Moreover, recent results suggest that when attention is directed not to a region of space but to a visual feature, variability and correlation decrease in the population that encodes this feature (Cohen and Maunsell, 2011), suggesting that a phenomenon analogous to desynchronization has occurred in a spatially
distributed neuronal assembly. The mechanisms of cortical state change have been a subject of investigation for many decades. Classical research yielded two schools of thought on this question. The first, espoused by Steriade and colleagues, held that cortical states are modulated primarily via the thalamus. In this view, increased XAV-939 nmr cholinergic input to thalamic relay cells leads to increased tonic firing and thus to a steady glutamatergic drive to cortex that causes desynchronization. The second perspective, espoused by Vanderwolf and colleagues, held that cortical state reflected direct neuromodulation of neocortex. Recent research provides support for both mechanisms. In the rodent somatosensory system, whisking causes increased tonic firing in thalamus; blocking thalamic firing with muscimol reduces the cortical depolarization caused by whisking, whereas stimulating Selleckchem PD-1/PD-L1 inhibitor 2 thalamus optogenetically causes cortical desynchronization (Poulet et al., 2012).
Support for direct cortical neuromodulation comes from the ability of locally applied neuromodulatory blockers to reduce the desynchronization caused by electrical stimulation of nucleus basalis or locomotion (Goard and Dan, 2009 and Polack et al., 2013). If attention does indeed consist of cortical state change occurring at a local level, one might expect the two phenomena to have similar circuit mechanisms. In particular, given the role of
top-down cortical connections in attention, it has been hypothesized that tonic glutamatergic input from higher-order cortex should also cause desynchronization in rodent cortex (Harris and Thiele, 2011). The study of Zagha et al. (2013) provides direct evidence for this hypothesis. Zagha et al. (2013) performed a number of elegant experiments to study the role of top-down connections from vibrissa motor cortex (vM1) to barrel cortex (S1). They found Linifanib (ABT-869) that blocking spiking in vM1 using muscimol shifted S1 toward more synchronized states, whereas optogenetically increasing vM1 activity shifted S1 toward more desynchronized states. This desynchronization was usually accompanied by an increase in firing rate of S1 neurons. Importantly, the effects on S1 state did not simply reflect the consequence of these manipulations on behavior. As might be expected, suppression or activation of vM1 activity caused a corresponding decrease or increase in the probability and amplitude of whisking. Nevertheless, an effect of manipulating vM1 on S1 state was seen even when analyzing data within whisking or nonwhisking periods.