Neuroscience
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Comparative Study
Long-term effects of maternal separation on ethanol intake and brain opioid and dopamine receptors in male Wistar rats.
Accumulating evidence indicates that an animal's response to a drug can be profoundly affected by early environmental influences. The brain opioid and dopamine systems may play a critical role in these effects, since various types of stress and drugs of abuse promote alterations in these brain systems. To study this further, we investigated long-term behavioural and neurochemical effects of repeated maternal separation in male Wistar rats. ⋯ Ethanol-induced changes were observed in D(2)-like receptor density in the ventral tegmental area in MS360, and in the ventral tegmental area and frontal-parietal cortex in animal facility-reared rats. These findings show that early experiences can induce long-lasting changes in especially brain dopamine receptor density and that ethanol consumption induces alterations in opioid and dopamine receptor density in distinct brain areas. It is also suggested that changes induced by repeated MS15 may provide protection against high voluntary ethanol intake.
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Comparative Study
A 14-day period of hindpaw sensory deprivation enhances the responsiveness of rat cortical neurons.
Hypodynamia-hypokinesia (HH) is a model of hindpaw sensory deprivation. It is obtained by unloading of the hindquarters during 14 days. In this situation, the feet are not in contact with the ground and as a consequence, the cutaneous receptors are not activated; the sensory input to the primary somatosensory cortex (SmI) is thus reduced. ⋯ Thin-spike cells were less frequently encountered in HH than in control rats. The analysis of regular cells revealed that after HH (1) spontaneous activity was unchanged and (2) cortical somatosensory neurons were more responsive: the cutaneous threshold was reduced and the response magnitude increased. Taken together, these results suggest a down-regulation of GABAergic function.
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Comparative Study
In vitro reconstitution of signal transmission from a hair cell to the growth cone of a chick vestibular ganglion cell.
Signal transmission from a chick hair cell to the growth cone of a vestibular ganglion cell was examined by placing an acutely dissociated hair cell on the growth cone of a cultured vestibular ganglion cell. Electrical stimuli were applied to the hair cell while monitoring the intracellular Ca(2+) concentration ([Ca(2+)](i)) at the growth cone or recording whole-cell currents from the vestibular ganglion cell. Electrical stimulation of the hair cell induced [Ca(2+)](i) increases at the growth cone and inward currents in the vestibular ganglion cell. ⋯ Glutamate (100 nM-300 microM) applied to the vestibular ganglion cell by the Y-tube method induced inward currents which were also antagonized by CNQX, but not by APV. These results indicate that the electrical stimulation of a hair cell induced glutamate or glutamate like agent release from the hair cell, which activated non-N-methyl-D-aspartate receptors at the growth cone of the vestibular ganglion cell, followed by action potentials and [Ca(2+)](i) elevation in the vestibular ganglion cell. This is the first demonstration of in vitro reconstitution of functional signal transmission from a hair cell to a vestibular ganglion cell.
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Comparative Study
Local sensory ganglion ischemia induced by endothelin vasoconstriction: vulnerability of diabetic neurons and microvessels.
In some disorders of the peripheral nervous system, it is relevant to understand how sensory neurons respond to selective ganglion ischemia. Sensory dorsal root ganglia may be susceptible to ischemic damage and irretrievable neuron loss because of their metabolic requirements. In diabetes, heightened sensitivity to ischemia associated with elevated endothelin levels might render ganglia particularly vulnerable. ⋯ Both intraganglionic axons and downstream sural sensory axons developed evidence of axonal degeneration. Local endothelin-induced vasoconstriction of microvessels supplying dorsal root ganglia provides a selective model of ischemia. Diabetic vessels and neurons, exposed to a greater depth and duration of ischemia from endothelin, are especially vulnerable.
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Cell surface glycoconjugates are thought to mediate cell-cell recognition and play roles in neuronal development and functions. We demonstrated here that exposure of neuronal cells to nanomolar levels of gangliosides Neu5Acalpha 8Neu5Acalpha 3Galbeta 4GlcCer, Galbeta 3GalNAcbeta 4(Neu5Acalpha 8Neu5Acalpha 3)Galbeta 4GlcCer (GD1b), Neu5Acalpha 3Galbeta 3GalNAcbeta 4(Neu5Acalpha 8Neu5Acalpha 3)Galbeta 4GlcCer (GT1b) or its oligosaccharide portion induced a rapid and transient activation of Ca2+/calmodulin-dependent protein kinase II (CaM-KII) in the subplasmalemma. Galbeta 3GalNAcbeta 4(Neu5Acalpha 3)Galbeta 4GlcCer (GM1), GalNAcbeta 4(Neu5Acalpha 3)Galbeta 4GlcCer, Neu5Acalpha 3Galbeta 4GlcCer, Neu5Acalpha 3Galbeta 3GalNAcbeta 4(Neu5Acalpha 3)Galbeta 4GlcCer (GD1a), and Neu5Acalpha 8Neu5Acalpha 3Galbeta 3GalNAcbeta 4(Neu5Acalpha 8Neu5Acalpha 3)-Galbeta 4GlcCer were ineffective. ⋯ The filopodia formation induced by the gangliosides may have a physiological relevance because long-term exposure of hippocampal neurons to GT1b oligosaccharide induced advanced dendritogenesis. Furthermore, exposure of cerebellar neurons to GT1b oligosaccharide facilitated CaM-KII-dependent dendritic outgrowth and branch formation of cerebellar Purkinje neurons, in which actin isoforms were localized to motile structures in dendrites. Thus, the ganglioside/CaM-KII signal plays a role in modulating dendritic morphogenesis by inducing cdc42-mediated actin reorganization.