Progress in brain research
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A central question in visual neuroscience is what circuits generate the responses of neurons in the primary visual cortex (V1). V1 neurons respond best to oriented stimuli of optimal size within their receptive field (RF) center. This size tuning is contrast dependent, i.e. a neuron's optimal stimulus size measured at high contrast (the high-contrast summation RF, or hsRF) is smaller than when measured using low-contrast stimuli (the low-contrast summation RF, or lsRF). ⋯ We review data showing that a subset of FB connections terminate in a patchy fashion in V1, and show modular and orientation specificity, consistent with their proposed role in orientation-specific center-surround interactions. We propose specific mechanisms by which each connection type contributes to the RF center and surround of V1 neurons, and implement these hypotheses into a recurrent network model. We show physiological data in support of the model's predictions, revealing that modulation from the "far" surround is not always suppressive, but can be facilitatory under specific stimulus conditions.
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The spinal cord is essential for normal autonomic nervous system regulation of the cardiovascular system as the preganglionic neurons controlling the heart and blood vessels originate in the thoracolumbar spinal segments. The site and extent of a spinal cord injury determine the degree of autonomic involvement in cardiovascular dysfunction after the injury. After complete cervical cord lesions the entire sympathetic outflow is separated from cerebral control; this may cause orthostatic hypotension. ⋯ This chapter will focus on orthostatic hypotension and paroxysmal hypertension in cord-injured people with lesions affecting the cervical and upper thoracic spinal cord. Conditions promoting these abnormalities in blood pressure will be elaborated. Possible mechanisms for the hypo- and hypertension will be discussed, as will strategies for managing these problems.
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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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On a daily basis, individuals with cervical and upper thoracic spinal cord injury face the challenge of managing their unstable blood pressure, which frequently results in persistent hypotension and/or episodes of uncontrolled hypertension. This chapter will focus on the clinical issues related to abnormal cardiovascular control in individuals with spinal cord injury, which include neurogenic shock, autonomic dysreflexia and orthostatic hypotension. Blood pressure control depends upon tonic activation of sympathetic preganglionic neurons by descending input from the supraspinal structures (Calaresu and Yardley, 1988). ⋯ This results in a variety of cardiovascular abnormalities that have been well documented in human studies, as well as in animal models (Osborn et al., 1990; Mathias and Frankel, 1992a, b; Krassioukov and Weaver, 1995; Maiorov et al., 1997, 1998; Teasell et al., 2000). However, the recognition and management of these cardiovascular dysfunctions following spinal cord injury represent challenging clinical issues. Moreover, cardiovascular disorders in the acute and chronic stages of spinal cord injury are among the most common causes of death in individuals with spinal cord injury (DeVivo et al., 1999).
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Spinal reflexes dominate cardiovascular control after spinal cord injury (SCI). These reflexes are no longer restrained by descending control and they can be impacted by degenerative and plastic changes within the injured cord. Autonomic dysreflexia is a condition of episodic hypertension that stems from spinal reflexes initiated by sensory input entering the spinal cord caudal to the site of injury. ⋯ One such treatment is an antibody to the integrin CD11d expressed by inflammatory leukocytes that enter the cord acutely after injury and cause significant secondary damage. This antibody blocks integrin-mediated leukocyte entry, resulting in greatly reduced white-matter damage and decreased autonomic dysreflexia after cord injury. Understanding the mechanisms for autonomic dysreflexia will provide us with strategies for treatments that, if given early after cord injury, can prevent this serious disorder from developing.