of terminal alpha(2)-adrenergic autoreceptors was attenuated since increasing frequency of stimulation of the ascending NE pathway produced a lesser degree of suppression of pyramidal neurons in rats administered bupropion than the control.
Enhancement of 5-HT and NE transmissions in hippocampus by prolonged bupropion may account for its effectiveness in major depression.”
“The question of the subtype(s) of the nicotinic acetylcholine receptor (nAChR) mediating the attention-enhancing effects of nicotine is still unsettled. While early studies pointed towards subtypes other than the homomeric alpha 7 nAChR, pro-cognitive effects of alpha 7 nAChR agonists have since been demonstrated.
This study tested YAP-TEAD Inhibitor 1 mouse whether the performance-enhancing effects of nicotine in a rodent model of attention could be reversed by the alpha 4 beta NU7441 chemical structure 2, alpha 4 beta 4, alpha 3 beta 2, and alpha 2 beta 2 nAChR antagonist dihydro-beta-erythroidine (DH beta E), or the alpha 7 antagonist methyllycaconitine (MLA).
tests, 12 rats trained to perform the 5-choice serial reaction time task were systemically injected with nicotine or vehicle in the presence of increasing doses of DH beta E or MLA.
DH beta E did not antagonize the attention-enhancing effects of nicotine reflected by measures of accuracy and omission errors, suggesting that its previously reported antagonism of nicotine effects on latency and anticipatory responses specifically reflected the
stimulant effects of nicotine. MLA dose-dependently reversed the reduction in omission errors by nicotine. In the absence of nicotine, low doses of MLA (0.4 and 1.3 mg/kg) not previously tested on attention improved response accuracy, resulting in an inverted U-shape dose-response function.
nAChR subtypes involved in the performance-enhancing effects of nicotine appear to vary depending on the function assessed. Our findings Thymidine kinase suggest a greater involvement of alpha 7 nAChRs in the effects of nicotine on attention than first suggested by preclinical studies, with different optimal receptor tones for aspects of stimulus detection and response readiness to task stimuli.”
“The placebo effect is a fascinating yet puzzling phenomenon, which has challenged investigators over the past 50 years. In previous studies, the investigators only focused on the placebo effect obtained within a single domain, and pain is the field in which most of the placebo research has been performed. However, recent research by our laboratory (Zhang and Luo in Psychophysiology 46:626-634, 2009; Zhang et al. 2011) showed that, in human subjects, the placebo effect can be transferred from one domain to the other, namely from pain to emotion.
The scope of this study was to investigate whether placebo analgesia could affect the depressive behavior in mice.
Female C57/BL6 mice were trained to associate the context cue with elevated pain tolerance via a set of procedures.