Sensory deficits are common within the schizophrenia spectrum (Cadenhead et al., 2014; Koychev et al., 2010; Silverstein & Keane, 2011) and are often endophenotypes of schizophrenia (Braff et al., 2007; Chkonia et al., 2010; Quednow et al., 2011). Sensory deficits may be reduced by nicotine consumption (Kumari et al., 2001; Leonard et al., 2007). Better sensory functioning was reported for participants with chronic nicotine consumption (Olincy et al., 1998; Petrovsky et al., 2013b; Wan et al., 2007) or acute nicotine consumption (Adler et al., 1993; Kumari et al., 2001). Here, we tested whether VBM performance, an endophenotype for schizophrenia (Chkonia et al., 2010), differs in people within the schizophrenia spectrum depending on their nicotine consumption.
First, our results support the notion that VBM deficits are an endophenotype for schizophrenia (Chkonia et al., 2010) because VBM deficits were highest in patients, followed by their relatives and finally controls (see Table 2). Second, we found higher SOAs in the high as compared to the low CogDis student group in study 2, replicating previous results (see Cappe et al., 2012). However, we could not replicate the results in study 3. One reason for the myeloperoxidase failure may be that effect size is small and hence, even large sample sizes of participants do not always lead to significant results (Francis, 2012). Third, only in study 1, smokers had lower SOAs (superior performance) than non-smokers, independent of illness status. However, we did not find this result in studies 2 and 3. Fourth, age correlated negatively with VBM performance, mainly in non-smoking controls and relatives in study 1 (age range up to 66years, while age range in the student populations was up to 30years).
Our findings can be explained in at least three ways. First, nicotine may not affect VBM performance. This explanation, however, is unlikely. As mentioned before, previous studies found significant differences in other visual tasks such as smooth-pursuit eye movements or contrast sensitivity. There is no reason to assume that chronic nicotine effects are only relevant to these visual functions. Second, effects of nicotine are often short term and are followed by fast adaptation of nicotinic receptors (Adler et al., 1998; Dome et al., 2010; Girod & Role, 2001). Adler et al. (1993) found transient effects of nicotine consumption on P50 gating. However, the beneficial effects of smoking disappeared within 30min after nicotine intake. Thus, only acute nicotine effects might impact VBM performance. A way to test this hypothesis is to administrate nicotine via a transdermal patch to non-smoking patients and determine VBM performance. Administration of nicotine with a transdermal patch improved attention in healthy non-smoking participants (Levin et al., 1998).
Third, our student samples had a lower nicotine dependence compared to other studies (Brinkmeyer et al., 2011; Rissling et al., 2007). For example, Brinkmeyer et al. (2011) found a difference on the P50 gating between heavy and light smokers as well as controls. Participants had much higher Fagerström score than in our study (5.64 vs. 2.75, respectively; we cannot compare study 3 with studies 1 and 2 since the Fagerström test was not applied in studies 1 and 2). Therefore, performance on the VBM might improve with a higher nicotine dependence (see also Herzig et al., 2010). Our third study showed that nicotine dependence increases with age. Also, study one showed that performance on the VBM task decreases with age (see also Kunchulia et al., 2014). Hence, the difference of study 1 compared to studies 2 and 3 may also be explained by the larger number of older participants in study 1.
Role of funding source
This work was supported by the National Centre of Competence in Research (NCCR) Synapsy (grant no. 565557 NCCR SYN P14 LPSY) of the Swiss National Science Foundation (SNF) (grant no. 320030_135741).