“From Humans to Animals: Animal Models in Schizophrenia”

Beirut campus, Byblos campus

The Department of Natural Sciences is holding a lecture entitled “From Humans to Animals: Animal Models in Schizophrenia,” to be given by Dr. Liesl Jones, assistant professor in the department of biological sciences in the City University of New York. The lecture will be held in Block A room 710-711 of the Byblos campus and in Nicol 222 on the Beirut campus.

Abstract: The use of animal models in mimicking diseases is crucial in designing drug therapies and understanding the eitiology of disease.  Here we present several possible models for schizophrenia. The aim of this chapter is to critically review current models for schizophrenia.  Schizophrenia is a devastating psychiatric illness.  Much research has shown that there are a variety of genes that are linked to schizophrenia. Anatomical studies have suggested cell in volume loss in the medial dorsal nucleus of the thalamus (MD) as well as alterations in cell density in the hippocampus.  Cellular changes include loss of dendrites and spines in the prefrontal cortex (PFC) as well as alterations in proteins involved in calcium signaling.  The one link to many of the studies appears to involve calcium signaling.  Much research suggests alterations in the hippocampus, PFC, MD and the amygdala.  Therefore a working animal model would have to show changes similar to that see in schizophrenia in the regions affected.  As mentioned above one of the most consistent findings in schizophrenia research is a decrease in volume and neuronal number in the MD.  The MD is reciprocally connected to the prefrontal cortex (PFC), another region implicated in schizophrenia.  Research suggests that the MD developmentally influences pyramidal cell morphology in the PFC in an activity-dependent and calcium dependent manner. Focusing on the interplay between the MD and the PFC, our research examines the hypothesis that morphological alterations observed in the PFC in schizophrenia could result from early damage to the MD. Unilateral electrolytic lesions of the MD in Long-Evans rat pups were made on postnatal day 4 (P4) and animals developed to P60.  Previously we examined dendritic morphology by examining MAP2 immunostaining and by using Golgi techniques to determine basilar dendrite number and spine density. Lesions causing mean MD volume decreases of 12.4% led to decreases in MAP2 staining in the prefrontal cortical regions examined. The lesion also caused a decrease in number of primary and secondary basilar dendrites in all three regions as well as a decrease in spine density. Research has suggested that there are schizophrenic associated alterations in MAP2 and cell density in the hippocampus.  To further examine or model for schizophrenia we examined cell density in the dentate gyrus and CA1 region of the hippocampus. Our data suggest alterations in cell density in the dentate gyrus. Our data are thus consistent with the hypothesis that early MD damage may lead to alterations similar to that observed in schizophrenia suggesting a possible working model for schizophrenia.  In addition to our neurodevelopmental model we will examine other neurodevelopmental models, pharmacological models and genetic models.  We will discuss how these models similarities and differences and suggest direction for future study.  For a disease as complex as schizophrenia understanding how to mimic the disease is important in determining drug therapies as well as possible methods for early detection and intervention.

All are welcome to attend.