Neuroscience and biobehavioral reviews
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Neurosci Biobehav Rev · Jun 2009
ReviewRodent models of insomnia: a review of experimental procedures that induce sleep disturbances.
Insomnia, the most common sleep disorder, is characterized by persistent difficulty in falling or staying asleep despite adequate opportunity to sleep, leading to daytime fatigue and mental dysfunction. As sleep is a sophisticated physiological process generated by a network of neuronal systems that cannot be reproduced in-vitro, pre-clinical development of hypnotic drugs requires in-vivo investigations. ⋯ Only few valid insomnia models are currently available, although many experimental conditions lead to disturbance of physiological sleep. We categorized these conditions as a function of the procedure used to induce perturbation of sleep, and we discuss their respective advantages and pitfalls with respect to validity, feasibility and translational value to human research.
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Neurosci Biobehav Rev · Jun 2009
ReviewStress-induced prefrontal reorganization and executive dysfunction in rodents.
The prefrontal cortex (PFC) mediates a range of higher order 'executive functions' that subserve the selection and processing of information in such a way that behavior can be planned, controlled and directed according to shifting environmental demands. Impairment of executive functions typifies many forms of psychopathology, including schizophrenia, mood and anxiety disorders and addiction, that are often associated with a history of trauma and stress. ⋯ In parallel, there is growing evidence that stress-induced alterations in PFC neuronal morphology are associated with deficits in rodent executive functions such as working memory, attentional set-shifting and cognitive flexibility, as well as emotional dysregulation in the form of impaired fear extinction. Although the molecular basis of stress-induced changes in PFC morphology and function are only now being elucidated, an understanding of these mechanisms could provide important insight into the pathophysiology of executive dysfunction in neuropsychiatric disease and foster improved strategies for treatment.
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Neurosci Biobehav Rev · Mar 2009
ReviewPain-related effects of trait anger expression: neural substrates and the role of endogenous opioid mechanisms.
Literature is reviewed indicating that greater tendency to manage anger via direct verbal or physical expression (trait anger-out) is associated with increased acute and chronic pain responsiveness. Neuroimaging data are overviewed supporting overlapping neural circuits underlying regulation of both pain and anger, consisting of brain regions including the rostral anterior cingulate cortex, orbitofrontal cortex, anterior insula, amygdala, and periaqueductal gray. These circuits provide a potential neural basis for observed positive associations between anger-out and pain responsiveness. ⋯ An opioid dysfunction hypothesis is presented in which inadequate endogenous opioid inhibitory activity in these brain regions contributes to links between trait anger-out and pain. A series of studies is presented that supports the opioid dysfunction hypothesis, further suggesting that gender and genetic factors may moderate these effects. Finally, possible implications of interactions between trait anger-out and state behavioral anger expression on endogenous opioid analgesic activity are described.
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Neurosci Biobehav Rev · Aug 2008
ReviewStress as a neuroinflammatory condition in brain: damaging and protective mechanisms.
Several neuropsychiatric diseases are related with stress (posttraumatic stress disorder, major depressive disorder, anxiety disorders, schizophrenia) and stress exposure modifies the onset and evolution of some neurological diseases (neurodegenerative diseases). It is accepted that brain inflammatory responses contribute to cell damage during these illnesses. Studies carried out with some stress protocols (physical, psychological or mixed) show a pro-inflammatory response in the brain and other systems mainly characterized by a complex release of several inflammatory mediators such as cytokines, prostanoids, free radicals and transcription factors. ⋯ Interestingly, anti-inflammatory pathways are also activated in brain in response to stress, constituting a possible endogenous mechanism of defence against excessive inflammation. The possibility of pharmacological modulation of these pathways to prevent the accumulation of pro-inflammatory mediators and subsequent brain damage in stress and in stress-related neuropsychological conditions is also reviewed. This dual response elicited by stress in brain, both pro- and anti-inflammatory deserves further attention in order to understand pathophysiological changes as well as possible new therapeutic approaches of stress-related neuropsychopathologies.
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Neurosci Biobehav Rev · Jul 2008
ReviewSpinal glial activation contributes to pathological pain states.
Chronic pain, a pathological state, affects millions of people worldwide. Despite decades of study on the neuronal processing of pain, mechanisms underlying the creation and maintenance of enhanced pain states after injury or inflammation remain far from clear. In the last decade, however, the discovery that glial activation amplifies pain has challenged classic neuronal views of "pain". ⋯ We overview the action of spinal glia (both microglia and astrocytes) in several persistent pain models, and provide new evidence that spinal glia activation contributes to the development and maintenance of arthritic pain facilitation. We also attempt to discuss some critical questions, such as how signals are conveyed from primary afferents to spinal glia following peripheral nerve injury and inflammation. What causes glia to become activated after peripheral/central injury/inflammation? And how the activated glia alter neuronal sensitivity and pain processing? Answers to these questions might open a new approach for treatment of pathological pain.