Enhancement of acetylcholine release during paradoxical sleep in the dorsal tegmental field of the cat brain stem

Kodama, Tohru; Takahashi, Yasuro; Honda, Yoshiaki

doi:10.1016/0304-3940(90)90576-u

Cited by 163 publications

(71 citation statements)

References 8 publications

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“…Anatomical studies also demonstrated that input terminals on spinal motoneurons contain GABA, glycine, or both (Taal and Holstege, 1994;Ornung et al, 1996). The present study suggests that both glycine and GABA release contribute to the active inhibition of muscle tone during electrical stimulation and after ACh stimulation of PIA, as well as during the normal release of ACh on the PIA in REM sleep (Kodama et al, 1990). Although it is likely that a similar pattern of release of inhibitory amino acids would be seen during the atonia of natural REM sleep, a direct test of this hypothesis is required.…”

Section: Discussionsupporting

confidence: 61%

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Changes in Inhibitory Amino Acid Release Linked to Pontine-Induced Atonia: AnIn VivoMicrodialysis Study

2003

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We hypothesized that cessation of brainstem monoaminergic systems and an activation of brainstem inhibitory systems are both involved in pontine inhibitory area (PIA) stimulation-induced muscle atonia. In our previous study (Lai et al., 2001), we found a decrease in norepinephrine and serotonin release in motoneuron pools during PIA stimulation-induced muscle tone suppression. We now demonstrate an increase in inhibitory amino acid release in motor nuclei during PIA stimulation in the decerebrate cat using in vivo microdialysis and HPLC analysis techniques. Microinjection of acetylcholine into the PIA elicited muscle atonia and simultaneously produced a significant increase in both glycine and GABA release in both the hypoglossal nucleus and the lumbar ventral horn. Glycine release increased by 74% in the hypoglossal nucleus and 50% in the spinal cord. GABA release increased by 31% in the hypoglossal nucleus and 64% in the spinal cord during atonia induced by cholinergic stimulation of the PIA. As with cholinergic stimulation, 300 msec train electrical stimulation of the PIA elicited a significant increase in glycine release in the hypoglossal nucleus and ventral horn. GABA release was significantly increased in the hypoglossal nucleus but not in the spinal cord during electrical stimulation of the PIA. Glutamate release in the motor nuclei was not significantly altered during atonia induced by electrical or acetylcholine stimulation of the PIA. We suggest that both glycine and GABA play important roles in the regulation of upper airway and postural muscle tone. A combination of decreased monoamine and increased inhibitory amino acid release in motoneuron pools causes PIA-induced atonia and may be involved in atonia linked to rapid eye-movement sleep.

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Section: Discussionsupporting

confidence: 61%

“…Application of acetylcholine (ACh) (George et al, 1964;Lai and Siegel, 1988;Kodama et al, 1990;Reinoso-Suarez et al, 1994), glutamate (Lai and Siegel, 1991;Onoe and Sakai, 1995), corticotropin-releasing factor (Lai and Siegel, 1992), and GABA antagonist (Xi et al, 2001) to the PIA can trigger muscle atonia and REM sleep.…”

Section: Introductionmentioning

confidence: 99%

Changes in Inhibitory Amino Acid Release Linked to Pontine-Induced Atonia: AnIn VivoMicrodialysis Study

2003

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“…), as well as the complete state of active sleep with all of its attendant physiological patterns of activity ( 1983; Baghdoyan et al, 1984Baghdoyan et al, , 1989Baghdoyan et al, , 1993Morales et al, 1987;Yamuy et al, 1993). Acetylcholine release in the NPO is significantly higher during active sleep than during quiet sleep or wakefulness (Kodama et al, 1990;Leonard and Lydic, 1997). In addition, the majority of the neurons in the NPO show an increased discharge rate during active sleep (McCarley and Hobson, 1971;Sakai, 1988;McCarley et al, 1995); many also increase their rate of discharge during waking movements (Siegel et al, 1977).…”

Section: Discussionmentioning

confidence: 99%

“…Supporting the role of cholinergic mechanisms in the generation of active sleep are findings of an increase in acetylcholine (ACh) release in this region during spontaneous active sleep (Kodama et al, 1990), as well as during carbachol-induced active sleep (Lydic et al, 1991). In addition, the induction of active sleep by cholinergic agonists within the NPO is blocked by muscarinic receptor antagonists (Baghdoyan et al, 1989;VelazquezMoctezuma et al, 1991).…”

Section: Introductionmentioning

confidence: 97%

Interactions between GABAergic and Cholinergic Processes in the Nucleus Pontis Oralis: Neuronal Mechanisms Controlling Active (Rapid Eye Movement) Sleep and Wakefulness

Xi¹,

Morales²,

Chase³

2004

J. Neurosci.

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The cholinergic system within the nucleus pontis oralis (NPO) of the pontine tegmentum is critically involved in the generation of active (rapid eye movement) sleep. Previously, we demonstrated that a GABAergic system in the NPO also plays an important role in the control of the behavioral states of wakefulness as well as active sleep. The present study examined interactions between these two neuronal systems vis-à-vis the occurrence of these behavioral states. Accordingly, cholinergic and GABAergic agonists and antagonists were injected into the NPO, and their combined effects on sleep and waking states of chronic, unanesthetized cats were examined. Microinjections of carbachol into the NPO elicited active sleep with a short latency. However, a preinjection of muscimol (a GABA A agonist) completely blocked the active sleep-inducing effects of carbachol. The induction of active sleep by carbachol was also suppressed by a subsequent injection of muscimol. On the other hand, the microinjection of scopolamine (a muscarinic receptor antagonist) did not block the induction of active sleep by bicuculline (a GABA A antagonist). We conclude that the excitatory cholinergic control of NPO neurons that are involved in the generation of active sleep is gated by a pontine GABAergic system that exerts its effects postsynaptically by inhibiting NPO neurons, resulting in the suppression of active sleep and the generation of wakefulness. In the absence of the activation of this GABAergic gating mechanism, active sleep occurs. These results reveal that specific interactions between cholinergic and GABAergic processes in the NPO play a critical role in the generation of active sleep and wakefulness.

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“…In humans, functional neuroimaging techniques, using H 2 15 O or 18 FDG positron emission tomography (PET) and functional magnetic resonance imaging (fMRI), allowed the mapping of the regional cerebral activity during this sleep stage, which is dominated by the activation of the pons, the thalamus, temporo-occipital and limbic/paralimbic areas (including the amygdala, the hippocampal formation and the anterior cingulate cortex), along with a relative quiescence of dorsolateral prefrontal and inferior parietal cortices. These results are in agreement with animal neurophysiological data about REM-sleep generation.…”

mentioning

confidence: 99%

Dreaming: a neuroimaging view

Dang‐Vu

Desseilles

Albouy

et al. 2005

Swiss Arch Neurol Psychiatr

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SummaryDang-Vu TT, Desseilles M, Albouy G, Darsaud A, Gais S, Rauchs G, Schabus M, Sterpenich V, Vandewalle G, Schwartz S, Maquet P. Dreaming: a neuroimaging view. Schweiz Arch Neurol 2005;156: 415-25. Our neurobiological knowledge about human dream organisation results primarily from the study of Rapid-Eye-Movement (REM) sleep. In humans, functional neuroimaging techniques, using H 2 15 O or 18 FDG positron emission tomography (PET) and functional magnetic resonance imaging (fMRI), allowed the mapping of the regional cerebral activity during this sleep stage, which is dominated by the activation of the pons, the thalamus, temporo-occipital and limbic/paralimbic areas (including the amygdala, the hippocampal formation and the anterior cingulate cortex), along with a relative quiescence of dorsolateral prefrontal and inferior parietal cortices. These results are in agreement with animal neurophysiological data about REM-sleep generation. They may also explain several hallmarks of dreaming experience that are found in dream reports after awakening from REM sleep. For instance, amygdala activation is consistent with the predominance of threatrelated emotions. Temporo-occipital activation is in keeping with visual dream imagery. Prefrontal deactivation is suggestive of the lack of orientational stability, the alteration in time perception, the delusional belief of being awake, the decrease in volitional control and the fragmented episodic memory recall. Inferior parietal deactivation may contribute to the lack of distinction between firstand third-person perspectives. Conversely, specific cognitive and emotional features in individual dreams could be used to predict some aspects of the regional functional organisation of the human brain during dreams, and also inspire the design of future dedicated neuroimaging studies by offering constraints to the analysis and interpretation of sleep data acquired just before dream reports. Therefore, we suggest that future functional brain imaging in humans should be combined with a careful neuropsychological analysis of dream reports, and especially their categorisation based on the presence of specific bizarre features, to test hypotheses about the brain correlates of dreams. As little is known about the physiology of non-REM sleep dreaming, future neuroimaging studies should also attempt to link dreaming experiences during this sleep stage with patterns of regional cerebral activity. Overall, although many questions arising from the study of oneiric behaviour remain unanswered, recent neurophysiological and neuroimaging research about REM sleep offers an increasingly detailed picture of the cerebral correlates of dreaming that might also provide new insights into dream functions.

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Enhancement of acetylcholine release during paradoxical sleep in the dorsal tegmental field of the cat brain stem

Cited by 163 publications

References 8 publications

Changes in Inhibitory Amino Acid Release Linked to Pontine-Induced Atonia: AnIn VivoMicrodialysis Study

Changes in Inhibitory Amino Acid Release Linked to Pontine-Induced Atonia: AnIn VivoMicrodialysis Study

Interactions between GABAergic and Cholinergic Processes in the Nucleus Pontis Oralis: Neuronal Mechanisms Controlling Active (Rapid Eye Movement) Sleep and Wakefulness

Dreaming: a neuroimaging view

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