The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry
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Review
In search of the motor engram: motor map plasticity as a mechanism for encoding motor experience.
Motor skill acquisition occurs through modification and organization of muscle synergies into effective movement sequences. The learning process is reflected neurophysiologically as a reorganization of movement representations within the primary motor cortex, suggesting that the motor map is a motor engram. ⋯ Here the authors review evidence that 1) motor map topography reflects the capacity for skilled movement, 2) motor skill learning induces reorganization of motor maps in a manner that reflects the kinematics of acquired skilled movement, 3) map plasticity is supported by a reorganization of cortical microcircuitry involving changes in synaptic efficacy, and 4) motor map integrity and topography are influenced by various neurochemical signals that coordinate changes in cortical circuitry to encode motor experience. Finally, the role of motor map plasticity in recovery of motor function after brain damage is discussed.
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It has been known for many years that the classic motor symptoms of Parkinson's disease are accompanied by deficits of executive function that resemble those seen after frontal lobe damage in humans. What is less clear is how different components of frontostriatal circuitry contribute to these impairments. Recently, improved methods of clinical assessment and classification, combined with novel technical approaches, such as functional neuroimaging, have led to great advances in our understanding of the fundamental mechanisms that drive frontostriatal circuitry. As a direct result, it has been possible to redefine impairments of executive function in Parkinson's disease more precisely in terms of the specific neuropsychological, neuroanatomical, and psychopharmacological mechanisms involved.
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Review
Neuroimmune activation and neuroinflammation in chronic pain and opioid tolerance/hyperalgesia.
One area that has emerged as a promising therapeutic target for the treatment and prevention of chronic pain and opioid tolerance/hyperalgesia is the modulation of the central nervous system (CNS) immunological response that ensues following injury or opioid administration. Broadly defined, central neuroimmune activation involves the activation of cells that interface with the peripheral nervous system and blood. ⋯ CNS innate immunity and Toll-like receptors, in particular, may be vital players in this orchestrated immune response and may hold the answers to what initiates this complex cascade. The challenge remains in the careful perturbation of injury/opioid-induced neuroimmune activation to down-regulate this process without inhibiting beneficial CNS autoimmunity that subserves neuronal protection following injury.
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Model systems are needed for the scientific investigation of consciousness. A good model system should include variable states of consciousness, allowing the relationship between brain activity and consciousness to be investigated. Examples include sleep, anesthesia, focal brain lesions, development, evolution, and epilepsy. ⋯ Abnormal decreased activity in these same networks may cause loss of consciousness in complex partial seizures. Thus, abnormally increased or decreased activity in the same networks can cause loss of consciousness. Information flow during normal conscious processing may require a dynamic balance between these two extremes of excitation and inhibition.
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Following injury, axons of the adult mammalian central nervous system (CNS) fail to regenerate. As a result, CNS trauma generally results in severe and persistent functional deficits. The inability of CNS axons to regenerate is largely associated with nonneuronal aspects of the CNS environment that are inhibitory to axonal elongation. ⋯ In vitro characterization of Nogo has demonstrated its function as a potent inhibitor of axon elongation. In vivo neutralization of Nogo activity results in enhanced axonal regeneration and functional recovery following CNS injury as well as increased plasticity in uninjured CNS fibers. These findings suggest that Nogo may be a major contributor to the nonpermissive nature of the CNS environment.