Progress in brain research
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Visual shape recognition--the ability to recognize a wide variety of shapes regardless of their size, position, view, clutter and ambient lighting--is a remarkable ability essential for complex behavior. In the primate brain, this depends on information processing in a multistage pathway running from primary visual cortex (V1), where cells encode local orientation and spatial frequency information, to the inferotemporal cortex (IT), where cells respond selectively to complex shapes. A fundamental question yet to be answered is how the local orientation signals (in V1) are transformed into selectivity for complex shapes (in IT). ⋯ Next, we found that responses to complex shapes were dictated by the curvature at a specific boundary location within the shape. Finally, using basis function decoding, we demonstrated that an ensemble of V4 neurons could successfully encode complete shapes as aggregates of boundary fragments. These findings identify curvature as a basis of shape representation in area V4 and provide insights into the neurophysiological basis for the salience of convex curves in shape perception.
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Review
Neural mechanisms of prefrontal cortical function: implications for cognitive rehabilitation.
Understanding the role of the frontal lobes in cognition remains a challenge for neurologists and neuroscientists. It is proposed that goal-directed behavior, at the core of what we consider human, depends critically on the function of the frontal lobes, and, specifically, the prefrontal cortex (PFC). In this chapter, we put forth the hypothesis that further insight into the neural mechanisms underlying normal PFC function may ultimately help us understand the frontal-lobe syndrome, and importantly, potentially lead to effective therapeutic interventions for frontal-lobe dysfunction. Thus, the aim of this chapter is to review current hypotheses and knowledge about the neural mechanisms underlying the normal function of the PFC in cognition that could guide the development of therapeutic interventions.
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Review
Mechanisms underlying the recovery of lower urinary tract function following spinal cord injury.
The lower urinary tract has two main functions, the storage and periodic expulsion of urine, which are regulated by a complex neural control system in the brain and lumbosacral spinal cord. This neural system coordinates the activity of two functional units in the lower urinary tract: (1) a reservoir (the urinary bladder) and (2) an outlet (consisting of bladder neck, urethra and striated muscles of the pelvic floor). During urine storage the outlet is closed and the bladder is quiescent, thereby maintaining a low intravesical pressure over a wide range of bladder volumes. ⋯ Following spinal cord injury, the bladder is initially areflexic but then becomes hyperreflexic due to the emergence of a spinal micturition reflex pathway. Studies in animals indicate that the recovery of bladder function after spinal cord injury is dependent in part on plasticity of bladder afferent pathways and the unmasking of reflexes triggered by capsaicin-sensitive C-fiber bladder afferent neurons. The plasticity is associated with changes in the properties of ion channels and electrical excitability of afferent neurons, and appears to be mediated in part by neurotrophic factors released in the spinal cord and the peripheral target organs.
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The autonomic nervous system modulates cardiac electrophysiology and abnormalities of autonomic function are known to increase the risk of ventricular arrhythmias. The abnormal and unstable autonomic control of the cardiovascular system following spinal cord injury also is well known. ⋯ Therefore, spinal cord injury may alter cardiac electrophysiology and increase the risk for ventricular arrhythmias. In this chapter, we discuss how the autonomic changes associated with cord injury can influence cardiac electrophysiology and the susceptibility to ventricular arrhythmias.
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In normal life, activity-dependent plasticity occurs in the spinal cord as well as in the brain. Like CNS plasticity elsewhere, this spinal cord plasticity can occur at many neuronal and synaptic sites and by a variety of mechanisms. Spinal cord plasticity is prominent in postnatal development and contributes to acquisition of standard behaviors such as locomotion and rapid withdrawal from pain. ⋯ This complexity is necessary, to preserve the full roster of behaviors, and is also inevitable, due to the ubiquity of activity-dependent plasticity in the CNS. Careful investigation of spinal cord plasticity is essential for understanding motor skills; and, because of the relative simplicity and accessibility of the spinal cord, is a logical and convenient starting point for exploring skill acquisition. Appropriate induction and guidance of activity-dependent plasticity in the spinal cord is likely to be a key part of the realization of effective new rehabilitation methods for spinal cord injuries, cerebral palsy, and other chronic motor disorders.