Cholinergic Modulation of General Anesthesia

2021 ◽  
Vol 19 ◽  
Author(s):  
L. Stan Leung ◽  
Tao Luo
Keyword(s):  
Inflammatory Response ◽  
General Anesthesia ◽  
Basal Forebrain ◽  
Animal Experiments ◽  
Cholinergic Neurons ◽  
Cognitive Disorder ◽  
General Anesthetic ◽  
Genetic Ablation ◽  
Behavioral Sensitivity ◽  
Anesthetic Exposure

: Acetylcholine in the brain serves arousal and cognitive functions. Cholinergic neurons in the mesopontine brainstem and basal forebrain are important for activation of the cerebral cortex, which is characterized by suppression of irregular slow waves and increase in gamma (30-100 Hz) activity in the electroencephalogram, and appearance of a hippocampal theta rhythm. During general anesthesia, decrease in acetylcholine release and cholinergic functions contribute to the desirable outcomes of general anesthesia such as amnesia, loss of awareness and consciousness, and immobility. Animal experiments indicate that inactivation, lesion or genetic ablation of cholinergic neurons in the basal forebrain potentiated the effects of inhalational and injectable anesthetics, including isoflurane, halothane, propofol, pentobarbital and in some cases, ketamine. Increased behavioral sensitivity to general anesthetic, faster induction time and delayed recovery of a loss of righting reflex have been shown in rodents with basal forebrain cholinergic deficits. Cholinergic stimulation in the prefrontal cortex, thalamus and basal forebrain hastens recovery from general anesthesia. Anticholinesterase accelerates emergence from general anesthesia, but with mixed success, in part depending on the anesthetic used. Cholinergic deficits may contribute to cognitive impairments after anesthesia and operations, which are severe in aged subjects. We propose a cholinergic hypothesis for postoperative cognitive disorder, in line with the cholinergic deficits and cognitive decline in aging and Alzheimer’s disease. The current animal literature suggests that brain cholinergic neurons can regulate the immune and inflammatory response after surgical operation and anesthetic exposure, and anticholinesterase and α7-nicotinic cholinergic agonists can alleviate postoperative inflammatory response and cognitive deficits.

scholarly journals ATPase Inhibitory Factor 1 Is Critical for Regulating Sevoflurane-Induced Microglial Inflammatory Responses and Caspase-3 Activation

2021 ◽  
Vol 15 ◽  
Author(s):  
Yaru Xu ◽  
Ge Gao ◽  
Xiaoru Sun ◽  
Qidong Liu ◽  
Cheng Li
Keyword(s):  
Inflammatory Response ◽  
Caspase 3 ◽  
Inflammatory Responses ◽  
Animal Experiments ◽  
Atp Synthesis ◽  
Inhibitory Factor ◽  
Inflammatory Factors ◽  
General Anesthetics ◽  
General Anesthetic ◽  
Inhibitory Factor 1

Postoperative delirium (POD) is one of the most important complications after surgery with general anesthesia, for which the neurotoxicity of general anesthetics is a high-risk factor. However, the mechanism remains largely unknown, which also hinders the effective treatment of POD. Here, we confirmed that a clinical concentration of the general anesthetic sevoflurane increased the expression of inflammatory factors and activated the caspase-3 by upregulating ATPase inhibitory factor 1 (ATPIF1) expression in microglia. Upregulation of ATPIF1 decreased the synthesis of ATP which is an important signaling molecule secreted by microglia. Extracellular supplementation with ATP attenuated the microglial inflammatory response and caspase-3 activation caused by sevoflurane or overexpression of ATPIF1. Additionally, the microglial inflammatory response further upregulated ATPIF1 expression, resulting in a positive feedback loop. Animal experiments further indicated that intraperitoneal injection of ATP significantly alleviated sevoflurane anesthesia-induced POD-related anxiety behavior and memory damage in mice. This study reveals that ATPIF1, an important protein regulating ATP synthesis, mediates sevoflurane-induced neurotoxicity in microglia. ATP supplementation may be a potential clinical treatment to alleviate sevoflurane-induced POD.

scholarly journals General anesthesia with remimazolam in a patient with mitochondrial encephalomyopathy: a case report

2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Yuji Suzuki ◽  
Matsuyuki Doi ◽  
Yoshiki Nakajima
Keyword(s):  
Lactic Acidosis ◽  
General Anesthesia ◽  
Mitochondrial Disease ◽  
Muscle Relaxation ◽  
Anesthetic Management ◽  
Perioperative Period ◽  
Mitochondrial Encephalomyopathy ◽  
Anesthesia Induction ◽  
General Anesthetic ◽  
Anesthetic Agents

Abstract Background Systemic anesthetic management of patients with mitochondrial disease requires careful preoperative preparation to administer adequate anesthesia and address potential disease-related complications. The appropriate general anesthetic agents to use in these patients remain controversial. Case presentation A 54-year-old woman (height, 145 cm; weight, 43 kg) diagnosed with mitochondrial encephalomyopathy with lactic acidosis and stroke-like episodes underwent elective cochlear implantation. Infusions of intravenous remimazolam and remifentanil guided by patient state index monitoring were used for anesthesia induction and maintenance. Neither lactic acidosis nor prolonged muscle relaxation occurred in the perioperative period. At the end of surgery, flumazenil was administered to antagonize sedation, which rapidly resulted in consciousness. Conclusions Remimazolam administration and reversal with flumazenil were successfully used for general anesthesia in a patient with mitochondrial disease.

scholarly journals Different cholinergic cell groups in the basal forebrain regulate social interaction and social recognition memory

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Kana Okada ◽  
Kayo Nishizawa ◽  
Tomoko Kobayashi ◽  
Shogo Sakata ◽  
Kouichi Hashimoto ◽  
...  
Keyword(s):  
Social Interaction ◽  
Recognition Memory ◽  
Basal Forebrain ◽  
Social Behaviour ◽  
Cholinergic Neurons ◽  
Social Recognition ◽  
Social Ability ◽  
Cell Groups ◽  
Cholinergic Cell ◽  
Social Recognition Memory

AbstractSocial behaviour is a complex construct that is reported to include several components of social approach, interaction and recognition memory. Alzheimer’s disease (AD) is mainly characterized by progressive dementia and is accompanied by cognitive impairments, including a decline in social ability. The cholinergic system is a potential constituent for the neural mechanisms underlying social behaviour, and impaired social ability in AD may have a cholinergic basis. However, the involvement of cholinergic function in social behaviour has not yet been fully understood. Here, we performed a selective elimination of cholinergic cell groups in the basal forebrain in mice to examine the role of cholinergic function in social interaction and social recognition memory by using the three-chamber test. Elimination of cholinergic neurons in the medial septum (MS) and vertical diagonal band of Broca (vDB) caused impairment in social interaction, whereas ablating cholinergic neurons in the nucleus basalis magnocellularis (NBM) impaired social recognition memory. These impairments were restored by treatment with cholinesterase inhibitors, leading to cholinergic system activation. Our findings indicate distinct roles of MS/vDB and NBM cholinergic neurons in social interaction and social recognition memory, suggesting that cholinergic dysfunction may explain social ability deficits associated with AD symptoms.

scholarly journals Contribution of the basal forebrain to corticocortical network interactions

2021 ◽  
Author(s):  
Peter Gombkoto ◽  
Matthew Gielow ◽  
Peter Varsanyi ◽  
Candice Chavez ◽  
Laszlo Zaborszky
Keyword(s):  
Sensory Processing ◽  
Basal Forebrain ◽  
Field Potential ◽  
Cholinergic Neurons ◽  
Attention And Memory ◽  
Cortical Circuits ◽  
Cholinergic Signaling ◽  
Spatial Changes ◽  
Gamma Power ◽  
Gamma Coherence

AbstractBasal forebrain (BF) cholinergic neurons provide the cerebral cortex with acetylcholine. Despite the long-established involvement of these cells in sensory processing, attention, and memory, the mechanisms by which cholinergic signaling regulates cognitive processes remain elusive. In this study, we recorded spiking and local field potential data simultaneously from several locations in the BF, and sites in the orbitofrontal and visual cortex in transgenic ChAT-Cre rats performing a visual discrimination task. We observed distinct differences in the fine spatial distributions of gamma coherence values between specific basalo-cortical and cortico-cortical sites that shifted across task phases. Additionally, cholinergic firing induced spatial changes in cortical gamma power, and optogenetic activation of BF increased coherence between specific cortico-cortical sites, suggesting that the cholinergic system contributes to selective modulation of cortico-cortical circuits. Furthermore, the results suggest that cells in specific BF locations are dynamically recruited across behavioral epochs to coordinate interregional cortical processes underlying cognition.

Co-expression of p75NTR- and calbindin-immunoreactivity in cholinergic neurons of the raccoon basal forebrain

1998 ◽  
Vol 797 (2) ◽  
pp. 351-356 ◽  
Author(s):  
Liisa Tremere ◽  
Gert Brückner ◽  
Kurt Brauer ◽  
Douglas D Rasmusson ◽  
Reinhild Poethke ◽  
...  
Keyword(s):  
Basal Forebrain ◽  
Cholinergic Neurons

scholarly journals Hydrophilic cell-derived extracellular matrix as a niche to promote adhesion and differentiation of neural progenitor cells

RSC Advances ◽  
2017 ◽  
Vol 7 (72) ◽  
pp. 45587-45594 ◽  
Author(s):  
Lingyan Yang ◽  
Ziyun Jiang ◽  
Linhong Zhou ◽  
Keli Zhao ◽  
Xun Ma ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Basal Forebrain ◽  
Progenitor Cell ◽  
Neural Progenitor Cells ◽  
Cholinergic Neurons ◽  
Neural Progenitor Cell ◽  
Neural Progenitor ◽  
Basal Forebrain Cholinergic Neurons ◽  
Adhesion Performance ◽  
Excellent Adhesion

Cell-derived extracellular matrix exhibits excellent adhesion performance for neural progenitor cell anchoring and residency, resulting in promoted proliferation of the stem cells to basal forebrain cholinergic neurons.

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