Neuroscience
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Comparative Study
Differential cavitation, angiogenesis and wound-healing responses in injured mouse and rat spinal cords.
The vascular disruption, blood vessel loss and cavitation that occur at spinal cord injury (SCI) epicenters in mice and rats are different, but few studies have compared the acute SCI response in the two species. This is of interest since key elements of the rat SCI response are shared with humans. In this study, we investigated acute SCI responses and characterized changes in pro- and anti-angiogenic factors and matrix deposition in both species. ⋯ We conclude that the more robust angiogenesis/wound-healing response in the mouse attenuates post-injury wound cavitation. Although the spinal cord functions that were monitored post-injury were similarly affected in both species, we suggest that the quality of the angiogenesis/wound-healing response together with the diminished lesion size seen after mouse SCI may protect against secondary axon damage and create an environment more conducive to axon sprouting/regeneration. These results suggest the potential therapeutic utility of manipulating the angiogenic response after human SCI.
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Genipin, an important bioactive component from Gardenia jasminoides Eills, was demonstrated to possess antidepressant-like effects in a previous study. However, the molecular mechanism of antidepressant-like effects on genipin was not clear. The present study aimed to investigate the possible mechanism of antidepressant-like effects on genipin with a chronic unpredictable mild stress (CUMS)-induced depression model in rats. ⋯ The mRNA and protein expression of CREB, BDNF were increased in genipin-treated rats compared to the CUMS-exposed model group. Moreover, the levels of corticosterone in serum were decreased by genipin-treated compared to the CUMS-exposed model group. These results suggest that the possible mechanism of antidepressant-like effects on genipin, at least in one part, resulted from monoaminergic neurotransmitter system and the potential dysfunctional regulation of the post-receptor signaling pathway, which particularly affected the 5-HT(1A)R, 5-HT(2A)R and BDNF levels in the hippocampus.
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Stress, a common if unpredictable life event, can have pronounced effects on physiology and behavior. Individuals show wide variation in stress susceptibility and resilience, which are only partially explained by variations in coding genes. Developmental programing of the hypothalamic-pituitary-adrenal stress axis provides part of the explanation for this variance. ⋯ Stress and the stress axis interacts bi-directionally with epigenetic marks within the brain. It is now clear that exposure to stress, particularly in early life, has both acute and lasting effects on these marks. They in turn influence cognitive function and behavior, as well as the risk for suicide and psychiatric disorders across the lifespan and, in some cases, unto future generations.
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Cajal-Retzius cells (CRc) represent a mostly transient neuronal cell type localized in the uppermost layer of the developing neocortex. The observation that CRc are a major source of the extracellular matrix protein reelin, which is essential for the laminar development of the cerebral cortex, attracted the interest in this unique cell type. In this review we will (i) describe the morphological and molecular properties of neocortical CRc, with a special emphasize on the question which markers can be used to identify CRc, (ii) summarize reports that identified the different developmental origins of CRc, (iii) discuss the fate of CRc, including recent evidence for apoptotic cell death and a possible persistence of some CRc, (iv) provide a detailed description of the electrical membrane properties and transmitter receptors of CRc, and (v) address the role of CRc in early neuronal circuits and cortical development. Finally, we speculate whether CRc may provide a link between early network activity and the structural maturation of neocortical circuits.
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Cell volume regulation (CVR) is essential for all types of cells in the central nervous system (CNS) to counteract cell volume changes that may be associated with neuronal activities or diseases and with osmosensing in the hypothalamus, to facilitate morphological changes during cell proliferation, differentiation and migration, and to execute apoptosis of cells. The regulation is attained by regulating the net influx or efflux of solutes and water across the plasma membrane. The volume-sensitive outwardly rectifying (VSOR) anion channel plays a major role in providing a pathway for anion flux during the regulation. ⋯ This property confers a means of intercellular communications through the opening of the channel in the CNS. Thus exploring the roles of VSOR anion channels is crucial to understand the basic principles of cellular functions in the CNS. Here we review biophysical and pharmacological characteristics of the VSOR anion channel in the CNS, discuss its activation mechanisms and roles in the CNS reported so far, and give some perspectives on the next issues to be examined in the near future.