Every time we undergo major surgery, we are reminded that anesthesia abolishes all consciousness for the duration of the anesthesia. The causal agent is that anesthetics disable communication (or connectivity) between neurons by minimizing synaptic transmission which can be measured by recording the drop in energy utilization of neocortical neurons during anesthesia (Attwell and Laughlin 2001; Herculano-Houzel 2011; Masohood et al. 2023; Richards 2002; Sibson et al. 1998; Shulman et al. 2009; also see Hebb 1968, pp. 123). Another way to study connectivity between neurons (but more directly) is to use TMS (transcranial magnetic stimulation) to activate the neocortex either during wakefulness (at which time human subjects are conscious) or during slow-wave sleep (at which time human subjects are unconscious). The effective spread of neocortical TMS (as verified using high-density EEG recording) was up to 12 cm from the center of of TMS activity during wakefulness and up to 4 cm from the center of TMS activity during slow-wave sleep, which agrees with the notion that synaptic transmission by neocortical neurons is what subserves consciousness (cf. Fig. 1 and Fig. 2, derived from Massimini, Tononi et al. 2005). The challenge now will be to determine how the brain integrates the information transmitted via synapses and how close this integration is to the predictions advanced by Tononi and colleagues (2008ab). For example, what are the connectivity properties of sensory maps as compared to individual neurons coding specific declarative attributes found in association cortex (Doty 1965, 1969; Ojemann 1991; Penfield and Roberts 1966; Tehovnik 2024; Tehovnik, Hasanbegović, Chen 2024; Tehovnik and Slocum 2013), and how does this connectivity coincide with consciousness generated externally versus internally. Normal conscious vision in mammals is mediated by having an intact V1, which is a retinotopic structure that links the entire visual field (Bartlett, Doty et al. 2005), such that its destruction produces a scotoma throughout the field (Tehovnik, Patel, Tolias et al. 2021). Cooling probes could be used (Schiller and Tehovnik 2015) to inactivate various combinations of topographic versus association cortices in primates, for example, to further test the theory of Tononi and colleagues.
As is known publicly, a protest letter has been published about the scientific usefulness of the Integration Information Theory of Tononi and colleagues (2008ab) suggesting that it represents pseudo-science. A word of advice to the signatories of the Fleming, Goodale et al. (2023) letter: beware of sharing your signature for short-term gain for science is a long-term project and as a living document of empirical knowledge it does not respond well to censorship (see Gomez-Marin 2023).
Figure 1: Field of activation of the neocortex by TMS of an awake human subject at 120 ms after TMS onset over the right premotor cortex. The top panel shows the TMS field, and the bottom panel shows the signal spread using EEG, marked in red. The approximate length of the neocortex from posterior to anterior is 17 cm (Tehovnik et al. 2000), and the maximal signal spread from the center of TMS is 12 cm extending to the posterior lateral part of neocortex. The figure is from Massimini, Tononi et al. (2005).
Figure 2: Field of activation of the neocortex by TMS of a human subject during slow-wave sleep at 120 ms after TMS onset over the right premotor cortex. The top panel shows the TMS field, and the bottom panel shows signal spread using EEG, marked in red. The approximate length of the neocortex from posterior to anterior is 17 cm (Tehovnik et al. 2000), and the maximal signal spread from the center of TMS is 4 cm extending through the supplementary motor area. The figure is from Massimini, Tononi et al. (2005).
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