Weekly original research reports in the Journal of Neuroscience have resumed for the year. YAY! And within the past week, there has been quite the chatter about the usefulness of transcranial electromagnetic stimulation (TMS) to induce and characterize the neuroanatomical origin, architecture, and propagation of slow wave activity; the predominant waveform of deep sleep that helps brain areas, globally, and neurons, locally, recover from a hectic (or just average) waking day.
TMS has been a popular research methodology to discuss in neurological and psychiatric research as it is a non-invasive, non-pharmacological alternative treatment strategy for migraines, Parkinson’s, and depression. Much like direct stimulation of a neuron or brain area through an electrode that is fed through an implanted cannula….in mice…… (obviously this technique is invasive), TMS evokes a classic excitatory and inhibitory neuronal state over a brief period of time. I.e. The action potential.
In a recent Journal of Neuroscience report (Bergmann et al.) and in a 2009 PNAS paper (Murphy et al. 2009) that we discussed in journal club on Tuesday, it is fairly evident that the induction and propagation of slow wave activity is largely influenced by TMS. Bergmann et al. 2011 used the technique to compare the temporality and architecture of slow wave activity (referred to as oscillations in the paper) with electrical activity arising from the motor cortex (abbreviated as MEPs) and TMS-evoked states across sleep and wakefulness. In brief, unlike MEPs which were spontaneously generated across sleep and often appeared after slow-wave oscillations, TMS-evoked states during sleep were altered, resembling slow-wave activity. In Murphy et al. 2009, which preceded the publication of Bergmann et al. by nearly two years, it was found that TMS-induced slow waves originate in a particular region of the cortex and then propagate from there, namely through the cingulate cortex, which serves as a gateway for bi-hemispheric higher-order cognition (attention and subsequent learning and memory) given its proximity to the corpus callosum. The beauty of this study was that high-density EEG was utilized, which is basically a hairnet with 256 (!!!) recording channels allowing for researchers to record from nearly every region of the cortex. Prior to its inception, sleep and cognitive neuroscientists systematically affixed a total of 6-8 electrodes to frontal, parietal, and occipital areas on either side of the brain. Although it would have been (and is) difficult to generate high quality waveforms with minimal electrical interference with the latter recording technique, both fields did rapidly advance. Now imagine what can be done and the impact that these two studies will have on better understanding the underlying neuronal activity and recruitment of neuronal pathways as they relate to neurological and psychiatric diseases.
Expression of DISC1, a protein linked to schizophrenia, in utero
Murphy, M., Riedner, B., Huber, R., Massimini, M., Ferrarelli, F., & Tononi, G. (2009). Source modeling sleep slow waves Proceedings of the National Academy of Sciences, 106 (5), 1608-1613 DOI: 10.1073/pnas.0807933106
Bergmann TO, Mölle M, Schmidt MA, Lindner C, Marshall L, Born J, & Siebner HR (2012). EEG-Guided Transcranial Magnetic Stimulation Reveals Rapid Shifts in Motor Cortical Excitability during the Human Sleep Slow Oscillation. The Journal of neuroscience : the official journal of the Society for Neuroscience, 32 (1), 243-253 PMID: 22219286