Behavioural pharmacology
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Behavioural pharmacology · Sep 2010
ReviewBrain-derived neurotrophic factor in traumatic brain injury, post-traumatic stress disorder, and their comorbid conditions: role in pathogenesis and treatment.
As US military service members return from the wars in Iraq and Afghanistan with elevated rates of traumatic brain injury (TBI) and post-traumatic stress disorder (PTSD), attention has been increasingly focused on TBI/PTSD comorbidity, its neurobiological mechanisms, and novel and effective treatment approaches. TBI and PTSD, and their comorbid conditions, present with a spectrum of common clinical features such as sleep disturbance, depression, anxiety, irritability, difficulty in concentrating, fatigue, suicidality, chronic pain, and alterations in arousal. These TBI and PTSD disorders are also thought to be characterized by overlapping neural mechanisms. ⋯ Induction of BDNF and activation of its intracellular receptors can produce neural regeneration, reconnection, and dendritic sprouting, and can improve synaptic efficacy. In this review, we consider treatment approaches that enhance BDNF-related signaling and have the potential to restore neural connectivity. Such treatment approaches could facilitate neuroplastic changes that lead to adaptive neural repair and reverse cognitive and emotional deficits in both TBI and PTSD.
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Behavioural pharmacology · Sep 2010
ReviewHistone deacetylases govern cellular mechanisms underlying behavioral and synaptic plasticity in the developing and adult brain.
Histone deacetylases (HDACs) are a family of enzymes that alter gene expression patterns by modifying chromatin architecture. There are 11 mammalian HDACs that are classified by homology into four subfamilies, all with distinct expression patterns in the brain. ⋯ We will discuss the latest findings on the specific or redundant roles of individual HDACs in the brain as well as the impact of HDAC function on complex behavior, with a focus on learning, memory formation, and affective behavior. Potential HDAC-mediated cellular mechanisms underlying those behaviors are discussed.
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Behavioural pharmacology · Sep 2010
Tianeptine reduces morphine antinociceptive tolerance and physical dependence.
Long-term use of morphine can cause neuronal dystrophic changes in specific areas of the brain. These changes may underlie the mechanism for developing morphine antinociceptive tolerance and physical dependence. We evaluated the effect of tianeptine, an antidepressant with prominent neuroprotective and neuroplastic properties, on the development of morphine antinociceptive tolerance and physical dependence. ⋯ The combination of tianeptine with morphine significantly reduced the development of morphine antinociceptive tolerance and suppressed the incidence of naloxone-precipitated withdrawal symptoms. We conclude that tianeptine is an effective inhibitor of morphine-induced antinociceptive tolerance and physical dependence in mice. Our results would imply that comedication with tianeptine and morphine might benefit those who need long-term morphine treatment.