Cholinergic suppression of visual responses in primate V1 is mediated by GABAergic inhibition

Disney, Anita A.; Aoki, Chiye; Hawken, Michael J.

doi:10.1152/jn.00188.2012

Cited by 51 publications

(93 citation statements)

References 86 publications

(159 reference statements)

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“…For example, the BF modulates the response gain of single neurons in the VC as well as enhancing the sensitivity of these neurons to low-contrast visual stimuli (45)(46)(47)(48)(49), highlighting that the BF augments the cortical representation of sensory stimuli, consistent with some aspects of attentional modulation (50). Along related lines, BF stimulation also accelerates visual learning and up-regulates cortical visually-evoked potentials (51,52) as well as boosting the reliability of neural signals about sensory information (53)(54)(55).…”

Section: Discussionmentioning

confidence: 86%

Basal forebrain contributes to default mode network regulation

Nair

Klaassen

Arató³

et al. 2018

Proc. Natl. Acad. Sci. U.S.A.

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The default mode network (DMN) is a collection of cortical brain regions that is active during states of rest or quiet wakefulness in humans and other mammalian species. A pertinent characteristic of the DMN is a suppression of local field potential gamma activity during cognitive task performance as well as during engagement with external sensory stimuli. Conversely, gamma activity is elevated in the DMN during rest. Here, we document that the rat basal forebrain (BF) exhibits the same pattern of responses, namely pronounced gamma oscillations during quiet wakefulness in the home cage and suppression of this activity during active exploration of an unfamiliar environment. We show that gamma oscillations are localized to the BF and that gamma-band activity in the BF has a directional influence on a hub of the rat DMN, the anterior cingulate cortex, during DMNdominated brain states. The BF is well known as an ascending, activating, neuromodulatory system involved in wake-sleep regulation, memory formation, and regulation of sensory information processing. Our findings suggest a hitherto undocumented role of the BF as a subcortical node of the DMN, which we speculate may be important for switching between internally and externally directed brain states. We discuss potential BF projection circuits that could underlie its role in DMN regulation and highlight that certain BF nuclei may provide potential target regions for up-or down-regulation of DMN activity that might prove useful for treatment of DMN dysfunction in conditions such as epilepsy or major depressive disorder.gamma suppression | anterior cingulate cortex | granger causality A highly consistent finding across a wide range of functional imaging studies in humans is that a network of brain regions, referred to as the "default mode network" (DMN), increases its activity during passive mental states compared with the performance of cognitive tasks. This was initially shown in a metaanalysis of several PET studies (1), in which a distribution of brain regions broadly including the medial prefrontal, retrosplenial, and anterior cingulate cortex (ACC), as well as lateral parietal and temporal cortices, was shown to be activated when subjects were in a state of quiet restfulness. The DMN areas are thought to form a cohesive set of intrinsically coupled brain regions, such that fMRI activations in its component regions exhibit similar time courses, allowing them to be identified reliably using seed-region analysis (2-4). Activity in the DMN exhibits anticorrelation with a complementary, largely nonoverlapping, set of fronto-parietal brain areas known as the "dorsal attention network" (DAN) (5). It should be noted, however, that particular brain structures may harbor functionally heterogeneous elements and thus may contribute to multiple functions, as was shown for the ACC (6). During wakefulness, the human brain thus alternates between DAN-and DMN-dominated activation states, corresponding to effortful cognitive task performance on the one hand and quiet restful...

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Section: Discussionmentioning

confidence: 86%

Basal forebrain contributes to default mode network regulation

Nair

Klaassen

Arató³

et al. 2018

Proc. Natl. Acad. Sci. U.S.A.

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“…The complexity of such regulatory pattern may be related to a higher degree of functional flexibility in the regions directly implicated in elaborating the decision-execution prefrontal tasks. These areas could be physiologically more similar to the Primate neocortex, where nicotinic targeting of FS cells seems more common (Disney et al, 2007, Disney et al, 2012; and references therein).…”

Section: Discussionmentioning

confidence: 99%

α4β2 ∗ nicotinic receptors stimulate GABA release onto fast-spiking cells in layer V of mouse prefrontal (Fr2) cortex

et al. 2017

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“…Muscarinic (m) AChRs mediate a complex and layer-specific array of inhibitory and excitatory effects at cortical interneurons and output neurons (Eggermann and Feldmeyer, 2009; Egorov et al, 2002; Gulledge and Stuart, 2005; Hasselmo and Bower, 1992). The specific role of frontal cortical mAChRs in attention is not well understood (Disney and Aoki, 2008; for evidence on the role of these receptors in temporal and sensory regions during attention and encoding see Disney et al, 2012; Herrero et al, 2008; Newman et al, 2013; Thiele et al, 2012). However, mAChR stimulation is essential for transferring the effects of cortical cholinergic activity to downstream regions (Nelson et al, 2005) including, presumably, to the striatum (Fig.…”

Section: Essential For Falls: Striatal Convergence Of Cortical Cholinmentioning

confidence: 99%

Where attention falls: Increased risk of falls from the converging impact of cortical cholinergic and midbrain dopamine loss on striatal function

Sarter

Albin

Kucinski

et al. 2014

Experimental Neurology

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Falls are a major source of hospitalization, long-term institutionalization, and death in older adults and patients with Parkinson’s disease (PD). Limited attentional resources are a major risk factor for falls. In this review, we specify cognitive–behavioral mechanisms that produce falls and map these mechanisms onto a model of multi-system degeneration. Results from PET studies in PD fallers and findings from a recently developed animal model support the hypothesis that falls result from interactions between loss of basal forebrain cholinergic projections to the cortex and striatal dopamine loss. Striatal dopamine loss produces inefficient, low-vigor gait, posture control, and movement. Cortical cholinergic deafferentation impairs a wide range of attentional processes, including monitoring of gait, posture and complex movements. Cholinergic cell loss reveals the full impact of striatal dopamine loss on motor performance, reflecting loss of compensatory attentional supervision of movement. Dysregulation of dorsomedial striatal circuitry is an essential, albeit not exclusive, mediator of falls in this dual-system model. Because cholinergic neuromodulatory activity influences cortical circuitry primarily via stimulation of α4β2* nicotinic acetylcholine receptors, and because agonists at these receptors are known to benefit attentional processes in animals and humans, treating PD fallers with such agonists, as an adjunct to dopaminergic treatment, is predicted to reduce falls. Falls are an informative behavioral endpoint to study attentional–motor integration by striatal circuitry.

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Cholinergic suppression of visual responses in primate V1 is mediated by GABAergic inhibition

Cited by 51 publications

References 86 publications

Basal forebrain contributes to default mode network regulation

Basal forebrain contributes to default mode network regulation

α4β2 ∗ nicotinic receptors stimulate GABA release onto fast-spiking cells in layer V of mouse prefrontal (Fr2) cortex

Where attention falls: Increased risk of falls from the converging impact of cortical cholinergic and midbrain dopamine loss on striatal function

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