The present research demonstrates that single or repeated sessions of frontocerebellar tDCS constitute an effective strategy to positively modulate mood. Following a single stimulation session, a mood improvement of approximately 5% was observed in both the F3+/Cb− condition of Experiment 1 and again in the F3−/Cb+ of Experiment 2. No significant change was noted in the Sham condition. Additionally, we demonstrated a successive elevation of mood from baseline in both experiments following three stimulations delivered second-daily over the course of 5 days, with a total increase of mood from baseline of > 6% for the F3+/Cb− condition and > 8% for the F3−/Cb+ condition. A significant mood increase was again observed between pre-/post-stimulation1 for both active conditions of repetitive stimulation analysis. A non-significant increase was observed between pre- and post-stimulation 3. As we used healthy participants, it is possible this lack of significance may reflect an approach to a ceiling with regard to mood measures.

A significant difference between BAI scores was observed between the active conditions F3+/Cb− and F3−/Cb+. However, whilst BAI and BDI-II scores both correlated significantly with baseline measures of POMS-VAS, there was no correlation between these scores and the degree of mood change, making it unlikely that the observed changes in Experiment 2 were driven by baseline levels of anxiety.

It must be considered that the differences in baseline levels between Experiment 1 and Experiment 2 may be driving the effect observed in the F3−/Cb+ reverse polarity montage. It is not possible for us to directly compare the results from these two experiments, however, it should be noted that data collection occurred at different times of the year. As season variation has been shown to impact upon a number of endocrine functions which influence mood and level of psychological arousal (Hansen et al. 2008, 2001; Lam and Levitan 2000; Persson et al. 2008), it is possible that had data collection occurred during the same seasonal period we would still have observed an equivalent POMS-VAS baseline in the F3−/Cb+ condition of Experiment 2, and still observed the same degree of mood increase.

Whilst not conclusive, there is some evidence to suggest an absence of polarity specific effects for mood modulation which warrant further investigation. Baseline levels of mood for the F3−/Cb+ condition of Experiment 2 are approximately 7% lower than those of either condition of Experiment 1. Following single stimulation the observed increase of mood for the F3−/Cb+ condition only slightly exceeds both pre and post-stimulation scores of the Sham condition. However, following repeated stimulation there is an elevation from baseline at all points of data collection for the F3−/Cb+ condition of Experiment 2 which is equivalent too or exceeds the greatest POMS-VAS score for the Sham condition. Additionally, comparison of the POMS-VAS dimensions exhibits an almost paralleled change across all dimensions for both Active conditions, but not for the Sham conditions. This is most is obvious following single stimulation (See online resources, Sect. 3) but is also present, albeit to a lesser degree, in dimensional analyses for repeated stimulation (See online resources, Sect. 3).

Whilst it may be intuitive to expect that polarity would influence the effects of the montage, as some evidence supports the classical notion of the influence of polarity upon neuronal excitability (e.g. Datta et al. 2009), this is perhaps somewhat over-simplistic. Orientation of somatodendritic axis and the distance of the axon to the locally applied direct current has resulting cellular influences (Holsheimer et al. 2007; Bikson et al. 2004; Gluckman et al. 1996) and can determine whether the applied field has an excitatory or inhibitory influence (Kabakov et al. 2012). Additionally, the physiological effects of the stimulation extend beyond the influence of electrode polarity and neuronal orientation and are also determined by whether the predominant influence of the affected network is excitatory or inhibitory (Lefaucheur et al. 2017).

Other considerations when examining polarity induced effects include stimulation intensity and current density at the electrode (Faria et al. 2011; Miranda et al. 2009, 2006). Increases in the amplitude of cathodal stimulation, from 1 to 2 mA, have been shown to induce (motor) cortical excitability enhancement, reflective of anodal stimulation (Batsikadze et al. 2013). Additionally, cortical folding produces polarity inversions of current flow and gyri and sulci produce the potential for current clustering (Datta et al. 2009; Sadleir et al. 2010). The cerebellum possesses both a disproportionally high density of neurons (Herculano-Houzel 2009), many of which are GABAergic (Galea et al. 2009; Pope and Miall 2012), and a large degree of cortical folding (Herculano-Houzel 2009). Therefore, whilst certain limitations of the study prevent us from drawing definitive conclusions, it is perhaps not surprising that at 2 mA polarity appears to have little, if any, influence over the degree to which mood was modulated.

To the best of our knowledge, the present study is the first to successfully demonstrate mood modulation in healthy subjects, in response to both single, and repeated, administration of tDCS. This may be partly attributable to methodological differences. In this research we used a VAS derived from the bipolar POMS questionnaire, whereas other studies [e.g. (Bennabi et al. 2015; Brunoni et al. 2013; Loo et al. 2010)] have used methods such as the Montgomery Asberg Depression Rating Scale, or the Hamilton Depression Rating Scale. Whilst reliable when assessing individuals with depression, the latter measures are perhaps not sensitive enough to detect transient fluctuations in mood of healthy individuals.

Another consideration is the time at which we assessed mood: It seems common practice to administer the measures immediately before (baseline) and following stimulation (e.g. Nitsche et al. 2012; Peña-Gómez et al. 2011; Plazier et al. 2012; Vanderhasselt et al. 2013), although Fregni et al. (2008) completed the final evaluation approximately 10 min after stimulation cessation, while Tadini et al. (2011) completed the final assessment approximately post 20 min. We administered the post-stimulation POMS-VAS at approximately 25 min post stimulation-cessation. Motor cortex studies have demonstrated peak MEP amplitudes occurring approximately 90 min after stimulation (e.g. Batsikadze et al. 2013). It is possible that the convention timing of re-assessment following tDCS does not allow for a sufficient period to detect tDCS-induced modulations of mood. Duration of stimulation may also contribute to differences in findings.

In our previous research (Austin et al. 2016) as in the current one, we used a stimulation duration of 12 min. Many prior studies, however (e.g. Bennabi et al. 2015; Brunoni et al. 2013; Fregni et al. 2008; Motohashi et al. 2013) used stimulation durations of 20 min or more. However, modulatory effects lasting approximately 1 h have been demonstrated for tDCS stimulation durations of 10 min (Fricke et al. 2011; Furubayashi et al. 2008; Nitsche and Paulus 2001) and a nonlinear influence has been demonstrated between stimulation duration and potentiated effect (Monte-Silva et al. 2013).

Frontocerebellar stimulation has previously been investigated in conjunction with a number of pathologies, however, differences such as electrode size and position exist between the montages previously used and the one utilised within the present research. For example, in the case of Ho et al. (2014), a 5 cm × 7 cm electrode was positioned over the left supraorbital region, while a large 5 cm x 10 cm cathode was situated centrally over the cerebellum. Here, we used the same 5 × 5 cm (25 cm2) electrode size as Minichino et al. (2014). However, whilst identification of the site of cerebellar stimulation was comparable, we identified the dlPFC as situated under the position of F3 of the 10-coordinate system, whereas Minichino et al. (2014) used the less conventional position of Fp1. Since tDCS relies on the presence of both polarity electrodes, current must always enter and exit the cortex via intermediary brain regions. Even small variations of electrode placement and size can influence tDCS field distribution (Saturnino et al. 2015; Faria et al. 2011; Miranda et al. 2009).

Without supporting physiological and/or neuroimaging data, it is only possible to speculate about the mechanism which might be responsible for this mood modulation. Previous mood modulation investigation has restricted the flow of current to the prefrontal cortices. Increased distance between electrodes reduces the degree of shunting across the scalp, increasing the amount of current which enters the brain (Bikson et al. 2010). In support of this, the computational model (Fig. 2) indicated particularly high current density in one area of the limbic system: the anterior cingulate cortex (ACC). Levels of ACC activity have been correlated with severity of depressive symptoms and treatment outcomes (Downey et al. 2016; Mayberg et al. 1997; Osuch et al. 2000), and deep brain stimulation of the ACC has demonstrated amelioration from treatment resistant depression (Anderson et al. 2012; Holtzheimer and Mayberg 2012; Mayberg 2009).

By directing the current contralaterally from the posterior to the anterior of the brain (or visa-versa), there is perhaps a greater chance of modulating neural activity in structures associated with affective processes and arousal. For example, the cerebellum has demonstrated reciprocal connections with brainstem regions linked to limbic and paralimbic regions (Snider and Maiti 1976), the hypothalamus (Aas and Brodal 1988; Haines et al. 1984), as well as brainstem regions that participate in the modulation of autonomic function (Almeida et al. 2002; Golanov et al. 2000; Andrezik et al. 1984; Miura and Reis 1969).

Shortcomings and future directions

Aside from the fact that data for all three conditions were not collected within the one experiment, the current research presents several limitations. Firstly, blinding may have been inadequately assessed. Whilst some studies have assessed the sham protocol as a suitable blind for tDCS studies using 1 mA (Gandiga et al. 2006), the experience of sensory side effects such as itching have been shown to be more prevalent in the active than the sham condition at 1.5 mA (Kessler et al. 2012). Additionally, it has been suggested that sham stimulation at 2 mA is an inadequate blinding procedure (O’Connell et al. 2012; Wallace et al. 2016). However, it should be noted that both studies utilised a within-subjects design, but despite this aspect a bias towards selection of the Active condition (85%) was demonstrated in the latter (Wallace et al. 2016), and correct identification following both sham and active stimulation conditions did not exceed 65% (O’Connell et al. 2012). As recorded side effects between the conditions of our experiment were comparable, we feel confident that our between-subjects research was suitably blinded. However, as we did not technically assess the reliability of our blinding procedure, it would be remiss to not at least acknowledge the possibility that the observed effects may, in part, be attributable to insufficient blinding.

Second, sample size also presented some limitations. Our decision to retrospectively exclude participants based on BAI and BDI-II scores reduced an already relatively small sample size. We made a priori assumptions regarding our sample and anticipated conducting an intention to treat analysis of psychologically healthy individuals. However, across both experiments, a greater number of participants (4 from the active condition of Experiment 1 and one from the sham condition) exceeded the scores for mild anxiety (BAI ≤ 16 REF) and depression (BDI-II ≤ 19 REF). Despite the fact that each of these participants who received an active stimulation reported an increase in mood, we considered that they should be removed from the sample for analyses to keep the focus of this research on individuals with sub-clinical levels of depression and/or anxiety, which may have been seen as driving the results observed in the active condition of Experiment 1.

Finally, we opted to replicate a previous second-daily design, of 3 repeat stimulations, which had demonstrated significant mood improvements for the F3 anode/F4 cathode electrode placement (Austin et al. 2016). Whilst direct comparisons cannot be made between the current research and prior studies conducted on a sample of depressed individuals, it is worth bearing in mind that daily stimulation is the norm for the latter (see Dedoncker et al. 2016). Additionally, it has been demonstrated that daily tDCS results in a greater increase in MEP amplitude than second-daily (Alonzo et al. 2012). Perhaps we would have observed a greater increase of mood improvement if we had opted for consecutive days.