Here we examined

Here we examined CB-5083 ic50 the effects of bupropion, in the absence and presence of zinc, on the ion current elicited by acetylcholine (ACh-current) in Xenopus oocytes expressing neuronal alpha 4 beta 4 nAChRs. We found that bupropion-inhibited ACh-currents depending on ACh and bupropion

concentrations. Thus, the IC50 of bupropion was lower with a higher ACh concentration: 3.51 and 2.27 mu M for the current elicited with 0.5 and 2 mu M ACh, respectively. The inhibitory effect of bupropion was more potent in the presence of zinc, e.g. the IC50 was 0.81 mu M in the presence of 100 mu M zinc and 2 mu M ACh. Furthermore, the zinc-potentiated ACh-current decreased with increasing bupropion concentration. Thus, zinc potentiation was 5.05 and 1.25 fold of the ACh-current inhibited

by 10 nM and 5 mu M bupropion, respectively. The ACh-current inhibited by 3 mu M bupropion was voltage-independent, decreasing to 0.48 of the ACh-current at all voltages. Zinc potentiation of the bupropion-inhibited DihydrotestosteroneDHT solubility dmso ACh-current was slight and voltage-independent. In addition, the zinc-potentiated ACh-current was slightly voltage-dependent: 1.8 fold of the ACh-current at -120 mV and 2.3 at -40 mV. Bupropion inhibition of the zinc-potentiated ACh-current was strong and voltage-independent, decreasing to 0.15 of the zinc-potentiated ACh-current at all voltages. Accordingly, zinc may interact within the ion channel, whereas bupropion, and bupropion in the presence of zinc (which causes greater inhibition) interact in an external region of the receptor channel complex. These results suggest that bupropion interacts with alpha 4 beta 4 nAChRs in a non-competitive manner, that zinc increases the sensitivity of nAChRs to bupropion, and that bupropion decreases the sensitivity of nAChRs to zinc. (C) 2011 Elsevier Ltd. All rights reserved.”
“Learning, attentional, and perseverative deficits are characteristic of cognitive aging. In this study, genetically check details diverse CD-1 mice underwent longitudinal training in a task asserted to tax working memory capacity

and its dependence on selective attention. Beginning at 3 mo of age, animals were trained for 12 d to perform in a dual radial-arm maze task that required the mice to remember and operate on two sets of overlapping guidance (spatial) cues. As previously reported, this training resulted in an immediate (at 4 mo of age) improvement in the animals’ aggregate performance across a battery of five learning tasks. Subsequently, these animals received an additional 3 d of working memory training at 3-wk intervals for 15 mo (totaling 66 training sessions), and at 18 mo of age were assessed on a selective attention task, a second set of learning tasks, and variations of those tasks that required the animals to modify the previously learned response. Both attentional and learning abilities (on passive avoidance, active avoidance, and reinforced alternation tasks) were impaired in aged animals that had not received working memory training.

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