Medial Septal Cholinergic Neurons Modulate Isoflurane Anesthesia

Tai, Siew Kian; Ma, Jingyi; Leung, L. Stan

doi:10.1097/aln.0b013e3182a7cab6

Cited by 22 publications

(19 citation statements)

References 31 publications

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“…Compared to the traditional chemical method, this approach has the merits of cell specificity and accuracy. BF cholinergic neuron lesioned mice were more sensitive to propofol and isoflurane in both behavior and EEG performance, and they have a longer recovery time, which are consistent with Leung's findings with rats (Leung et al, 2011;Tai et al, 2014). However, there are still concerns about the lesion approach, as it has reported that lesion experiment of the sleep-wake nucleus may lead to changes in sleep debt, suggesting that the lesion itself might affect anesthetic efficacy (Tung et al, 2002).…”

Section: Discussionsupporting

confidence: 83%

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Basal Forebrain Cholinergic Activity Modulates Isoflurane and Propofol Anesthesia

et al. 2020

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Cholinergic neurons in the basal forebrain (BF) have long been considered to be the key neurons in the regulation of cortical and behavioral arousal, and cholinergic activation in the downstream region of the BF can arouse anesthetized rats. However, whether the activation of BF cholinergic neurons can induce behavior and electroencephalogram (EEG) recovery from anesthesia is unclear. In this study, based on a transgenic mouse line expressing ChAT-IRES-Cre, we applied a fiber photometry system combined with GCaMPs expression in the BF and found that both isoflurane and propofol inhibit the activity of BF cholinergic neurons, which is closely related to the consciousness transition. We further revealed that genetic lesion of BF cholinergic neurons was associated with a markedly increased potency of anesthetics, while designer receptor exclusively activated by designer drugs (DREADD)-activated BF cholinergic neurons was responsible for slower induction and faster recovery of anesthesia. We also documented a significant increase in δ power bands (1-4 Hz) and a decrease in β (12-25 Hz) power bands in BF cholinergic lesioned mice, while there was a clearly noticeable decline in EEG δ power of activated BF cholinergic neurons. Moreover, sensitivity to anesthetics was reduced after optical stimulation of BF cholinergic cells, yet it failed to restore wakelike behavior in constantly anesthetized mice. Our results indicate a functional role of BF cholinergic neurons in the regulation of general anesthesia. Inhibition of BF cholinergic neurons mediates the formation of unconsciousness induced by general anesthetics, and their activation promotes recovery from the anesthesia state.

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Section: Discussionsupporting

confidence: 83%

“…To determine whether a nucleus is involved in general anesthesia, lesion method used to be the most common and only approach (Leung et al, 2011(Leung et al, , 2013Tai et al, 2014). However, the effects of general anesthetics on neuronal activity are often overlooked due to the inherent limitation of the technique.…”

Section: Discussionmentioning

confidence: 99%

Basal Forebrain Cholinergic Activity Modulates Isoflurane and Propofol Anesthesia

et al. 2020

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“…The medial septal region has been proposed to function as a node for the ascending brainstem pathways, sending inputs to the posterior cingulate, enthorinal cortex and hippocampus ( Bland et al, 2000 ). Recent studies have implicated the medial septal nucleus in general anesthesia ( Ma et al, 2002 ; Leung et al 2013 , Tai et al, 2014 ). The septal area has also been associated with analgesia induced by acupuncture ( Xiong and Zheng 1990 ; Zhao 2008 ).…”

Section: Discussionmentioning

confidence: 99%

Butorphanol Suppression of Histamine Itch Is Mediated by Nucleus Accumbens and Septal Nuclei: A Pharmacological fMRI Study

Papoiu

Kraft

Coghill

et al. 2015

Journal of Investigative Dermatology

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Opioid receptors in the central nervous system are important modulators of itch transmission. In this study, we examined the effect of mixed-action opioid butorphanol on histamine itch, cowhage itch and heat pain in healthy volunteers. Using functional MRI, we investigated significant changes in cerebral perfusion to identify the critical brain centers mediating the antipruritic effect of butorphanol. Butorphanol suppressed the itch induced experimentally with histamine, reduced the intensity of cowhage itch by approximately 35%, and did not affect heat pain sensitivity. In comparison with the placebo, butorphanol produced a bilateral deactivation of claustrum, insula and putamen, areas activated during itch processing. Analysis of cerebral perfusion patterns of brain processing of itch vs. itch inhibition under the effect of the drug, revealed that the reduction of cowhage itch by butorphanol was correlated with changes in cerebral perfusion in the midbrain, thalamus, S1, insula and cerebellum. The suppression of histamine itch by butorphanol was paralleled by the activation of nucleus accumbens and septal nuclei, structures expressing high levels of kappa opioid receptors. In conclusion, important relays of the mesolimbic circuit were involved in the inhibition of itch by butorphanol and could represent potential targets for the development of antipruritic therapy.

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“…Although many endogenous sleep or arousal pathways (i.e., the GABAergic [ 10 , 11 ], noradrenergic [ 12 , 13 ], histaminergic [ 7 , 14 ], and cholinergic [ 15 , 16 ] pathways) have been implicated in the mechanism of general anesthesia, few studies have investigated the role of the dopaminergic pathways in general anesthesia. Very recently, using a D1 receptor agonist (chloro-APB), Taylor et al successfully induced the emergence from isoflurane anesthesia in rats [ 4 ].…”

Section: Discussionmentioning

confidence: 99%

The Role of Dopaminergic VTA Neurons in General Anesthesia

et al. 2015

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Recent studies have demonstrated that the central dopaminergic system is implicated in the mechanism underlying general anesthesia. Here, we investigated whether dopaminergic ventral tegmental area (VTA) neurons participate in general anesthesia. Dopaminergic VTA neurons were selectively ablated from male Sprague Dawley rats via the bilateral infusion of 6-hydroxydopamine (6-OHDA) into the VTA. Two weeks after infusion, the number of dopaminergic neurons in the bilateral VTA was markedly reduced in the 6-OHDA-treated rats compared with the vehicle-treated rats. These bilateral VTA lesions significantly prolonged the recovery time for propofol but did not significantly alter its onset time or 50% effective dose (ED50) value. In addition, the anesthetic responses to isoflurane and ketamine were unaffected by the VTA lesions. Our findings suggested that dopaminergic VTA neurons might be involved in the emergence from propofol anesthesia.

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Medial Septal Cholinergic Neurons Modulate Isoflurane Anesthesia

Abstract: These findings suggest a role of the septal cholinergic neurons in modulating the sensitivity to isoflurane anesthesia, which affects both induction and emergence. The sensitivity of hippocampal gamma power to isoflurane appears to indicate anesthesia (LORR) sensitivity.

Cited by 22 publications

References 31 publications

Basal Forebrain Cholinergic Activity Modulates Isoflurane and Propofol Anesthesia

Basal Forebrain Cholinergic Activity Modulates Isoflurane and Propofol Anesthesia

Butorphanol Suppression of Histamine Itch Is Mediated by Nucleus Accumbens and Septal Nuclei: A Pharmacological fMRI Study

The Role of Dopaminergic VTA Neurons in General Anesthesia

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