Progress in brain research
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Do seizures cause neuronal death? At least in the immature hippocampus, this may not be the critical question for determining the mechanisms of epileptogenesis. Neuronal injury and death have clearly been shown to occur in most epilepsy models in the mature brain, and are widely considered a prerequisite to seizure-induced epilepsy. In contrast, little neuronal death occurs after even a severe and prolonged seizure prior to the third postnatal week. ⋯ Rather, findings in the experimental prolonged febrile seizure model suggest that persistent functional alterations of gene expression ('neuroplasticity') in diverse hippocampal neuronal populations may promote pro-epileptogenic processes induced by these seizures. These findings also suggest that during development, relatively short, intense bursts of neuronal activity may disrupt 'normal' programmed maturational processes to result in permanent, selective alterations of gene expression, with profound functional consequences. Therefore, determining the cascade of changes in the programmed expression of pertinent genes, including their temporal and cell-specific spatial profiles, may provide important information for understanding the process of transformation of an evolving, maturing hippocampal network into one which is hyperexcitable.
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Historical Article
Central control of information transmission through the intraspinal arborizations of sensory fibers examined 100 years after Ramón y Cajal.
About 100 years ago, Santiago Ramón y Cajal reported that sensory fibers entering the spinal cord have ascending and descending branches, and that each of them sends collaterals to the gray matter where they have profuse ramifications. To him this was a fundamental discovery and proposed that the intraspinal branches of the sensory fibers were "centripetal conductors by which sensory excitation is propagated to the various neurons in the gray matter". In addition, he assumed that "conduction of excitation within the intraspinal arborizations of the afferent fibers would be proportional to the diameters of the conductors", and that excitation would preferentially flow through the coarsest branches. ⋯ The PAD produced by single, or by small groups of GABAergic interneurons in group I muscle afferents, can remain confined to some sets of intraspinal arborizations of the afferent fibers and not spread to nearby collaterals. In muscle spindle afferents this local character of PAD allows cutaneous and descending inputs to differentially inhibit the PAD in segmental and ascending collaterals of individual fibers, which may be an effective way to decouple the information flow arising from common sensory inputs. This feature appears to play an important role in the selection of information flow in muscle spindles that occurs at the onset of voluntary contractions in humans.