patients with mixed positive and negative symptoms also occur in patients with predominantly negative symptoms, and investigated their correlation to clinical symptoms and cognitive deficits. Twenty schizophrenia patients suffering from predominant negative symptoms and 25 healthy subjects underwent neuropsychological and electromagnetic assessments. ERFs were recorded during a three-stimuli novelty oddball and a sensory gating paradigm, and M50, P300m and Novelty-P3m components were investigated. Patients displayed impaired M50 ratios, reduced left P300m and frontal Novelty-P3m amplitudes. These electromagnetic measures correlated significantly with the severity of negative symptoms (SANS scale). The electrophysiological abnormalities which have been proposed as candidate biomarkers for schizophrenia are also manifested in patients with predominantly negative symptoms.

Different signal transduction cascades are activated simultaneously in the rat insular cortex and hippocampus following novel taste learning.

Novel taste learning is a robust one-trial incidental learning process, dependent on functional activity of the insular (taste) cortex. In contrast to that of the cortex, the role of the hippocampus in taste learning is controversial. We set out to identify the time courses of the activation of mitogen-associated protein kinase (MAPK), transcription factor cAMP-response element-binding protein (CREB) and Akt/PKB (protein kinase B) in the insular cortex and hippocampus of rats subsequent to novel taste learning. Following taste learning, an early response (20 min) occurred at the same time in the insular cortex and the hippocampus. However, whereas MAPK was activated specifically in the insular cortex, CREB and Akt were phosphorylated in the hippocampus but not in the cortex. In addition, the immediate early gene, CCAAT/enhancer binding protein (C/EBPbeta) was induced in both the hippocampus and the insular cortex 18 h following taste learning. The results demonstrate, for the first time, correlative activation and gene expression in the hippocampus following novel taste learning. Moreover, the results suggest that different signal transduction cascades necessary for taste learning are activated in concert in different brain structures, to enable taste learning and consolidation.