The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry
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During the development of the nervous system, neurons must first migrate to their appropriate locations and then send out axons to make connections. Various environmental cues guide these migrating neurons and growing axons. After axons reach their target regions, neuronal contacts are created through the formation of synapses. ⋯ Here, we discuss semaphorins and plexins, the largest family of axon guidance ligand-receptor pairs. Because the roles of semaphorins in neuronal migration and axonal repulsion have been extensively reviewed, we will focus on plexin receptors. We will discuss how semaphorin signals are specifically passed through these receptors into cells and how plexins mediate their newly identified roles in axon pruning and synaptic development.
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What does the visual cortex of the blind do during Braille reading? This process involves converting simple tactile information into meaningful patterns that have lexical and semantic properties. The perceptual processing of Braille might be mediated by the somatosensory system, whereas visual letter identity is accomplished within the visual system in sighted people. Recent advances in functional neuroimaging techniques, such as functional magnetic resonance imaging, have enabled exploration of the neural substrates of Braille reading. The primary visual cortex of early-onset blind subjects is functionally relevant to Braille reading, suggesting that the brain shows remarkable plasticity that potentially permits the additional processing of tactile information in the visual cortical areas.
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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.