Effects of ketamine and pentobarbitone on acetylcholine release from the rat frontal cortex in vivo

Kikuchi, Takayuki; Wang, Y; Shinbori, Hironobu; Sato, Kazuo; Okumura, Fukuichiro

doi:10.1093/bja/79.1.128

Cited by 39 publications

(29 citation statements)

References 7 publications

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“…Although cortical ACh decreases during administration of GABAergic anaesthetics, 16 33 34 the present findings show a significant increase in ACh concentrations during ketamine-induced unconsciousness. However, this increase was considerably lower than that reported by Kikuchi and colleagues 16 (∼105% in the present study vs ∼281% in the study by Kikuchi and colleagues). 16 We demonstrate that a dramatic increase (∼325%) in cortical ACh is associated with emergence and recovery, which could result from increased arousal because of decreased plasma ketamine concentrations.…”

Section: Discussioncontrasting

confidence: 90%

“…However, this increase was considerably lower than that reported by Kikuchi and colleagues 16 (∼105% in the present study vs ∼281% in the study by Kikuchi and colleagues). 16 We demonstrate that a dramatic increase (∼325%) in cortical ACh is associated with emergence and recovery, which could result from increased arousal because of decreased plasma ketamine concentrations. Higher ACh concentrations are typically correlated with an activated cortex, as in the waking state 35 or rapid eye movement sleep, 35 which is also characterized by decreased gamma coherence.…”

Section: Discussioncontrasting

confidence: 90%

“…Studies of ketamine and neurochemistry have focused on acetylcholine (ACh) but (i) without concomitant neurophysiological recordings, 16 17 (ii) using subanaesthetic doses of ketamine, 16 17 or (iii) without formal testing of loss of righting reflex (LORR) as a surrogate of anaesthetic-induced unconsciousness. 16 To address this gap in knowledge, the objective of the present study was to identify the relationship of electroencephalographic coherence, cortical ACh, and the state of ketamine-induced unconsciousness.…”

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confidence: 99%

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Electroencephalographic coherence and cortical acetylcholine during ketamine-induced unconsciousness

Pal

Hambrecht-Wiedbusch

Silverstein

et al. 2015

British Journal of Anaesthesia

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Background: There is limited understanding of cortical neurochemistry and cortical connectivity during ketamine anaesthesia. We conducted a systematic study to investigate the effects of ketamine on cortical acetylcholine (ACh) and electroencephalographic coherence. Methods: Male Sprague-Dawley rats (n=11) were implanted with electrodes to record electroencephalogram (EEG) from frontal, parietal, and occipital cortices, and with a microdialysis guide cannula for simultaneous measurement of ACh concentrations in prefrontal cortex before, during, and after ketamine anaesthesia. Coherence and power spectral density computed from the EEG, and ACh concentrations, were compared between conscious and unconscious states. Loss of righting reflex was used as a surrogate for unconsciousness. Results: Ketamine-induced unconsciousness was associated with a global reduction of power (P=0.02) in higher gamma bandwidths (>65 Hz), a global reduction of coherence (P≤0.01) across a broad frequency range (0.5-250 Hz), and a significant increase in ACh concentrations (P=0.01) in the prefrontal cortex. Compared with the unconscious state, recovery of righting reflex was marked by a further increase in ACh concentrations (P=0.0007), global increases in power in theta (4-10 Hz; P=0.03) and low gamma frequencies (25-55 Hz; P=0.0001), and increase in power (P≤0.01) and coherence (P≤0.002) in higher gamma frequencies (65-250 Hz). Acetylcholine concentrations, coherence, and spectral properties returned to baseline levels after a prolonged recovery period. Conclusions: Ketamine-induced unconsciousness is characterized by suppression of high-frequency gamma activity and a breakdown of cortical coherence, despite increased cholinergic tone in the cortex.

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Section: Discussioncontrasting

confidence: 90%

Section: Discussioncontrasting

confidence: 90%

mentioning

confidence: 99%

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Electroencephalographic coherence and cortical acetylcholine during ketamine-induced unconsciousness

Pal

Hambrecht-Wiedbusch

Silverstein

et al. 2015

British Journal of Anaesthesia

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“…Jentsch et al (1998) reported that the acute administration of PCP in rats increases cortical acetylcholine (ACh) release measured by means of microdialysis. Similarly, Kikuchi et al (1997) reported substantial increases in frontal cortical ACh release following ketamine administration. These data, in concert with the finding that amphetamine also increases and, following repeated administration, sensitizes increases in cortical ACh release (Nelson et al 2000), suggest that increases in cortical cholinergic transmission may represent a common effect of psychotogenic treatments (see also Sarter et al 2001).…”

Section: Introductionmentioning

confidence: 88%

Effects of acute and repeated systemic administration of ketamine on prefrontal acetylcholine release and sustained attention performance in rats

et al. 2002

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The robust stimulation of cortical acetylcholine release represents a potent component of the pharmacological effects of ketamine. The effects of acute ketamine on attentional performance were limited to high rates of omissions. Repeated ketamine administration 'sensitized' neither cortical acetylcholine release nor attentional performance. These effects of repeated ketamine differ substantially from those of another major psychotogenic drug, amphetamine, and thus support the view that ketamine and amphetamine model fundamentally different aspects of schizophrenia.

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“…In addition, the central cholinergic system has been implicated in modulating the depressant action of pentobarbital. In vivo studies indicate that acute treatment with pentobarbital can inhibit Ach release and decrease muscarinic receptor binding in the frontal cortex, striatum and hippocampus of rats and mice (Inoue et al, 1992;Kikuchi et al, 1997;Sato et al, 1996). Intra-septal microinjection of arecoline is reported to significantly shorten the duration of pentobarbital-induced LORR (Zucker et al, 1987).…”

mentioning

confidence: 99%

Systemic Administration of Arecoline Reduces Ethanol‐Induced Sleeping Through Activation of Central Muscarinic Receptor in Mice

Sun

Liu²,

Luo³

et al. 2009

Alcoholism Clin & Exp Res

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Background: Epidemiological evidence of co-use of alcohol and areca nuts suggests a potential central interaction between arecoline, a major alkaloid of areca and a muscarinic receptor agonist, and ethanol. Moreover, the central cholinergic system plays an important role in the depressant action of ethanol and barbiturates. The purpose of this study was to investigate the effects of arecoline on pentobarbital-and ethanol-induced hypnosis in mice.Methods: Male ICR mice were tested for locomotor activity following acute systemic administration of ethanol alone, arecoline alone, or ethanol plus arecoline. For the loss of the righting reflex (LORR) induced by pentobarbital and ethanol, sleep latency and sleeping duration were evaluated in mice treated with arecoline alone or the combination of arecoline and scopolamine or methscopolamine.Results: Ethanol (1.0 to 3.0 g ⁄ kg, i.p.) reduced locomotor activity significantly and a declining trend was observed after treatment with arecoline (0.25 to 1.0 mg ⁄ kg, i.p.), but there were no synergistic effects of ethanol and arecoline on locomotor activity. The experiments on LORR demonstrated that arecoline (0.125 to 1.0 mg ⁄ kg, s.c.) shortened the duration of sleeping induced by ethanol (4.0 g ⁄ kg, i.p.), but not pentobarbital (45 mg ⁄ kg, i.p.). In addition, alterations of sleep latency were not obvious in both pentobarbital-and ethanol-induced LORR. Statistical analyses revealed that scopolamine (centrally acting), but not methscopolamine (peripherally acting), could antagonize the effect of arecoline on the duration of ethanol-induced LORR in mice.Conclusions: These results suggest that central muscarinic receptor is a pharmacological target for the action of arecoline to modulate ethanol-induced hypnosis.

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Effects of ketamine and pentobarbitone on acetylcholine release from the rat frontal cortex in vivo

Cited by 39 publications

References 7 publications

Electroencephalographic coherence and cortical acetylcholine during ketamine-induced unconsciousness

Electroencephalographic coherence and cortical acetylcholine during ketamine-induced unconsciousness

Effects of acute and repeated systemic administration of ketamine on prefrontal acetylcholine release and sustained attention performance in rats

Systemic Administration of Arecoline Reduces Ethanol‐Induced Sleeping Through Activation of Central Muscarinic Receptor in Mice

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