Topographic Mapping between Basal Forebrain Cholinergic Neurons and the Medial Prefrontal Cortex in Mice

Bloem, Bernard; Schoppink, Luc; Rotaru, Diana C.; Faiz, Amu; Hendriks, Patrick; Mansvelder, Huibert D.; Berg, Wilma D. J. van de; Wouterlood, Floris G.

doi:10.1523/jneurosci.3011-14.2014

Cited by 121 publications

(120 citation statements)

References 64 publications

(37 reference statements)

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“…The projections from basal forebrain cholinergic neurons to frontal cortical targets are the most completely described (Bloem et al, 2014; Chandler and Waterhouse, 2012; Chandler et al, 2013). Medial frontal cortex receives projections from more medial and anterior located cholinergic neurons within the basal forebrain nuclear groups.…”

Section: Cholinergic Neurons and Cholinergic Signaling Mechanisms mentioning

confidence: 99%

“…Medial frontal cortex receives projections from more medial and anterior located cholinergic neurons within the basal forebrain nuclear groups. The dorsal regions of prefrontal cortical areas receive projections from medially located NB/SI and DB neurons, whereas more ventral regions of prefrontal cortex receive projections from more laterally located BFCNs (Fig 1A & Bloem et al, 2014). More rostrally positioned BFCNs appear to project to both superficial and deep layers of frontal cortex, while more caudally placed BFCNs preferentially project to deep layers of cortex (Bloem et al, 2014).…”

Section: Cholinergic Neurons and Cholinergic Signaling Mechanisms mentioning

confidence: 99%

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Basal Forebrain Cholinergic Circuits and Signaling in Cognition and Cognitive Decline

Ballinger

Ananth

Talmage

et al. 2016

Neuron

548

517

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Recent work continues to place cholinergic circuits at center stage for normal executive and mnemonic functioning, and provides compelling evidence that the loss of cholinergic signaling and cognitive decline are inextricably linked. This review focuses on the last few years of studies on the mechanisms by which cholinergic signaling contributes to circuit activity related to cognition. We attempt to identify areas of controversy, as well as consensus, on what is and is not yet known about how cholinergic signaling in the CNS contributes to normal cognitive processes. In addition, we delineate the findings from recent work on the extent to which dysfunction of cholinergic circuits contributes to cognitive decline associated with neurodegenerative disorders.

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Section: Cholinergic Neurons and Cholinergic Signaling Mechanisms mentioning

confidence: 99%

Section: Cholinergic Neurons and Cholinergic Signaling Mechanisms mentioning

confidence: 99%

Basal Forebrain Cholinergic Circuits and Signaling in Cognition and Cognitive Decline

Ballinger

Ananth

Talmage

et al. 2016

Neuron

548

517

View full text Add to dashboard Cite

show abstract

“…Indeed, the BF contains multiple nuclei composed of cholinergic, GABAergic, and glutamatergic corticopetal projection neurons, which are organized in segregated pools with specific projection pathways and cortical targets (32). Anatomical studies have shown that medial frontal cortical structures, including the cingulate cortex, are major targets of both cholinergic and noncholinergic BF neurons (32)(33)(34), such that in anatomical terms the BF possesses considerable connections to DMN frontal cortical structures. It has been shown that the GABAergic corticopetal BF projection, in particular, can produce robust gamma oscillations in cortical targets (35), providing a potential functional pathway by which the BF could influence DMN activation (36).…”

Section: Significancementioning

confidence: 99%

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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“…Reflecting the seemingly diffuse organization of this projection system, functional conceptualizations traditionally have described acetylcholine (ACh) as a neuromodulator that influences broadly defined behavioral and cognitive processes such as wakefulness, arousal, and gating of input processing (1,2). However, anatomical studies have revealed a topographic organization of BF cholinergic cell bodies with highly segregated cortical projection patterns (3)(4)(5)(6)(7). Such an anatomical organization favors hypotheses describing the cholinergic mediation of discrete cognitive-behavioral processes.…”

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confidence: 99%

Cortical cholinergic signaling controls the detection of cues

Gritton

Howe

Mallory

et al. 2016

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

166

208

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The cortical cholinergic input system has been described as a neuromodulator system that influences broadly defined behavioral and brain states. The discovery of phasic, trial-based increases in extracellular choline (transients), resulting from the hydrolysis of newly released acetylcholine (ACh), in the cortex of animals reporting the presence of cues suggests that ACh may have a more specialized role in cognitive processes. Here we expressed channelrhodopsin or halorhodopsin in basal forebrain cholinergic neurons of mice with optic fibers directed into this region and prefrontal cortex. Cholinergic transients, evoked in accordance with photostimulation parameters determined in vivo, were generated in mice performing a task necessitating the reporting of cue and noncue events. Generating cholinergic transients in conjunction with cues enhanced cue detection rates. Moreover, generating transients in noncued trials, where cholinergic transients normally are not observed, increased the number of invalid claims for cues. Enhancing hits and generating false alarms both scaled with stimulation intensity. Suppression of endogenous cholinergic activity during cued trials reduced hit rates. Cholinergic transients may be essential for synchronizing cortical neuronal output driven by salient cues and executing cue-guided responses.V irtually all cortical regions and layers receive inputs from cholinergic neurons originating in the nucleus basalis of Meynert, the substantia innominata, and the diagonal band of the basal forebrain (BF). Reflecting the seemingly diffuse organization of this projection system, functional conceptualizations traditionally have described acetylcholine (ACh) as a neuromodulator that influences broadly defined behavioral and cognitive processes such as wakefulness, arousal, and gating of input processing (1, 2). However, anatomical studies have revealed a topographic organization of BF cholinergic cell bodies with highly segregated cortical projection patterns (3-7). Such an anatomical organization favors hypotheses describing the cholinergic mediation of discrete cognitive-behavioral processes. Studies assessing the behavioral effects of cholinergic lesions, recording from or stimulating BF neurons in behaving animals have supported such hypotheses, proposing that cholinergic activity enhances sensory coding and mediates the ability of reward-predicting stimuli to control behavior (8-17).In separate experiments using two different tasks, we reported the presence of phasic cholinergic release events (transients) in the medial prefrontal cortex (mPFC) of rodents trained to report the presence of cues (18,19). These studies used choline-sensitive microelectrodes to measure changes in extracellular choline concentrations that reflect the hydrolysis of newly released ACh by endogenous acetylcholinesterase (SI Results and Discussion). Importantly, such cholinergic transients were not observed in trials in which cues were missed and in which the absence of a cue was correctly reported and rewarded. Cho...

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Topographic Mapping between Basal Forebrain Cholinergic Neurons and the Medial Prefrontal Cortex in Mice

Cited by 121 publications

References 64 publications

Basal Forebrain Cholinergic Circuits and Signaling in Cognition and Cognitive Decline

Basal Forebrain Cholinergic Circuits and Signaling in Cognition and Cognitive Decline

Basal forebrain contributes to default mode network regulation

Cortical cholinergic signaling controls the detection of cues

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