Neuroscience
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The prefrontal cortex (PFC) mediates higher-order cognitive and executive functions that subserve various complex, adaptable behaviors, such as cognitive flexibility, attention, and working memory. Deficits in these functions typify multiple neuropsychiatric disorders that are caused or exacerbated by exposure to psychological stress. Here we review recent evidence examining the effects of stress on executive and cognitive functions in rodents and discuss an emerging body of evidence that implicates the N-methyl-D-aspartate receptor (NMDAR) as a potentially critical molecular mechanism mediating these effects. Future work in this area could open up new avenues for developing pharmacotherapies for ameliorating cognitive dysfunction in neuropsychiatric disease.
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During the last 30 years there have been many attempts to develop animal models of obsessive compulsive disorder (OCD), in the hope that they may provide a route for furthering our understanding and treatment of this disorder. The present review provides the reader with an overview of the currently active animal models of OCD, their strengths and limitations, so that the reader can use the review as a guide for establishing new animal models of OCD, evaluating existing animal models and choosing among them according to one's needs. ⋯ On the basis of this evaluation we discuss the usefulness of the different models for screening drugs for anti-compulsive activity, detecting new targets for high frequency stimulation, studying the neural mechanisms of OCD and unraveling the role of gonadal hormones. We then describe potential new treatment strategies that emerge from the convergence of data obtained in different models on the one hand, and how different models can be used to model different subtypes or dimensions of OCD, on the other hand.
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Animal experimentation in the Parkinson's disease (PD) field is a classic example of how the use of animal models to study diseases can have a significant impact on human health. Among the different neurotoxin-based animal models of PD that are presently available, the 6-hydroxydopamine (6-OHDA) and the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) models have been established and validated as useful models for the development of therapeutic strategies aimed to treat motor symptoms and to study alterations of the basal ganglia that occur in this disease. The 6-OHDA rat model and the MPTP primate model have contributed enormously to translate animal experimentation into clinical practice, including pharmacological treatments and deep brain stimulation of the subthalamic nucleus. ⋯ At the same time, the lack of any effective neuroprotective strategy for PD is preventing the validation of any one particular model as a screening tool for such neuroprotective strategies. Therefore, it seems that we are trapped in a vicious circle that casts doubt on the suitability of the neurotoxin-based models for this purpose. Here, we discuss how epidemiological data may help to validate a specific model with data linking a lower risk of developing PD with nutritional/consumption habits or with a specific chronic drug therapy.
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Feeding is a fundamental process for basic survival and is influenced by genetics and environmental stressors. Recent advances in our understanding of behavioral genetics have provided a profound insight on several components regulating eating patterns. ⋯ The animal model is an essential tool in the investigation of eating behaviors and their pathological forms, yet development of an appropriate animal model for eating disorders still remains challenging due to our limited knowledge and some of the more ambiguous clinical diagnostic measures. Therefore, this review will serve to focus on the basic clinical features of eating disorders and the current advances in animal models of eating disorders.