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Enhanced LTP Persistence Associated with Memory Alteration in the Maternal Immune Activation Model of Schizophrenia.

Enhanced LTP Persistence Associated with Memory Alteration in the Maternal Immune Activation Model of Schizophrenia.

Individuals with schizophrenia display a number of structural and cytoarchitectural alterations in the hippocampus, suggesting that functional processes such as synaptic plasticity may also be modified. Altered hippocampal plasticity is likely to affect memory function, and may therefore contribute to the cognitive symptoms of schizophrenia.  

Our goal was to determine whether environmental risk factors that have previously been associated with schizophrenia produced changes in hippocampal synaptic plasticity and associated memory processes, using the maternal immune activation (MIA) animal model. Pregnant rat dams were administered either Poly I:C or vehicle on GD15 to initiate MIA. Long-term potentiation (LTP) was measured in the dentate gyrus of their freely-moving, adult offspring. 

The memory performance of these animals was also tested in the Morris water-maze and in a plus-maze. MIA did not alter basal synaptic transmission in either the dentate gyrus or CA1 of freely moving adult rats. It did, however, result in increased paired-pulse facilitation of the dentate gyrus population spike and an enhanced persistence of dentate LTP across several days. MIA animals also displayed slower reversal learning in both the water maze, and the plus maze.

MIA animals displayed a reduced flexibility to change behavior in response to changes in task requirements. The effect could result from more persistent memory for the original goals, an interpretation that corresponds well with the LTP data. The results support the hypothesis that hippocampal plasticity is altered in schizophrenia and that this may underlie aspects of cognitive dysfunction in this disorder. Supported by funding from the Health Research Council of New Zealand.

Speakers: David Bilkey
Conference: MAPrc
Areas of Interest / Categories: MAPrc 2014, Schizophrenia

MAPrc 2014

The effect of symptomatic improvement on gamma synchrony in psychosis: a pilot study.

Impaired functional connectivity, as measured by synchronous gamma activity, has been observed in both the early and chronic stages of schizophrenia, as well as in unaffected first-degree relatives. This suggests gamma synchrony may be a trait-like marker of psychosis susceptibility, and not just a state-dependant characteristic. To conduct a pilot study into the short-term temporal stability of gamma synchrony and its relationship to symptomatic improvement in young patients who have been treated for recent onset psychosis. 20 medicated subjects underwent both clinical (PANSS) and electrophysiological (auditory oddball task during EEG) evaluation at both baseline and 8 weeks follow-up.

The effect of symptomatic improvement on gamma synchrony in psychosis: a pilot study.

Impaired functional connectivity, as measured by synchronous gamma activity, has been observed in both the early and chronic stages of schizophrenia, as well as in unaffected first-degree relatives. This suggests gamma synchrony may be a trait-like marker of psychosis susceptibility, and not just a state-dependant characteristic. To conduct a pilot study into the short-term temporal stability of gamma synchrony and its relationship to symptomatic improvement in young patients who have been treated for recent onset psychosis. 20 medicated subjects underwent both clinical (PANSS) and electrophysiological (auditory oddball task during EEG) evaluation at both baseline and 8 weeks follow-up.

Cerebral cortical grey matter deficits in schizophrenia and their associations with ageing, psychopathology, cognition and treatment response.

The diagnosis of schizophrenia lacks a broadly accepted biological basis and its heterogeneity may well represent a group of disorders with different aetiologies. Even so, brain imaging can map and quantify structural brain abnormalities in vivo as an intermediate (or endo-) phenotype of the disorder. To identify the degree of regional grey matter deficits in relation to age, the severity of psychopathology and cognitive/ neurological impairment, and treatment response in schizophrenia. Eighteen schizophrenia patients (32.2 years [SD 14.3], meeting DSM-IV criteria were examined. Eighteen pair-wise age (±2 years) and gender-matched healthy volunteers (31.9 years [SD 14.3]) served as control group.

A healthy lifestyle intervention among people with psychotic disorders: Results from a RCT.

People with psychotic disorders have higher rates of CVD risk factors compared to the general community. To our knowledge, this is the first RCT of its kind. To determine the efficacy of a multi-component intervention (smoking, diet and activity) delivered face to face compared to a largely telephone delivered intervention (smoking) among smokers with psychotic disorders. Participants with psychotic disorders residing in the community and smoking =15 cigarettes/day (CPD) were randomly assigned to either condition.

Schizophrenia and neurodevelopment – Where do we stand today?

The schizophrenia brain is differentiated from the normal brain by subtle changes, with significant overlap in measures between normal and disease states. For the past 25 years, schizophrenia has increasingly been considered a neurodevelopmental disorder. This frame of reference challenges biological researchers to consider how pathological changes identified in adult brain tissue can be accounted for by aberrant developmental processes occurring during fetal, childhood or adolescent periods. The objective is to place schizophrenia neuropathology in a neurodevelopmental context. This requires solid, scrutinized evidence of changes occurring during normal development of the cerebral cortex. We review literature on the development of the prefrontal cortex and chart major molecular and cellular events on a similar time line. Whilst neurogenesis, neuronal migration and myelination undergo most dramatic changes prenatally, these processes also extend into adolescence.

Serum epidermal growth factor levels are reduced in people with treatment resistant schizophrenia and modulated by clozapine treatment.

Up to 45% of patients with schizophrenia are treatment resistant to conventional drugs leaving clozapine as the only effective option. Its severe side-effects however limit it to a late stage option and the development of a biomarker to predict treatment response would be of high clinical utility. Our previous data demonstrate clozapine augments epidermal growth factor receptor (EGFR) signaling and hence we examined if EGF levels may be altered in treatment resistant schizophrenia (TRS) and are influenced by clozapine treatment. Study objectives: To determine if EGF levels are influenced by clozapine in TRS and can serve as a biomarker for clozapine response.

The Weight of Evidence: The Role of Metformin in Cardiometabolic Protection in Early Psychosis.

The relationship between weight gain and the treatment of first episode psychosis (FEP) with psychotropic medication is well established, with weight gain and increased cardiovascular risk as common sequelae. Such metabolic abnormalities create further disease burden and shorten the life expectancy of a population already dealing with mental illness. Antipsychotic-induced weight gain has been shown to commence within the first months of initiating treatment in drug-naïve youth, thus early intervention is necessary in order to attenuate the progression of metabolic abnormalities. Initial studies using metformin in this population have shown promising results.

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