Synapse
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Luteinizing hormone-releasing hormone (LHRH) neurons play a pivotal role in the neuroendocrine control of mammalian reproduction. Astrocytes were shown to be involved in the regulation of LHRH neuronal function, but little is known about the contribution of astroglial-derived factors in the regulation of LHRH neuron development. In order to gain insight into the mechanisms regulating the development of these cells, at morphological and biochemical levels we characterized the neurotrophic effects exerted by young astrocytes (maintained in culture for 8 days in vitro) and old astrocytes (maintained 26 days) on the differentiation, proliferation, and phenotypic expression of immortalized hypothalamic LHRH (GT(1-1)) neurons in vitro. ⋯ Treatment of old glia with bFGF rescued its neurotrophic and functional effects on GT(1-1) cells. Moreover, the ACM of aged bFGF-treated old glia was the most powerful neurotrophic stimulus for GT(1-1) neurons. These results suggest that: 1) soluble peptidic factors, including bFGF, and mechanism(s) requiring coculture are responsible for the highly potent neurotrophic and functional effects of young glia; 2) the inhibitory effects of old glia on neurite outgrowth and LHRH release are mediated in part by soluble inhibitory molecules and in part by factors requiring coculture with old glia; 3) old glia may revert to a growth-supporting state when treated with bFGF and this functional shift involves a diffusible molecule with potent neurotrophic and functional effects on immortalized LHRH neurons. (c) 2000 Wiley-Liss, Inc.
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Combined administration of the amphetamine analogs phentermine and fenfluramine (PHEN/FEN) has been used in the treatment of obesity. While these medications are thought to modulate monoamine transmission, the precise neurochemical effects of the PHEN/FEN mixture have not been extensively studied. To assess the mechanism of PHEN/FEN action, in vivo microdialysis studies were performed in the nucleus accumbens of conscious freely moving rats. ⋯ Thus, dual activation of DA and 5-HT neurotransmission with monoamine releasing agents may be an effective treatment strategy for substance use disorders, as well as for obesity. Synapse 36:102-113, 2000. Published 2000 Wiley-Liss, Inc.
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We examined the acute effect of the irreversible GABA-transaminase inhibitor, gamma-vinyl GABA (GVG, Sabril((R)), Vigabatrin((R))) on increases in nucleus accumbens (NAc) dopamine (DA) following acute administration of methamphetamine, heroin, or ethanol. Methamphetamine (2.5 mg/kg) produced a dose-dependent increase (2, 700%) in NAc DA. GVG preadministration (300 or 600 mg/kg), however, inhibited this response by approximately 39 and 61%, respectively. ⋯ Finally, at half the dose necessary for heroin, GVG (150 mg/kg) also completely abolished ethanol-induced increases in NAc DA following a 0.25 g/kg challenge dose (140%). Taken with our previous findings using nicotine or cocaine as the challenge drug, these results indicate that GVG attenuates increases in NAc DA by a mechanism common to many drugs of abuse. However, it appears unlikely that an acute dose of GVG can completely inhibit increases in NAc DA following challenges with a drug whose mechanism of action is mediated primarily through the DA reuptake site.
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ERRATUM: Everett A. W. 1999. Membrane Recycling Due to Low and High Rates of Nerve Stimulation at Release Sites in the Amphibian (Bufo marinus) Neuromuscular Junction. ⋯ In the above-referenced article, Figure 1 was erroneously reproduced in black and white as converted from a color original, not providing an accurate representation of the staining. The figure is reproduced here as the author intended, from an original black and white rendering. The Publisher sincerely apologizes for this error.
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The paraventricular nucleus of the thalamus (PVT) is a midline thalamic nucleus that responds strongly to exposure to various stressors. Many of the projection targets of PVT neurons, including the medial prefrontal cortex, nucleus accumbens, and central/basolateral nuclei of the amygdala, are also activated by stress. We sought to determine if PVT neurons that respond to stress are those that project to one or more of these forebrain sites. ⋯ Stress markedly increased Fos protein-like immunoreactivity in PVT neurons, but without regard to the projection target of the thalamic neurons. Thus, the percentage of PVT cells that were retrogradely labeled from either the prefrontal cortex, nucleus accumbens, or amygdala, and that expressed Fos-like immunoreactivity did not differ substantially across the three forebrain sites. These data suggest that the PVT may have a role as a generalized relay for information relating to stress, and may serve an important role in the stress-induced activation of limbic forebrain areas.