Progress in brain research
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Assessing the level of consciousness of noncommunicative brain-damaged patients is difficult, as one has to make inferences based on the patients' behavior. However, behavioral responses of brain-damaged patients are usually limited not only by their cognitive dysfunctions, but also by their frequent motor impairment. For these reasons, it is essential to resort to para-clinical markers of the level of consciousness. ⋯ Specifically, we emphasize the principled approach provided by the Integrated Information Theory of Consciousness (IITC). We describe the different conditions where the theory predicts markedly reduced states of consciousness, and discuss several technical and conceptual issues limiting its applicability to measuring the level of consciousness of individual patients. Nevertheless, we argue that some of the predictions of the theory are potentially testable using available imaging techniques.
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Gamma aminobutyric acid (GABA) is an inhibitor neurotransmitter that plays many important roles in the central nervous system. Because the half-life time of GABA is very short in vivo, GABA itself is not used for clinical practice. An analogue of GABA, baclofen, is an agonist of GABA-B receptor, and has very strong antispastic effect by acting to the posterior horn of the spinal cord. ⋯ The mechanism of SCS on pain is known to be mediated through the spinal GABA neuronal system. Thus, ITB and SCS have a common background, spinal GABA neuronal mechanism. The effect of GABA agonists on recovery of consciousness is not yet established, but review of such case studies becomes a clue to solve problems in PVS, and there may be hidden serendipity.
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Human death is a unitary phenomenon that physicians can determine in two ways: (1) showing the irreversible cessation of all brain clinical functions; or (2) showing the permanent cessation of circulatory and respiratory functions. Over the last 40 years the determination of human death using neurological tests ("brain death") has become an accepted practice throughout the world but has remained controversial within academic circles. Brain death has a rigorous biophilosophical basis by defining death as the irreversible loss of the critical functions of the organism as a whole. ⋯ Among physicians, the area of greatest controversy in death determination now is the use of circulatory-respiratory tests, particularly as applied to organ donation after circulatory death. Circulatory-respiratory tests are valid only because they produce destruction of the whole brain, the criterion of death. Clarifying the distinction between the permanent and irreversible cessation of circulatory and respiratory functions is essential to understanding the use of these tests, and explains why death determination in organ donation after circulatory death does not violate the dead donor rule.
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Review
The age of plasticity: developmental regulation of synaptic plasticity in neocortical microcircuits.
Proper wiring of neural circuits during development depends on both molecular cues that guide connectivity and activity-dependent mechanisms that use patterned activation to adjust the strength and number of synaptic connections. In this chapter, we discuss some of the plasticity mechanisms underlying the experience-dependent rewiring of visual cortical microcircuits focusing on layer 4 of rat primary visual cortex. The microcircuit in layer 4 has the ability to regulate its excitability by shifting the balance between excitatory and inhibitory synaptic transmission in an experience-dependent manner. ⋯ In contrast, during the classical sensitive period for rodent visual system plasticity, this homeostatic response is replaced by mechanisms that reduce the responsiveness of deprived cortex. We discuss this developmentally regulated switch in plasticity within layer 4 and how this might depend on the maturation of excitatory and inhibitory monosynaptic connections. Based on our published data, we propose inhibitory plasticity as an important player in circuit refinement that can contribute both to the compensatory forms of circuit plasticity in the early stages of development and to the pathological loss of function induced by visual deprivation during the critical period.
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Here we review the functional anatomy of brainstem circuits important for triggering saccades. Whereas the rostral part of the superior colliculus (SC) is considered to be involved in visual fixation, the caudal part of the SC plays an important role in generation of saccades. We determined the neural connections from the rostral and caudal parts of the SC to inhibitory burst neurons (IBNs) and omnipause neurons (OPNs) in the nucleus raphe interpositus. ⋯ Further, IBNs receive disynaptic inhibition from the rostral part of the SC, on either side, via OPNs. Intracellular recording revealed that OPNs receive excitation from the rostral parts of the bilateral SCs, and disynaptic inhibition from the caudal SC mainly via IBNs. The neural connections determined in this study are consistent with the notion that the "fixation zone" is localized in the rostral SC, and suggest that IBNs, which receive monosynaptic excitation from the caudal "saccade zone," may inhibit tonic activity of OPNs and thereby trigger saccades.