Neuroscience and biobehavioral reviews
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Neurosci Biobehav Rev · Jun 2009
ReviewContribution of the activation of satellite glia in sensory ganglia to pathological pain.
Peripheral tissue injury/inflammation can alter the properties of somatic sensory pathways, resulting in behavioral hypersensitivity and pathological and/or chronic pain, including increased responses to pain caused by both noxious stimuli (hyperalgesia) and normally innocuous stimuli (allodynia). Although there are increasing reports that glia in the spinal cord contribute to the maintenance of pathological pain, recent evidence suggests that activation of satellite glia in sensory ganglia may also play an important role in the development of hyperalgesia and allodynia. ⋯ The focus of the present review is on the contribution of the activation of satellite glia in sensory ganglia to pathological pain. In addition, we discuss potential therapeutic targets in satellite glia-neuronal interactions for the prevention of pathological pain.
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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 · Apr 2009
Childhood neglect and parental care perception in cocaine addicts: relation with psychiatric symptoms and biological correlates.
Childhood neglect and poor child-parent relationships have been reported to increase substance use disorders susceptibility. Stressful environmental factors, including emotional neglect, could affect individual personality traits and mental health, possibly inducing stable changes in hypothalamic-pituitary-adrenal (HPA) axis and brain mono-amine function, in turn involved in addictive behavior vulnerability. Therefore, we decided to investigate homovanillic (HVA) and prolactin (PRL) plasma levels, as expression of possible changes in dopamine function, ACTH and cortisol plasma levels, as measures of HPA axis function, and concomitant psychiatric symptoms profile in abstinent cocaine addicts, in relationship to their childhood history of neglect and poor parental care perception. ⋯ These findings suggest the possibility that childhood experience of neglect and poor parent-child attachment may partially contribute to a complex neurobiological derangement including HPA axis and dopamine system dysfunctions, playing a crucial role in addictive and affective disorders susceptibility.
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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.