For things needing your attention: the role of neocortical gamma in sensory perception

Pritchett, Dominique L.; Siegle, Joshua H.; Deister, Christopher A.; Moore, Christopher I.

doi:10.1016/j.conb.2015.02.004

Cited by 46 publications

(43 citation statements)

References 82 publications

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“…In sum, these findings are consistent with prior claims (Pritchett et al, 2015;Ray and Maunsell, 2015) that gamma band LFP power does not index a viable temporal carrying signal that promotes sensory processing. However, persistent spiking gamma observed in the gnsFS predicted perceptual success, was not perturbed by sensory input, and was negatively related to the gamma band LFP.…”

Section: Gamma Spiking By Gnsfs Is Negatively Correlated With the Gamsupporting

confidence: 89%

“…Hypotheses proposing a role for gamma in sensory neocortical relay fall into two broad categories Pritchett et al, 2015). First, gamma could enhance relay by improving rate coding locally; for example by increasing firing in appropriate projection neurons (Azouz and Gray, 2000;Fellous et al, 2003;Tiesinga et al, 2004); or through effective inhibition of distracting 'surround' neurons that carry non-informative signals (Gieselmann and Thiele, 2008;Vinck and Bosman, 2016); or both (Borgers et al, 2008).…”

Section: Introductionmentioning

confidence: 99%

“…First, gamma could enhance relay by improving rate coding locally; for example by increasing firing in appropriate projection neurons (Azouz and Gray, 2000;Fellous et al, 2003;Tiesinga et al, 2004); or through effective inhibition of distracting 'surround' neurons that carry non-informative signals (Gieselmann and Thiele, 2008;Vinck and Bosman, 2016); or both (Borgers et al, 2008). In these scenarios, the exact frequency and duration of expression could vary within and between areas while still achieving effective rate enhancement (Pritchett et al, 2015).…”

Section: Introductionmentioning

confidence: 99%

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Persistent Gamma Spiking in Non-Sensory Fast-Spiking Cells Predicts Perceptual Success

Shin

Moore

2018

Preprint

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Persistent gamma oscillations (30-55Hz) are hypothesized to temporally coordinate stimulus encoding, enabling perception. This prediction poses a conundrum: How can gamma serve as a template when the stimulus itself drives its mediators, presumably perturbing its maintenance? Specifically, fast-spiking interneurons (FS), a key gamma generator, can be highly sensory responsive. Further, the gamma-band local field potential (LFP) shows properties inconsistent with temporal coordination. Combining tetrode recording with controlled psychophysics revealed an FS subtype (gnsFS) that was not sensory responsive, whose inter-spike intervals peaked at gamma, and that fired with higher periodicity than other FS. Successful detection was predicted by increased regularity in gnsFS spiking at gamma, persisting from before to after sensory onset. In contrast, gamma LFP power negatively predicted detection, and was negatively related to gamma band spiking by gnsFS. These results suggest that a distinct interneuron subgroup, not 'distracted' by sensory input, mediates perceptually-relevant oscillations independent of LFP.

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Section: Gamma Spiking By Gnsfs Is Negatively Correlated With the Gamsupporting

confidence: 89%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Persistent Gamma Spiking in Non-Sensory Fast-Spiking Cells Predicts Perceptual Success

Shin

Moore

2018

Preprint

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“…Beta oscillations have previously been implicated as information carriers in the sensorimotor system: synchronous beta activity in motor cortex appears to mediate directionally-specific information flow (Rubino et al, 2006), and postcentral beta causally influences precentral beta (Brovelli et al, 2004). Conversely, gamma oscillations may mediate bottom-up, or feed-forward, sensory processing (Bressler and Richter, 2015), perhaps providing local gain on subsets of neurons (Pritchett et al, 2015). It is unclear whether our observed increase in gamma indicates an attempt at communication, or is simply the response of a circuit that has become disconnected and unbalanced.…”

Section: Discussionmentioning

confidence: 99%

Disruption of corticocortical information transfer during ketamine anesthesia in the primate brain

et al. 2016

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The neural mechanisms of anesthetic-induced unconsciousness have yet to be fully elucidated, in part because of the diverse molecular targets of anesthetic agents. We demonstrate, using intracortical recordings in macaque monkeys, that information transfer between structurally connected cortical regions is disrupted during ketamine anesthesia, despite preserved primary sensory representation. Furthermore, transfer entropy, an information-theoretic measure of directed connectivity, decreases significantly between neuronal units in the anesthetized state. This is the first direct demonstration of a general anesthetic disrupting corticocortical information transfer in the primate brain. Given past studies showing that more commonly used GABAergic drugs inhibit surrogate measures of cortical communication, this finding suggests the potential for a common network-level mechanism of anesthetic-induced unconsciousness.

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“…Fast oscillations in cortical networks are also critically dependent on the synchronized firing of fast-spiking inhibitory interneurons, which is a phenomenon associated with Up states of the slow oscillation (Hasenstaub et al, 2005 ). The suggested functional roles of synchronized fast oscillations in cortical processing during waking are myriad (Fries, 2009 ; Bosman et al, 2014 ; Pritchett et al, 2015 ), though their roles in slow-wave sleep, if any, are uncertain. The fast oscillations associated with REM sleep have been proposed to be a correlate of dreaming mentation (Llinás and Ribary, 1993 ).…”

Section: Functions Of the Slow Oscillationmentioning

confidence: 99%

The Slow Oscillation in Cortical and Thalamic Networks: Mechanisms and Functions

Neske

2016

Front. Neural Circuits

217

243

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During even the most quiescent behavioral periods, the cortex and thalamus express rich spontaneous activity in the form of slow (<1 Hz), synchronous network state transitions. Throughout this so-called slow oscillation, cortical and thalamic neurons fluctuate between periods of intense synaptic activity (Up states) and almost complete silence (Down states). The two decades since the original characterization of the slow oscillation in the cortex and thalamus have seen considerable advances in deciphering the cellular and network mechanisms associated with this pervasive phenomenon. There are, nevertheless, many questions regarding the slow oscillation that await more thorough illumination, particularly the mechanisms by which Up states initiate and terminate, the functional role of the rhythmic activity cycles in unconscious or minimally conscious states, and the precise relation between Up states and the activated states associated with waking behavior. Given the substantial advances in multineuronal recording and imaging methods in both in vivo and in vitro preparations, the time is ripe to take stock of our current understanding of the slow oscillation and pave the way for future investigations of its mechanisms and functions. My aim in this Review is to provide a comprehensive account of the mechanisms and functions of the slow oscillation, and to suggest avenues for further exploration.

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For things needing your attention: the role of neocortical gamma in sensory perception

Cited by 46 publications

References 82 publications

Persistent Gamma Spiking in Non-Sensory Fast-Spiking Cells Predicts Perceptual Success

Persistent Gamma Spiking in Non-Sensory Fast-Spiking Cells Predicts Perceptual Success

Disruption of corticocortical information transfer during ketamine anesthesia in the primate brain

The Slow Oscillation in Cortical and Thalamic Networks: Mechanisms and Functions

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