The neuroadaptations involved in opiate tolerance, dependence and withdrawal will be re-visited since they share many features with synaptic learning mechanisms.

This article

is part of a Special Issue entitled ‘Synaptic Plasticity and Addiction’. Published by Elsevier Ltd.”
“Background. The net metabolic cost of walking (C-w) as well as the level of neural activation of agonist and antagonist leg muscles are higher in healthy old compared with young adults. This study examined the association between C-w and agonist muscle activity and antagonist Selleckchem Selonsertib coactivity in young and old adults.

Methods. Young and old adults walked at 0.98 m/s on a treadmill set at 6% decline, level, and 6% incline, while C-w and neural activation of leg muscles were measured.

Results.

C-w was 7.0% (incline), 19.2% (level), and 47.3% (decline) higher in old adults (overall 18.3%). Old (67.1%) versus young (40.1%) adults activated their leg muscles 67.3% A-1210477 mw more during the gait tasks and had 152.8% higher antagonist muscle coactivation (old: 67.1%, young: 19.9%). Agonist muscle activation was unrelated to C-w on incline, but it explained up to 42% (level), 48% (decline), and 70% (three tasks combined) of variance in C-w. Antagonist coactivation accounted for up to 41% (incline), 45% (level), 59% (decline), 39% (three tasks combined) of variance in C-w.

Conclusions. Age-related adaptations in the recruitment pattern of leg muscles during gait significantly

contribute to the high C-w in old adults. Clinical interventions optimizing the neural control of leg muscles during www.selleck.cn/products/erastin.html gait could reduce C-w consequently the relative effort needed for exercise and activities of daily living in old adults.”
“Synaptic plasticity in the most general terms represents the flexibility of neurotransmission in response to neuronal activity. Synaptic plasticity is essential both for the moment-by-moment modulation of neural activity in response to dynamic environmental cues and for long-term learning and memory formation. These temporal characteristics are served by an array of pre- and post-synaptic mechanisms that are frequently modulated by ethanol exposure. This modulation likely makes significant contributions to both alcohol abuse and dependence. In this review. I discuss the modulation of both short-term and long-term synaptic plasticity in the context of specific ethanol-sensitive cellular substrates. A general discussion of the available preclinical, animal-model based neurophysiology literature provides a comparison between results from in vitro and in vivo studies. Finally, in the context of alcohol abuse and dependence, the review proposes potential behavioral contributions by ethanol modulation of plasticity. This article is part of a Special Issue entitled ‘Synaptic Plasticity and Addiction’. (C) 2010 Elsevier Ltd. All rights reserved.”
“Background.