Cortical input to the basal forebrain

Záborszky, László; Gaykema, Ronald P.; Swanson, D.J.; Cullinan, William E.

doi:10.1016/s0306-4522(97)00049-3

Cited by 199 publications

(162 citation statements)

References 90 publications

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“…Thus, the fact that decrements in sustained attention tend to occur concomitantly with feelings of sleepiness, is consistent with studies indicating that the same mechanisms implicated in the control of the homeostatic sleep drive, are also involved in the regulation of attention (Zaborszky et al 1997). Moreover, neurons within the BF project to components of the cortical sustained attention network, whose activation is linked with optimal human performance on the PVT (Drummond et al 2005a).…”

Section: Sleep Deprivation Adenosine and Vigilant Attentionsupporting

confidence: 82%

Adenosine, Caffeine, and Performance: From Cognitive Neuroscience of Sleep to Sleep Pharmacogenetics

Urry

Landolt

2014

Current Topics in Behavioral Neurosciences

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An intricate interplay between circadian and sleep-wake homeostatic processes regulate cognitive performance on specific tasks, and individual differences in circadian preference and sleep pressure may contribute to individual differences in distinct neurocognitive functions. Attentional performance appears to be particularly sensitive to time of day modulations and the effects of sleep deprivation. Consistent with the notion that the neuromodulator, adenosine adenosine , plays an important role in regulating sleep pressure, pharmacologic and genetic data in animals and humans demonstrate that differences in adenosinergic tone affect sleepiness, arousal and vigilant attention attention in rested and sleep-deprived states. Caffeine Caffeine -the most often consumed stimulant in the world-blocks adenosine receptors and normally attenuates the consequences of sleep deprivation on arousal, vigilance, and attention. Nevertheless, caffeine cannot substitute for sleep, and is virtually ineffective in mitigating the impact of severe sleep loss on higher-order cognitive functions. Thus, the available evidence suggests that adenosinergic mechanisms, in particular adenosine A2A receptor-mediated signal transduction, contribute to waking-induced impairments of attentional processes, whereas additional mechanisms must be involved in higher-order cognitive consequences of sleep deprivation. Future investigations should further clarify the exact types of cognitive processes affected by inappropriate sleep. This research will aid in the quest to better understand the role of different brain systems (e.g., adenosine and adenosine receptors) in regulating sleep, and sleep-related subjective state, and cognitive processes. Furthermore, it will provide more detail on the underlying mechanisms of the detrimental effects of extended wakefulness, as well as lead to the development of effective, evidence-based countermeasures against the health consequences of circadian misalignment and chronic sleep restriction. In press (accepted): January 14, 2014 Addresses for correspondence:Hans-Peter Landolt, Ph.D.

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Section: Sleep Deprivation Adenosine and Vigilant Attentionsupporting

confidence: 82%

Adenosine, Caffeine, and Performance: From Cognitive Neuroscience of Sleep to Sleep Pharmacogenetics

Urry

Landolt

2014

Current Topics in Behavioral Neurosciences

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“…BF cholinergic neurons respond to glutamate, and they are innervated by a robust glutamatergic input that represents Ͼ50% of their afference (Hur et al 2009;Khateb et al 1995;Momiyama and Fukazawa 2007;Sim and Griffith 1996). This input appears to arise from multiple sources, including the lateral hypothalamus, the amygdala, the intralaminar and midline nuclei of the thalamus, and the brain stem, but not the cortex, which sends glutamatergic connections back to the BF, but only to noncholinergic neurons (Carnes et al 1990;Fadel et al 2005;Jolkkonen et al 2002;Zaborszky et al 1984Zaborszky et al , 1991Zaborszky et al , 1997. It remains unclear, however, which of these regions serves as the source of the excitatory glutamatergic input to BF cholinergic neurons.…”

Section: Discussionmentioning

confidence: 99%

Adenosine inhibits glutamatergic input to basal forebrain cholinergic neurons

Hawryluk

Ferrari

Keating

et al. 2012

Journal of Neurophysiology

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Hawryluk JM, Ferrari LL, Keating SA, Arrigoni E. Adenosine inhibits glutamatergic input to basal forebrain cholinergic neurons. J Neurophysiol 107: 2769 -2781, 2012. First published February 22, 2012 doi:10.1152/jn.00528.2011.-Adenosine has been proposed as an endogenous homeostatic sleep factor that accumulates during waking and inhibits wake-active neurons to promote sleep. It has been specifically hypothesized that adenosine decreases wakefulness and promotes sleep recovery by directly inhibiting wake-active neurons of the basal forebrain (BF), particularly BF cholinergic neurons. We previously showed that adenosine directly inhibits BF cholinergic neurons. Here, we investigated 1) how adenosine modulates glutamatergic input to BF cholinergic neurons and 2) how adenosine uptake and adenosine metabolism are involved in regulating extracellular levels of adenosine. Our experiments were conducted using whole cell patch-clamp recordings in mouse brain slices. We found that in BF cholinergic neurons, adenosine reduced the amplitude of AMPAmediated evoked glutamatergic excitatory postsynaptic currents (EPSCs) and decreased the frequency of spontaneous and miniature EPSCs through presynaptic A 1 receptors. Thus we have demonstrated that in addition to directly inhibiting BF cholinergic neurons, adenosine depresses excitatory inputs to these neurons. It is therefore possible that both direct and indirect inhibition may synergistically contribute to the sleep-promoting effects of adenosine in the BF. We also found that blocking the influx of adenosine through the equilibrative nucleoside transporters or inhibiting adenosine kinase and adenosine deaminase increased endogenous adenosine inhibitory tone, suggesting a possible mechanism through which adenosine extracellular levels in the basal forebrain are regulated. magnocellular preoptic nucleus; substantia innominata; adenosine A 1 receptors; electrophysiology; excitatory postsynaptic currents; in vitro; mice IN THE LAST EIGHTY YEARS, a large number of studies have been directed toward identifying the endogenous sleep factors that could build during the waking period to drive the need for sleep and then be dissipated by sleep itself (Achermann

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“…In contrast, the recruitment of prefrontal cholinergic inputs in task-performing animals is thought to be mediated via direct prefrontal projections to the basal forebrain as well as via multi-synaptic circuits involving the nucleus accumbens and perhaps also the amygdala (Holland et al, 2000;Lee et al, 2006;Neigh-McCandless et al, 2002;Sarter et al, 2001Sarter et al, , 2005aZaborszky, 1997Zaborszky, , 2002Zahm, 2000). Together with evidence demonstrating the disruption of the prefrontal modulation of accumbens neurons following repeated psychostimulant exposure (Goto and Grace, 2005), the present findings suggest that repeated AMPH-exposure disrupts such telencephalic innervation of basal forebrain cholinergic neurons and thus, prefrontal ACh release.…”

Section: Discussionmentioning

confidence: 99%

Toward a Neuro-Cognitive Animal Model of the Cognitive Symptoms of Schizophrenia: Disruption of Cortical Cholinergic Neurotransmission Following Repeated Amphetamine Exposure in Attentional Task-Performing, but Not Non-Performing, Rats

Kozak

Martı́nez

Young

et al. 2007

Neuropsychopharmacol

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Impairments in attentional functions and capacities represent core aspects of the cognitive symptoms of schizophrenia. Attentional performance has been demonstrated to depend on the integrity and activity of cortical cholinergic inputs. The neurobiological, behavioral, and cognitive effects of repeated exposure to psychostimulants model important aspects of schizophrenia. In the present experiment, prefrontal acetylcholine (ACh) release was measured in attentional task-performing and non-performing rats pretreated with an escalating dosing regimen of amphetamine (AMPH) and following challenges with AMPH. In non-performing rats, pretreatment with AMPH did not affect the increases in ACh release produced by AMPH-challenges. In contrast, attentional task performanceassociated increases in ACh release were attenuated in AMPH-pretreated and AMPH-challenged rats. This effect of repeated AMPH exposure on ACh release was already present before task-onset, suggesting that the loss of cognitive control that characterized these animals' performance was a result of cholinergic dysregulation. The findings indicate that the demonstration of repeated AMPH-induced dysregulation of the prefrontal cholinergic input system depends on interactions between the effects of repeated AMPH exposure and cognitive performance-associated recruitment of this neuronal system. Repeated AMPH-induced disruption of prefrontal cholinergic activity and attentional performance represents a useful model to investigate the cholinergic mechanisms contributing to the cognitive impairments of schizophrenia.

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Cortical input to the basal forebrain

Cited by 199 publications

References 90 publications

Adenosine, Caffeine, and Performance: From Cognitive Neuroscience of Sleep to Sleep Pharmacogenetics

Adenosine, Caffeine, and Performance: From Cognitive Neuroscience of Sleep to Sleep Pharmacogenetics

Adenosine inhibits glutamatergic input to basal forebrain cholinergic neurons

Toward a Neuro-Cognitive Animal Model of the Cognitive Symptoms of Schizophrenia: Disruption of Cortical Cholinergic Neurotransmission Following Repeated Amphetamine Exposure in Attentional Task-Performing, but Not Non-Performing, Rats

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