Changes in cortical acetylcholine output induced by modulation of the nucleus basalis

Casamenti, Fiorella; Deffenu, G; Abbamondi, Anna Laura; Pepeu, Giancarlo

doi:10.1016/0361-9230(86)90140-1

Cited by 208 publications

(75 citation statements)

References 24 publications

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“…Stimulations of BF increase the cortical acetylcholine level (Casamenti et al 1986;Kurosawa et al 1989). Both electrical and chemical BF stimulations cause an ipsilateral increase in cortical blood¯ow (Biesold et al 1989;Lacombe et al 1989;Adachi et al 1990).…”

Section: Cerebral Blood¯ow As a Marker Of Neuronal Activity During Sleepmentioning

confidence: 99%

Functional neuroimaging of normal human sleep by positron emission tomography

Maquet

2000

Journal of Sleep Research

566

312

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Functional neuroimaging using positron emission tomography has recently yielded original data on the functional neuroanatomy of human sleep. This paper attempts to describe the possibilities and limitations of the technique and clarify its usefulness in sleep research. A short overview of the methods of acquisition and statistical analysis (statistical parametric mapping, SPM) is presented before the results of PET sleep studies are reviewed. The discussion attempts to integrate the functional neuroimaging data into the body of knowledge already acquired on sleep in animals and humans using various other techniques (intracellular recordings, in situ neurophysiology, lesional and pharmacological trials, scalp EEG recordings, behavioural or psychological description). The published PET data describe a very reproducible functional neuroanatomy in sleep. The core characteristics of this ‘canonical’ sleep may be summarized as follows. In slow‐wave sleep, most deactivated areas are located in the dorsal pons and mesencephalon, cerebellum, thalami, basal ganglia, basal forebrain/hypothalamus, prefrontal cortex, anterior cingulate cortex, precuneus and in the mesial aspect of the temporal lobe. During rapid‐eye movement sleep, significant activations were found in the pontine tegmentum, thalamic nuclei, limbic areas (amygdaloid complexes, hippocampal formation, anterior cingulate cortex) and in the posterior cortices (temporo‐occipital areas). In contrast, the dorso‐lateral prefrontal cortex, parietal cortex, as well as the posterior cingulate cortex and precuneus, were the least active brain regions. These preliminary studies open up a whole field in sleep research. More detailed explorations of sleep in humans are now accessible to experimental challenges using PET and other neuroimaging techniques. These new methods will contribute to a better understanding of sleep functions.

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Section: Cerebral Blood¯ow As a Marker Of Neuronal Activity During Sleepmentioning

confidence: 99%

Functional neuroimaging of normal human sleep by positron emission tomography

Maquet

2000

Journal of Sleep Research

566

312

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“…First, cholinolytic atropine blocks EEG activation (Phillis & York, 1968;Szerb, 1964). Second, stimulation of the NB produces cortical EEG activation and release of acetylcholine in the cortex (Casamenti, Deffenu, Abbamondi, & Pepeu, 1986;Celesia & Jasper, 1966;Détári, Juhász, & Kukorelli, 1983Détári, Juhász, & Kukorelli, 1987;Jiménez-Capdeville, Dykes, & Myasnikov, 1997;Juhász, Détári, & Kukorelli, 1985;Kukorelli, Feuer, Juhász, & Détári, 1986;Rasmusson, Clow, & Szerb, 1992Rasmusson, Szerb, & Jordan, 1996;Szymusiak & McGinty, 1986). Third, specific neurotoxic lesions of NB cholinergic corticopetal neurons deplete the cortex of ACh and impair EEG activation, i.e., increase slow wave activity and decrease fast (e.g., γ) waves (Berntson, Shafi, & Sarter, 2002;Wenk, Stoehr, Quintana, Mobley, & Wiley, 1994).…”

Section: Involvement Of the Cholinergic Systemmentioning

confidence: 99%

The level of cholinergic nucleus basalis activation controls the specificity of auditory associative memory

Weinberger

Miasnikov

Chen

2006

Neurobiology of Learning and Memory

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Learning involves not only the establishment of memory per se, but also the specific details of its contents. In classical conditioning, the former concerns whether an association was learned while the latter discloses what was learned. The neural bases of associativity have been studied extensively while neural mechanisms of memory specificity have been neglected. Stimulation of the cholinergic nucleus basalis (NBs) paired with a preceding tone induces CS-specific associative memory. As different levels of acetylcholine may be released naturally during different learning situations, we asked whether the level of activation of the cholinergic neuromodulatory system can control the degree of detail that is encoded and retrieved. Adult male rats were tested pre-and post-training for behavioral responses (interruption of ongoing respiration) to tones of various frequencies (1-15 kHz, 70 dB, 2 s). Training consisted of 200 trials/day of tone (8.0 kHz, 70 dB, 2 s) either paired or unpaired with NBs (CS-NBs = 1.8 s) at moderate (65.7 ± 9.0 μA, one day) or weak (46.7 ± 12.1 μA, three training days) levels of stimulation, under conditions of controlled behavioral state (pre-trial stable respiration rate). Post-training (24 h) responses to tones revealed that moderate activation induced both associative and CS-specific behavioral memory, whereas weak activation produced associative memory lacking frequency specificity. The degree of memory specificity 24 h after training was positively correlated with the magnitude of CS-elicited increase in γ activity within the EEG during training, but only in the moderate NBs group. Thus, a low level of acetylcholine released by the nucleus basalis during learning is sufficient to induce associativity whereas a higher level of release enables the storage of greater experiential detail. γ waves, which are thought to reflect the coordinated activity of cortical cells, appear to index the encoding of CS detail. The findings demonstrate that the amount of detail in memory can be directly controlled by neural intervention.

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“…Such fifing behavior may engage limbic cortices into theta oscillations. Indeed, limbic theta rhythmicity accompanies neocortical (apparent) desynchronization (Green and Arduini, 1954;Vanderwolf, 1969) and both processes are controlled by BF cholinergic influences (Stewart et al, 1984;Bland, 1986;Casamenti et al, 1986;BuzsZlki et al, 1988;Stewart and Fox, 1990;Metherate et al, 1992). On the other hand, it may be that the awakening effect reported after intracerebroventricular injections of NT (Caste1 et al, 1989) results from NT actions outside the BF.…”

Section: Nt Internalizationmentioning

confidence: 99%

“…Thus, ACh has long been known to be maximal during cortical activation (Kanai and Szerb, 1965;Celesia and Jasper, 1966;Jasper and Tessier, 197 1) and to decrease with the disappearance of low-voltage fast activity (the typical EEG desynchronized or arousal pattern) following lesions of the BF (Lo Conte et al, 1982;Stewart et al, 1984;Buzsaki et al, 1988). In turn, stimulation of the BF has been shown to result in cortical ACh release and cortical activation (Belardetti et al, 1977;Casamenti et al, 1986;Kurosawa et al, 1989;Metherate et al, 1992). On the other hand, since there is also considerable evidence that the BF participates in the regulation of sleep (Sterman and Clemente, 1962;Detari and Vanderwolf, 1987;Szymusiak and McGinty, 1989), it appears that BF neurons may influence cortical-functional state across the sleep-waking cycle.…”

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confidence: 99%

Neurotensin promotes oscillatory bursting behavior and is internalized in basal forebrain cholinergic neurons

1994

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Cholinergic neurons of the basal forebrain magnocellular complex (BF) constitute the primary source of ACh to the cerebral cortex and are thought to be instrumental in mediating cortical activation and plasticity. Recent light and electron microscopic studies have revealed a selective association of receptors for the neuropeptide neurotensin (NT) with BF cholinergic neurons, suggesting that this peptide may be playing a key role in the control of BF cholinergic function. In the present study, we have investigated by means of intracellular recording in guinea pig brain slices the neuromodulatory actions of NT on the intrinsic excitability of BF cholinergic neurons that were identified electrophysiologically by their low-threshold discharge, slow afterhyperpolarization, and transient outward rectification (TOR). In all cholinergic neurons tested (n = 39), bath application of NT (20–200 nM for 1–4 min) produced, via a direct mechanism, a membrane potential depolarization associated with a decrease in apparent input conductance. Most significantly, NT led to the emergence of a very prominent slow rhythmic bursting pattern that could shape into complex spindle-like sequences that were intrinsically generated by the cholinergic cells. These NT actions were also accompanied by a reduction of both the slow afterhyperpolarization and TOR. Bursting oscillations relied on the activation of Ca2+ conductances as opposed to Na+ conductances, since they were absent during Ca(2+)-conductance block with Mn2+, but still occurred in the presence of the Na(+)- channel blocker TTX. NT actions were specific, since they could be reproduced by application of the active (NT 8–13) but not of the inactive (NT 1–8) fragment of the peptide. Identification of the BF cholinergic neurons as direct NT targets was further provided by confocal laser scanning microscopic demonstration of internalization of a fluoresceinylated derivative of NT (fluo-NT) within biocytin-filled, electrophysiologically identified cholinergic neurons. The results demonstrate the electrophysiological functionality of NT receptors on BF cholinergic neurons and the existence of a receptor-mediated internalization of NT in these cells. They also suggest that the peptide is an important player in the control of BF function and, in particular, in the generation of forebrain network oscillations.

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Changes in cortical acetylcholine output induced by modulation of the nucleus basalis

Cited by 208 publications

References 24 publications

Functional neuroimaging of normal human sleep by positron emission tomography

Functional neuroimaging of normal human sleep by positron emission tomography

The level of cholinergic nucleus basalis activation controls the specificity of auditory associative memory

Neurotensin promotes oscillatory bursting behavior and is internalized in basal forebrain cholinergic neurons

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