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EEG neurofeedback (EEG-NFB) is a promising tool for the treatment of depressive disorders. However, many methods for the presentation of neurobiological reactions are available and it is widely unknown which of these feedback options are preferrable. Moreover, the influence of motivation on NFB training success is insufficiently studied. This study analyzed the efficacy of a novel EEG protocol (FC3/Pz) based on findings for NFB in depression. The role of four feedback options (Rumination, Anxiety, Meditation Master, Moving Art) from the NFB software "Brain Assistant" and motivation in EEG-based NFB performance was studied. Regarding "Anxiety" and "Rumination" visual feedback was used to evoke emotions; reinforcement (both negative and positive operant conditioning) was continuous. Regarding "Meditation Master" visual feedback was combined with continuous positive reinforcement. Regarding "Moving Art" 20-min calm nature films with neutral character were used; both visual and auditive feedback were applied. The reinforcement was positive and continuous. 13 healthy participants completed 15 EEG sessions over four months combining simultaneous frontal (aims: reduction of theta-, alpha- and high beta-activity, increase of low and mid beta-activity) and parietal training (aims: reduction of theta-, alpha 1-, mid and high beta-activity, increase of alpha 2- and low beta-activity). We observed significantly more pronounced percentage change in the expected direction for Anxiety than Moving Art (mean difference = 3.32; p = 0.003). The association between motivation and performance was non-significant. Based on these results we conclude that feedback with both negative and positive operant conditioning and emotion evoking effects should be preferred., Competing Interests: Declaration of Conflicting InterestsThe author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

Nicotinic acetylcholine receptors (nAChRs) of the hippocampus have been thought to contribute to cognitive enhancement by cigarette smoking. Although positive modulation on cognitive functions is linked to the smoked, low-dose nicotine, the cellular correlate behind this modulation is unknown. It has been accepted that cellular mechanisms underlying plastic effects on memory involve the association of backpropagating action potentials (bAPs) with synaptic activity in the hippocampus. Here, we show the effects of low-dose (1 microM) nicotine on bAP-evoked Ca2+ transients in basal dendrites and spines of pyramidal neurons in rat hippocampal slices. Although nicotine application failed to have any direct effect in low concentration, it could significantly enhance bAP-evoked Ca2+ transients through presynaptic nAChRs located on axon terminals innervating pyramidal cells. The activation of these receptors is known to release neurotransmitters and induce postsynaptic currents. High-dose (250-500 microM) nicotine could induce firing and Ca2+ accumulation in spines. Large amplitude currents were observed occasionally (8 out of 18 cells) in voltage clamp recordings in response to pressure application of high-dose nicotine. This may explain the relatively low incidence of nicotine-induced firing (7 out of 27 cells) under current clamp. These data indicate that (i) activation of presynaptic nAChRs can modulate backreporting in dendrites of pyramidal neurons and (ii) there is a group of pyramidal neurons with higher nicotine-sensitivity, producing firing at strong stimulations. Our data revealed a subcellular effect of nicotine through regulation of Ca2+ levels in the computational units of pyramidal neurons., ((c) 2008 Wiley-Liss, Inc.)

Ca2+ permeability of central nicotinic acetylcholine receptors (nAChRs), especially the alpha7 subunits, are exceptionally high and this important feature provide a special functional importance for these receptors at the system level. Although studies at the cellular level extensively characterized the molecular properties of Ca2+ influx following nAChR activation, much less is known about the time-related Ca2+ dynamics during nicotine administration in integration units of neurons. Such studies are of particular relevance to understanding in situ nonsynaptic actions of nicotine. Puff ejection of drugs produce a rapid drug delivery and elimination from the cell surface allowing the activation of extrasynaptic receptors within desensitization time-frame. In this report we provide evidence that rapid nicotine application is able to produce irregular Ca2+ transients in the dendrites of stratum radiatum interneurons in the hippocampal CA1 region. Potential components and mechanisms of nAChR-mediated Ca2+ influx are discussed in details to demonstrate the unique feature of activation of nAChRs involved in nonsynaptic function in interneurons as compared to other types of nicotinic activity.

Two-photon microscopy is an especially powerful tool for combining anatomical and physiological experiments in the central nervous system: the possibility of simultaneously studying physiological phenomena in well-defined anatomical compartments allows fluorescence imaging of neurons in deeper layers of the brain. In this review we summarize the most commonly used brain preparation techniques together with the methods of loading neurons with fluorescent indicators. We will focus primarily on issues of drug delivery specifically related to two-photon experiments highlighting the different ways of drug administration. Methods of chemical stimulation via caged neurotransmitters are also discussed. Finally a few specific areas of two-photon applications in drug research on neuronal tissue are highlighted.