gamma oscillations, and theta activity has been proposed to support large-scale
integration of subsystems serving the formation and recall of memories.” That
is to say, “short distance synchronization tends to preferentially occur at higher
frequencies (gamma band) than long-distance synchronization, which often
manifests itself in the beta- but also in the theta- and alpha-frequency range.”
The thalamic generation of alpha activity fits very well with proposals like those
of Shipp (2003), Saalmann et al. (2012), Saalmann and Kastner (2011), accord-
ing to which the thalamus (specifical ly, the pulvinar) synchronizes oscillations
between interconnected cortical areas, thereby modulating the efficacy of cor-
tico-cortical information transfer. (On thalamocortical phase synchronization
entrains gamma oscillations during long-term memory retrieval, see also Staudigl
et al. (2012).)
The thalamus, then, is key to providing oscilla tory coherence, acting as the
network’s metronome, as it were; regulating the flow of neural ‘traffic’ via rhyth-
mic synchrony, which Miller (2013) views as brain’s way of achieving coherent,
meaningful though t. Viewed in this light, a healthy brain amounts to a ‘conso-
nant’ brain. When parts of the network are damaged, synchronization breaks
down, leading to the fragmentation of thought. “Imprecise synchrony leads to
imprecise connectivity that can only support imprecise temporal dynamics” (Uhl-
haas et al. 2008). Singer (2011) goes as far as claiming that “abnormal com-
municaton is the centr al pathophysiological feature of neuropsychiatric disorders”.
Focusing on schizophrenia, Uhlhaas and Singer (2010) claim that in this disorder
the relevant brain circu its are “characterized by imprecise temporal dynamics are
unable to support the neural coding regime [required]”. Yizhar et al. (2011)
note that behavioral impairment in both autism and schizo phrenia has been
associated with elevated baseline (non-evoked) high-frequency activity in the
30–80 Hz range, which could account for descriptions of these disorders in
terms of “over excitation”, “excitation leaks” or “under-inhibition”.
In light of this, we can only concur with Tsatsanis et al. (2003), who write
that “an examination of the thalamus may pro vide insight into autism as an
information-processing disorder, particularly with regard to shaping the neural
architecture of the brain in a way that leads to less functional connectivity and
thus a less synchronized network.” Given the central role of the thalamus in
the context of early brain development, as well as in the processing of sensory
information from the environment, it is indeed the case that both genetic or
epigenetic disturbances of the mechanisms responsible for the generation of
temporally structured activity patterns coordinated by the thalamus may impede
the activity-dependent specification of developing circuitry which in turn leads
to abnormal temporal patterns. This latter point is stressed by Uhlhaas et al.
(2010), who write: “Considering the important role of neural syn chrony in the
shaping of cortical circuits at different developmental periods, we hypothesise
that [in autism] abnormal brain maturation during early prenatal and postnatal
periods results in cortical circuits that are unable to support the expression of
high-frequency oscillations during infancy. These impaired oscillations might in
turn reduce the temporal precision of coordinated firing patterns and thereby
The central role of the thalamus 243