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Zhang, K.;  Pan, J.;  Yu, Y. In Vivo Calcium Imaging under General Anesthesia. Encyclopedia. Available online: https://encyclopedia.pub/entry/25122 (accessed on 08 July 2025).
Zhang K,  Pan J,  Yu Y. In Vivo Calcium Imaging under General Anesthesia. Encyclopedia. Available at: https://encyclopedia.pub/entry/25122. Accessed July 08, 2025.
Zhang, Kai, Jiacheng Pan, Yonghao Yu. "In Vivo Calcium Imaging under General Anesthesia" Encyclopedia, https://encyclopedia.pub/entry/25122 (accessed July 08, 2025).
Zhang, K.,  Pan, J., & Yu, Y. (2022, July 14). In Vivo Calcium Imaging under General Anesthesia. In Encyclopedia. https://encyclopedia.pub/entry/25122
Zhang, Kai, et al. "In Vivo Calcium Imaging under General Anesthesia." Encyclopedia. Web. 14 July, 2022.
In Vivo Calcium Imaging under General Anesthesia
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This entry is adapted from the peer-reviewed paper 10.3390/biom12070898

General anesthesia has been widely utilized since the 1840s, but its underlying neural circuits remain to be completely understood. Calcium ions are popular targets used to detect neuronal activities that link circuit dynamics to behaviors in modern neuroscience research.

general anesthesia neural nuclei and circuits in vivo calcium imaging

1. Introduction

General anesthesia has been used since the 1840s and is a necessary safety guarantee for most surgeries today. From destroying the lipid bilayer on the cell surface [1] to protein targets [2] and the specific molecular sites on specific receptors [3], the mechanisms of general anesthetics have been well documented. However, the neural circuits underlying general anesthesia remain relatively unclear, compared with the protein and molecular targets of general anesthetics. Growing evidence suggests that many neural circuits that regulate the sleep–wake cycle are involved in the general-anesthesia effect as well. For example, varieties of neurons and their projections that are important to promote wakefulness, including monoaminergic [4][5], cholinergic [6], glutamatergic [7], and orexinergic neurons [8], participate in promoting emergence from general anesthesia. The γ-aminobutyric acid (GABA) neurons in the ventrolateral preoptic nucleus (VLPO) extensively innervate and suppress multiple arousal-promoting brain regions [9][10]. The VLPO is vital for both the initiation and maintenance of sleep [11]. It is reported that VLPO is necessary for propofol-induced inhibition of locus coeruleus (LC) activity [12]. Whereas directly specific activation of GABAergic in the VLPO modulates sleep–wake architecture but not anesthetic-state transitions [13]. Therefore, although there may be some common pathways between general anesthesia and sleep, we are still a long way from fully understanding the neural circuitry of general anesthesia.
An explicit exploration of the role of specific neural circuits under general anesthesia requires advanced neural labeling and modulation technologies. In the following contents, in vivo calcium imaging are introduced. In vivo calcium imaging records the activity of specific neurons and neural circuits in target brain regions [14].

2. In Vivo Calcium Imaging

Calcium ions are popular targets used to detect neuronal activities that link circuit dynamics to behaviors in modern neuroscience research [15][16]. Exploiting calcium ion properties, two main categories of calcium-ion indicators have been developed: chemical calcium dyes [17] and genetically encoded calcium indicators (GECIs) [18][19]. However, chemical calcium dyes, such as Fluo-4 and Oregon Green BAPTA-1 (OGB-1), are delivered through cell permeabilization, which can damage the cell integrity. Additionally, chemical calcium dyes are normally only capable of recording neuronal activity for several hours. These limitations constrain subsequent imaging conditions [20][21]. In contrast, GECIs could be easily expressed via virus-delivery methods, such as for adeno-associated-virus or lentivirus vectors, and cause the least cellular damage. Furthermore, GECIs could even be successfully expressed by transgenic methods without invasive procedures [22][23]. Thus, GECIs can be stably expressed in neurons and allow recording of the neural-firing patterns over a long period of time. Most importantly, GECIs are capable of selective yet unbiased labeling of neuronal types through their specific gene promoters, enabling research on the activities of each neuronal cell type. Moreover, GECIs can also be expressed at the nerve-projection terminals, so in vivo calcium imaging can directly monitor the activity of specific neural circuits [24]. Thus, in vivo calcium imaging has several advantages over traditional in vivo electrophysiological recording in studying neural endpoints and circuits under general anesthesia. Nowadays, GECIs, such as the GCaMP6s series, which possess a high time sensitivity and fluorescence signal-to-noise ratio [25], have become one of the most widely used calcium-ion detection tools [26][27].
GECIs bind to calcium ions and emit fluorescence signals that can be used to determine intracellular calcium concentration [19] (Figure 1A). These GECI-based signals can be detected by several methods, including optical-fiber photometry, miniscope imaging and two-photon imaging (Figure 1B). GECIs fluorescence is stimulated through an optical fiber in optical-fiber photometry. It has the advantages of not restricting animal movements and of monitoring deep-brain regions. Thus, optical-fiber photometry coupled with the GECI technology allows the activities of neurons and neural projections in any deep-brain area related to a specific behavior to be captured in freely moving animals [28]. Among the three in vivo calcium imaging technologies, optical-fiber photometry is currently the most widely used one in the study of neural-circuit mechanisms in general anesthesia. However, despite many advantages, optical-fiber photometry has its disadvantages. For example, compared with other in vivo calcium imaging techniques, its spatial resolution is relatively low, and it can only monitor changes in fluorescence intensity in neuron populations rather than at the single-neuron level. Therefore, it is difficult to detect relatively tiny excitability changes in cell groups using optical-fiber photometry. Further, the GECI-delivery methods, such as viral transfection or dyes, and the optical-fiber implantation, inevitably cause damage to the brain tissue, especially when targeting deep-brain regions.
Biomolecules 12 00898 g001
Figure 1. Schematic diagram of imaging principles of in vivo calcium imaging. (A) In basal condition: CaM and M13 are not bound to each other, and the fluorescence intensity of EGFP generally remains constant and low; in stimulated condition: the fluorescence intensity of EGFP increases significantly when calcium ions bind directly to EGFP. CaM, calmodulin; M13, calmodulin-binding peptide; EGFP, enhanced green fluorescent protein. (B) The schematic diagram of imaging device principles (top) and calcium-signal characterization for the three in vivo calcium imaging techniques (bottom).
Miniscope imaging has a high spatial resolution, and individual neuronal activity can be readily monitored [29]. The development of a head-mounted miniscope combined with Gradient Index (GRIN) lens-implantation technology also enables neural activities to be monitored in the deep-brain regions of freely moving animals [30]. However, viral transfection or lens implantation could also cause brain tissue damage. Additionally, this method is relatively more complex than fiber photometry in both surgical operation and imaging [31]. Two-photon microscopic-imaging technology with higher resolution is also applied, to identify the neural-population codes underlying complex brain functions [32]. Traditionally, the monitoring depth of this method is relatively shallow and generally limited to the study of neuronal activity in the cortex or hippocampus. In addition, it requires animal-head fixation, restricting the animal’s free movement [33][34]. These shortcomings may limit its wide application in the study of anesthesia neural circuitry to some extent. Fortunately, a newly developed miniature two-photon miniscope for large-scale calcium imaging in freely moving mice allows stable simultaneous recording of neuronal dynamics of densely active cortical regions in several behavioral tasks, without impediment to the animal’s behavior [35]. In summary, despite these limitations, with the continuous improvement of in vivo calcium imaging technology, it remains a valuable fundamental research technique with tremendous potential, especially in its application prospect in anesthesiology, such as the study of neural targets of analgesics and sedatives commonly used in the operating room.
In vivo calcium imaging technologies are widely applied to investigate whether specific neural endpoints or projections associated with the sleep–wake cycle participate in general anesthesia. The cortex is organized into six layers, and excitatory cells within each layer receive inputs from other excitatory cells in the same layer and from inhibitory cells. Simultaneously, the cerebral cortex receives a lot of subcortical projections, whose activity is critical for consciousness [36][37]. A recent two-photon calcium imaging study found that different anesthetics selectively synchronized activity in cortical pyramidal neurons within layer 5, which may contribute to the loss of consciousness induced by general anesthesia [38].
Monoaminergic neurons that drive arousal produce dopamine, serotonin, histamine, or norepinephrine, and they extensively innervate many brain regions. These monoaminergic cell groups share similar activity patterns, exhibiting high firing rates during wakefulness and slow firing rates during sleep [39]. The ventral tegmental area (VTA) mainly contains dopaminergic neurons and projects to abundant arousal-promoting brain areas [5]. Using real-time in vivo fiber photometry, researchers have shown that calcium signals of VTA dopaminergic neurons significantly decline after sevoflurane-induced loss of righting reflex (LORR) and robustly increase due to recovery of righting reflex (RORR) [40]. The nucleus accumbens (NAc) is situated in the ventral striatum and receives projections from dopaminergic neurons of VTA [41]. NAc neurons are similarly inhibited in the induction phase of propofol anesthesia and are markedly activated during recovery, and these effects are mediated by dopamine receptor 1 [40][42]. Moreover, the calcium signals of the ventral periaqueductal gray (vPAG) dopaminergic neurons also decrease during induction and increase during emergence, respectively, with isoflurane anesthesia [43]. Serotonergic (5-HTergic) neurons in the dorsal raphe nucleus (DRN), which project heavily to the midbrain and forebrain, are implicated in the modulation of the sleep–wake transition [44]. The calcium activity of DRN 5-HT neurons gradually declines after the initiation of isoflurane administration and begins to restore after the termination of anesthetics inhalation [45].
Together, these results suggest that similar to the role of promoting wakefulness during the sleep–wake cycle, the dopaminergic and serotonergic neurons in the brain may contribute to the consciousness transition that occurs during general anesthesia with various anesthetics. Two additional important awakening monoaminergic cell groups include the histaminergic neurons in the tuberopapillary nucleus and norepinephrine neurons in the LC. The actions of these neuron populations have not yet been reported using in vivo calcium imaging under general anesthesia. However, recently in a larval-fish model, a two-photon laser-based ablation study indicated that the LC neurons play a regulatory role in both the induction of and emergence from intravenous general anesthesia [46].
The basal forebrain (BF) is a heterogeneous region containing cholinergic, GABAergic, and glutamatergic neurons, and these BF neurons heavily innervate the cortex. In addition, it is worth noting that BF GABAergic neurons are functionally heterogeneous. Some BF GABAergic neurons are primarily active during the awake state, while others are more active during sleep. However, as a whole, BF plays a vital role in promoting quick cortical activity and arousal [47][48]. During both isoflurane and propofol anesthesia, calcium signals in BF cholinergic neurons decrease gradually during the induction period, begin to rise during the pre-awakening stage, and peak almost at the moment of RORR. Due to the reliable time accuracy and record stability advantages of optical-fiber photometry technology, researchers have observed that neuronal activity changes always precede behavioral changes. Therefore, BF cholinergic neuronal events may be the impetus for changes in the state of consciousness rather than the target of changes [49]. Given that the function of GABAergic BF neurons is clearly distinct in the sleep–wake cycle, it is odd that there have been no in vivo calcium imaging studies of these cell groups in general anesthesia. Future experiments are needed to target BF GABA neurons in both the induction to and emergence from general anesthesia.
Glutamatergic neurons in the parabrachial nucleus (PBN) are vital in contributing to both behavioral and cortical electroencephalogram arousal [50]. An optical-fiber photometry study in rats showed an obvious increase in the activity of PBN neurons during emergence from both isoflurane and propofol anesthesia but no significant change in the induction period [51]. On the other hand, the lateral habenula (LHb), another brain region clustered with glutamatergic neurons, plays an important role in promoting sleep but not arousal [52]. The average calcium activity of LHb is significantly increased during isoflurane anesthesia maintenance and begins to decline during RORR. Calcium signals of glutamatergic neurons in LHb show no change during the induction stage [53]. These interesting findings suggest that the glutamatergic neurons may play distinct roles in general anesthesia and the sleep–wake cycle. Compared with the dopaminergic and cholinergic systems, the glutamatergic system may only participate in the recovery phase, but not the induction phase of general anesthesia. Future research should focus on the responses of glutamatergic neurons and their projections in other brain nuclei during the induction phase of general anesthesia.
The lateral septum contains GABAergic neurons that project to multiple wakefulness-promoting subregions. The calcium activity of the dorsal–intermediate lateral septal GABAergic neuron changes in both the processes of induction and emergence, similar to the trend observed in the sleep–wake cycle [54]. Collectively, these in vivo calcium imaging findings suggest that multiple brain nuclei and neural circuits known to regulate the sleep–wake cycle play a similar role in general anesthesia (Table 1).
Table 1. Main findings with the three technologies in the neural nuclei and circuits of general anesthesia.
Neuron Type of Brain Region and Its Projections Technology Anesthetic Method Experimental Animals (Numbers) The Role of Induction to or Emergence from General Anesthesia
Layer 5 cortical pyramidal neurons In vivo two-photon calcium imaging Isoflurane, Fentanyl-Medetomidine-Midazolam, and Ketamine-Xylazine Rbp4-cre mice (22) Both
VTA dopaminergic neurons and VTA-NAc and VTA-PrL dopaminergic projection Optical-fiber photometry, optogenetics and chemogenetics Sevoflurane DAT-cre mice (64); Rats (67) Both
NAc neurons and NAc GABAergic neurons Optical-fiber photometry Sevoflurane and propofol Mice (18); Rats (12) Both
vPAG dopaminergic neurons Optical-fiber photometry Isoflurane Rats (12) Both
DRN 5-HT neurons Optical-fiber photometry Isoflurane Sert-cre mice (6) Both
Chemogenetics Sert-cre mice (24) Emergence
LC TH neurons and LC-PVT Chemogeneticsand optogenetics Isoflurane Rats (32); TH-cre mice (54) Emergence
BF cholinergic neurons Optical-fiber photometry and chemogenetics Isoflurane and propofol ChAT-cre mice (40) Both
PBN glutamatergic neurons Optical-fiber photometry, Chemogeneticsoptogenetics Isoflurane and propofol Rats (42) Emergence
Sevoflurane Vglut2-cre mice (32) Both
LHb glutamatergic neurons Optical-fiber photometry, chemogenetics, optogenetics Isoflurane Vglut2-cre mice (68) Emergence
LHA glutamatergic neurons and LHA-LHb glutamatergic projection Optogenetics andchemogenetics, Isoflurane Vglut2-cre mice (48) Emergence
LHA orexinergic neurons and LHA-PVT orexinergic projection Chemogenetics and optogenetics Isoflurane Hcrt-cre mice (83) Emergence
Desflurane Hcrt-cre mice (83) Both
LHA orexinergic neurons, LHA-BF, LHA-LC, and LHA-VTA orexinergic projections Optogenetics Isoflurane Hcrt-cre mice (69) Emergence
Dorsal–intermediate lateral septum GABAergic neurons, and dorsal–intermediate lateral septum-VTA GABAergic projection Optical-fiber photometry, chemogenetics and optogenetics Isoflurane Vgat-cre mice (56) Both
Hypothalamus preoptic area’s GABAergic neurons Chemogeneticsand optogenetics Isoflurane, propofol, and ketamine Mice (39) Emergence
VTA GABAergic neurons, and VTA–LHA GABAergic projections Chemogenetics Isoflurane Vgat-cre mice (30) Both
RMTg GABAergic neurons Chemogenetics Sevoflurane Vgat-cre mice (18) Both
In vivo calcium imaging has recently been used to explore the neural responses and other effects of anesthetics and to study the neural-circuitry mechanisms during a loss of consciousness induced by general anesthesia. For example, Qiu et al. recently used fiber photometry to explore the role of the VTA in dexmedetomidine-induced sedation [55]. They demonstrated that selective activation of dopaminergic neurons in the VTA attenuates the depth of sedation in mice. Another study successfully employed optical-fiber photometry and miniscope technology to show that different general anesthetic drugs activate a shared population of central amygdala neurons to potently suppress pain reflexes [56]. Moreover, optical-fiber photometry and two-photon imaging have been successfully applied to study complications of brain dysfunction caused by different anesthetics [57][58]. Additionally, based on the principle of genetically encoded calcium ion indicators, several fluorescent proteins that can be used to characterize specific neurotransmitter concentrations have been developed, including the dopamine neurotransmitter probe [55], glutamatergic neurotransmitter probe [59], adenosine neurotransmitter probe [60] and orexin sensor probe [34]. These improvements provide a broader potential for the application of in vivo calcium imaging in many fields in the future.

References

  1. Antkowiak, B. How do general anaesthetics work? Naturwissenschaften 2001, 88, 201–213.
  2. Franks, N.; Lieb, W.R. Do general anaesthetics act by competitive binding to specific receptors? Nature 1984, 310, 599–601.
  3. Solt, K.; Forman, S.A. Correlating the clinical actions and molecular mechanisms of general anesthetics. Curr. Opin. Anaesthesiol. 2007, 20, 300–306.
  4. Vazey, E.M.; Aston-Jones, G. Designer receptor manipulations reveal a role of the locus coeruleus noradrenergic system in isoflurane general anesthesia. Proc. Natl. Acad. Sci. USA 2014, 111, 3859–3864.
  5. Taylor, N.E.; Van Dort, C.J.; Kenny, J.D.; Pei, J.; Guidera, J.A.; Vlasov, K.Y.; Lee, J.T.; Boyden, E.S.; Brown, E.N.; Solt, K. Optogenetic activation of dopamine neurons in the ventral tegmental area induces reanimation from general anesthesia. Proc. Natl. Acad. Sci. USA 2016, 113, 12826–12831.
  6. Pal, D.; Dean, J.G.; Liu, T.; Li, D.; Watson, C.J.; Hudetz, A.G.; Mashour, G.A. Differential Role of Prefrontal and Parietal Cor-tices in Controlling Level of Consciousness. Curr. Biol. 2018, 28, 2145–2152.e5.
  7. Wang, T.X.; Xiong, B.; Xu, W.; Wei, H.H.; Qu, W.M.; Hong, Z.Y.; Huang, Z.L. Activation of Parabrachial Nucleus Glutamatergic Neurons Accelerates Reanimation from Sevoflurane Anesthesia in Mice. Anesthesiology 2019, 130, 106–118.
  8. Kelz, M.B.; Sun, Y.; Chen, J.; Cheng Meng, Q.; Moore, J.T.; Veasey, S.C.; Dixon, S.; Thornton, M.; Funato, H.; Yanagisawa, M. An essential role for orexins in emergence from general anesthesia. Proc. Natl. Acad. Sci. USA 2008, 105, 1309–1314.
  9. Jiang-Xie, L.F.; Yin, L.; Zhao, S.; Prevosto, V.; Han, B.X.; Dzirasa, K.; Wang, F. A Common Neuroendocrine Substrate for Diverse General Anesthetics and Slee. Neuron 2019, 102, 1053–1065.e4.
  10. Uschakov, A.; Gong, H.; McGinty, D.; Szymusiak, R. Efferent projections from the median preoptic nucleus to sleep- and arousal-regulatory nuclei in the rat brain. Neuroscience 2007, 150, 104–120.
  11. Chung, S.; Weber, F.; Zhong, P.; Tan, C.L.; Nguyen, T.N.; Beier, K.T.; Hörmann, N.; Chang, W.C.; Zhang, Z.; Do, J.P.; et al. Identification of preoptic sleep neurons using retrograde labelling and gene profiling. Nature 2017, 545, 477–481.
  12. Zhang, Y.; Yu, T.; Yuan, J.; Yu, B.W. The ventrolateral preoptic nucleus is required for propofol-induced inhibition of locus coeruleus neuronal activity. Neurol. Sci. 2015, 36, 2177–2184.
  13. Vanini, G.; Bassana, M.; Mast, M.; Mondino, A.; Cerda, I.; Phyle, M.; Chen, V.; Colmenero, A.V.; Hambrecht-Wiedbusch, V.S.; Mashour, G.A. Activation of Preoptic GABAergic or Glutamatergic Neurons Modulates Sleep-Wake Architecture, but Not Anesthetic State Transitions. Curr. Biol. 2020, 30, 779–787.e4.
  14. Wang, D.; Li, Y.; Feng, Q.; Guo, Q.; Zhou, J.; Luo, M. Learning shapes the aversion and reward responses of lateral habenula neurons. Elife 2017, 6, e23045.
  15. Oh, J.; Lee, C.; Kaang, B.K. Imaging and analysis of genetically encoded calcium indicators linking neural circuits and behaviors. Korean J. Physiol. Pharmacol. 2019, 23, 237–249.
  16. Gründemann, J.; Bitterman, Y.; Lu, T.; Krabbe, S.; Grewe, B.F.; Schnitzer, M.J.; Lüthi, A. Amygdala ensembles encode behavioral states. Science 2019, 364, eaav8736.
  17. Paredes, R.M.; Etzler, J.C.; Watts, L.T.; Zheng, W.; Lechleiter, J.D. Chemical calcium indicators. Methods 2008, 46, 143–151.
  18. Rose, T.; Goltstein, P.M.; Portugues, R.; Griesbeck, O. Putting a finishing touch on GECIs. Front. Mol. Neurosci. 2014, 7, 88.
  19. Yang, Y.; Liu, N.; He, Y.; Liu, Y.; Ge, L.; Zou, L.; Song, S.; Xiong, W.; Liu, X. Improved calcium sensor GCaMP-X overcomes the calcium channel perturbations induced by the calmodulin in GCaM. Nat. Commun. 2018, 9, 1504.
  20. Grienberger, C.; Konnerth, A. Imaging calcium in neurons. Neuron 2012, 73, 862–885.
  21. Inoue, M.; Takeuchi, A.; Horigane, S.I.; Ohkura, M.; Gengyo-Ando, K.; Fujii, H.; Kamijo, S.; Takemoto-Kimura, S.; Kano, M.; Nakai, J.; et al. Rational design of a high-affinity, fast, red calcium indicator R-CaMP2. Nat. Methods 2015, 12, 64–70.
  22. Huang, L.; Ledochowitsch, P.; Knoblich, U.; Lecoq, J.; Murphy, G.J.; Reid, R.C.; de Vries, S.E.; Koch, C.; Zeng, H.; Buice, M.A.; et al. Relationship between simultaneously recorded spiking activity and fluorescence signal in GCaMP6 transgenic mice. Elife 2021, 10, e51675.
  23. Kobayashi, S.; O’Hashi, K.; Kaneko, K.; Kobayashi, S.; Ogisawa, S.; Tonogi, M.; Fujita, S.; Kobayashi, M. A new phenotype identification method with the fluorescent expression in cross-sectioned tails in Thy1-GCaMP6s transgenic mice. J. Oral. Sci. 2022, 64, 156–160.
  24. Markowitz, J.E.; Gillis, W.F.; Beron, C.C.; Neufeld, S.Q.; Robertson, K.; Bhagat, N.D.; Peterson, R.E.; Peterson, E.; Hyun, M.; Linderman, S.W.; et al. The Striatum Organizes 3D Behavior via Moment-to-Moment Action Selection. Cell 2018, 174, 44–58.e17.
  25. Chen, T.W.; Wardill, T.J.; Sun, Y.; Pulver, S.R.; Renninger, S.L.; Baohan, A.; Schreiter, E.R.; Kerr, R.A.; Orger, M.B.; Jayaraman, V.; et al. Ultrasensitive fluorescent proteins for imaging neuronal activity. Nature 2013, 499, 295–300.
  26. Li, Y.; Zeng, J.; Zhang, J.; Yue, C.; Zhong, W.; Liu, Z.; Feng, Q.; Luo, M. Hypothalamic Circuits for Predation and Evasion. Neuron 2018, 97, 911–924.e5.
  27. Luo, L.; Callaway, E.M.; Svoboda, K. Genetic Dissection of Neural Circuits: A Decade of Progress. Neuron 2018, 98, 256–281.
  28. Guo, Q.; Zhou, J.; Feng, Q.; Lin, R.; Gong, H.; Luo, Q.; Zeng, S.; Luo, M.; Fu, L. Multi-channel fiber photometry for population neuronal activity recording. Biomed. Opt. Express 2015, 6, 3919–3931.
  29. Roukos, V.; Misteli, T. Deep Imaging: The next frontier in microscopy. Histochem Cell Biol. 2014, 142, 125–131.
  30. Shuman, T.; Aharoni, D.; Cai, D.J.; Lee, C.R.; Chavlis, S.; Page-Harley, L.; Vetere, L.M.; Feng, Y.; Yang, C.Y.; Mollinedo-Gajate, I.; et al. Breakdown of spatial coding and interneuron synchronization in epileptic mice. Nat. Neurosci. 2020, 23, 229–238.
  31. Zhang, L.; Liang, B.; Barbera, G.; Hawes, S.; Zhang, Y.; Stump, K.; Baum, I.; Yang, Y.; Li, Y.; Lin, D.T. Miniscope GRIN Lens System for Calcium Imaging of Neuronal Activity from Deep Brain Structures in Behaving Animals. Curr. Protoc. Neurosci. 2019, 86, e56.
  32. Kislin, M.; Sword, J.; Fomitcheva, I.V.; Croom, D.; Pryazhnikov, E.; Lihavainen, E.; Toptunov, D.; Rauvala, H.; Ribeiro, A.S.; Khiroug, L.; et al. Reversible Disruption of Neuronal Mitochondria by Ischemic and Traumatic Injury Revealed by Quantitative Two-Photon Imaging in the Neocortex of Anesthetized Mice. J. Neurosci. 2017, 37, 333–348.
  33. Yang, W.; Yuste, R. In vivo imaging of neural activity. Nat. Methods 2017, 14, 349–359.
  34. Duffet, L.; Kosar, S.; Panniello, M.; Viberti, B.; Bracey, E.; Zych, A.D.; Radoux-Mergault, A.; Zhou, X.; Dernic, J.; Ravotto, L.; et al. A genetically encoded sensor for in vivo imaging of orexin neuropeptides. Nat. Methods 2022, 19, 231–241.
  35. Zong, W.; Obenhaus, H.A.; Skytøen, E.R.; Eneqvist, H.; de Jong, N.L.; Vale, R.; Jorge, M.R.; Moser, M.B.; Moser, E.I. Large-scale two-photon calcium imaging in freely moving mice. Cell 2022, 185, 1240–1256.e30.
  36. Brown, R.; Lau, H.; LeDoux, J.E. Understanding the Higher-Order Approach to Consciousness. Trends Cogn. Sci. 2019, 23, 754–768.
  37. Mashour, G.A.; Roelfsema, P.; Changeux, J.P.; Dehaene, S. Conscious Processing and the Global Neuronal Workspace Hypothesis. Neuron 2020, 105, 776–798.
  38. Bharioke, A.; Munz, M.; Brignall, A.; Kosche, G.; Eizinger, M.F.; Ledergerber, N.; Hillier, D.; Gross-Scherf, B.; Conzelmann, K.K.; Macé, E.; et al. General anesthesia globally synchronizes activity selectively in layer 5 cortical pyramidal neurons. Neuron 2022, 110, 2024–2040.e10.
  39. Scammell, T.E.; Arrigoni, E.; Lipton, J.O. Neural circuitry of wakefulness and sleep. Neuron 2017, 93, 747–765.
  40. Gui, H.; Liu, C.; He, H.; Zhang, J.; Chen, H.; Zhang, Y. Dopaminergic Projections from the Ventral Tegmental Area to the Nucleus Accumbens Modulate Sevoflurane Anesthesia in Mice. Front. Cell Neurosci. 2021, 15, 671473.
  41. Ross, S.; Peselow, E. The neurobiology of addictive disorders. Clin. Neuropharmacol. 2009, 32, 269–276.
  42. Zhang, Y.; Gui, H.; Duan, Z.; Yu, T.; Zhang, J.; Liang, X.; Liu, C. Dopamine D1 Receptor in the Nucleus Accumbens Modulates the Emergence from Propofol Anesthesia in Rat. Neurochem Res. 2021, 46, 1435–1446.
  43. Liu, C.; Zhou, X.; Zhu, Q.; Fu, B.; Cao, S.; Zhang, Y.; Zhang, L.; Zhang, Y.; Yu, T. Dopamine neurons in the ventral periaqueductal gray modulate isoflurane anesthesia in rats. CNS Neurosci. Ther. 2020, 26, 1121–1133.
  44. Monti, J.M. Serotonin control of sleep-wake behavior. Sleep Med. Rev. 2011, 15, 269–281.
  45. Li, A.; Li, R.; Ouyang, P.; Li, H.; Wang, S.; Zhang, X.; Wang, D.; Ran, M.; Zhao, G.; Yang, Q.; et al. Dorsal raphe serotonergic neurons promote arousal from isoflurane anesthesia. CNS Neurosci. Ther. 2021, 27, 941–950.
  46. Du, W.J.; Zhang, R.W.; Li, J.; Zhang, B.B.; Peng, X.L.; Cao, S.; Yuan, J.; Yuan, C.D.; Yu, T.; Du, J.L. The Locus Coeruleus Modulates Intravenous General Anesthesia of Zebrafish via a Cooperative Mechanism. Cell Rep. 2018, 24, 3146–3155.e3.
  47. Xu, M.; Chung, S.; Zhang, S.; Zhong, P.; Ma, C.; Chang, W.C.; Weissbourd, B.; Sakai, N.; Luo, L.; Nishino, S.; et al. Basal forebrain circuit for sleep-wake control. Nat. Neurosci. 2015, 18, 1641–1647.
  48. Kim, T.; Thankachan, S.; McKenna, J.T.; McNally, J.M.; Yang, C.; Choi, J.H.; Chen, L.; Kocsis, B.; Deisseroth, K.; Strecker, R.E.; et al. Cortically projecting basal forebrain parvalbumin neurons regulate cortical gamma band oscillations. Proc. Natl. Acad. Sci. USA 2015, 112, 3535–3540.
  49. Luo, T.Y.; Cai, S.; Qin, Z.X.; Yang, S.C.; Shu, Y.; Liu, C.X.; Zhang, Y.; Zhang, L.; Zhou, L.; Yu, T.; et al. Basal Forebrain Cholinergic Activity Modulates Isoflurane and Propofol Anesthesia. Front. Neurosci. 2020, 14, 559077.
  50. Fuller, P.; Sherman, D.; Pedersen, N.P.; Saper, C.B.; Lu, J. Reassessment of the structural basis of the ascending arousal system. J. Comp. Neurol. 2011, 519, 933–956.
  51. Luo, T.; Yu, S.; Cai, S.; Zhang, Y.; Jiao, Y.; Yu, T.; Yu, W. Parabrachial Neurons Promote Behavior and Electroencephalographic Arousal from General Anesthesia. Front. Mol. Neurosci. 2018, 11, 420.
  52. Zhang, B.; Gao, Y.; Li, Y.; Yang, J.; Zhao, H. Sleep Deprivation Influences Circadian Gene Expression in the Lateral Habenula. Behav. Neurol. 2016, 2016, 7919534.
  53. Liu, C.; Liu, J.; Zhou, L.; He, H.; Zhang, Y.; Cai, S.; Yuan, C.; Luo, T.; Zheng, J.; Yu, T.; et al. Lateral Habenula Glutamatergic Neurons Modulate Isoflurane Anesthesia in Mice. Front. Mol. Neurosci. 2021, 14, 628996.
  54. Wang, D.; Guo, Q.; Zhou, Y.; Xu, Z.; Hu, S.W.; Kong, X.X.; Yu, Y.M.; Yang, J.X.; Zhang, H.; Ding, H.L.; et al. GABAergic Neurons in the Dorsal-Intermediate Lateral Septum Regulate Sleep-Wakefulness and Anesthesia in Mice. Anesthesiology 2021, 135, 463–481.
  55. Qiu, G.; Wu, Y.; Yang, Z.; Li, L.; Zhu, X.; Wang, Y.; Sun, W.; Dong, H.; Li, Y.; Hu, J. Dexmedetomidine Activation of Dopamine Neurons in the Ventral Tegmental Area Attenuates the Depth of Sedation in Mice. Anesthesiology 2020, 133, 377–392.
  56. Hua, T.; Chen, B.; Lu, D.; Sakurai, K.; Zhao, S.; Han, B.X.; Kim, J.; Yin, L.; Chen, Y.; Lu, J.; et al. General anesthetics activate a potent central pain-suppression circuit in the amygdala. Nat. Neurosci. 2020, 23, 854–868.
  57. Zhang, K.; Lian, N.; Ding, R.; Guo, C.; Dong, X.; Li, Y.; Wei, S.; Jiao, Q.; Yu, Y.; Shen, H. Sleep Deprivation Aggravates Cognitive Impairment by the Alteration of Hippocampal Neuronal Activity and the Density of Dendritic Spine in Isoflurane-Exposed Mice. Front. Behav. Neurosci. 2020, 14, 589176.
  58. Chen, K.; Hu, Q.; Gupta, R.; Stephens, J.; Xie, Z.; Yang, G. Inhibition of unfolded protein response prevents post-anesthesia neuronal hyperactivity and synapse loss in aged mice. Aging Cell 2022, 21, e13592.
  59. Marvin, J.S.; Scholl, B.; Wilson, D.E.; Podgorski, K.; Kazemipour, A.; Müller, J.A.; Schoch, S.; Quiroz, F.J.U.; Rebola, N.; Bao, H.; et al. Stability, affinity, and chromatic variants of the glutamate sensor iGluSnFR. Nat. Methods 2018, 15, 936–939.
  60. Peng, W.; Wu, Z.; Song, K.; Zhang, S.; Li, Y.; Xu, M. Regulation of sleep homeostasis mediator adenosine by basal forebrain glutamatergic neurons. Science 2020, 369, eabb0556.
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Subjects: Biology
Contributors MDPI registered users' name will be linked to their SciProfiles pages. To register with us, please refer to https://encyclopedia.pub/register :
Kai Zhang
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Jiacheng Pan
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Yonghao Yu
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Update Date: 15 Jul 2022
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