Journals / Experimed / 2020 / Cilt: 10 - Sayı: 3

Molecular Mechanism of General Anesthesia

Genel Anesteziklerin Moleküler Mekanizması

Journal
Experimed
Pages
140–143
Publication Date
2020-12-24
DOI
—
🏛️Bibliographic metadata and full text access for this article are provided via DergiPark.
DergiPark Record ↗
✨

AI Summary & Key Takeaways

AI Insight
⚡ TL;DR(Too Long; Didn't Read)

In this article, receptors responsible for anesthesia in CNS and their mechanism of action will be reviewed.

📌 3 Key Takeaways

🎯
Objective & Hypothesis:Despite the widespread changes induced by general anesthetic agents, their exact effect sites are not clearly defined in the central nervous system (CNS).
📊
Key Findings & Data:Protein base theory of anesthesia, which focuses on ion channels, took the place of lipid-based theory in the 1980’s.
💡
Conclusion & Impact:In this article, receptors responsible for anesthesia in CNS and their mechanism of action will be reviewed.
🔬Design:Review & Systematic Survey
📍Scope:Comprehensive Sample
⚙️Variables:Genel Anestezi · Moleküler Farmakoloji · Bilinç

Abstract

Despite the widespread changes induced by general anesthetic agents, their exact effect sites are not clearly defined in the central nervous system (CNS). Recent molecular studies have pointed out specific sites in CNS on which anesthetic drugs show their effects. Hypnosis, amnesia, sedation are mediated by different receptors, neurotransmitters and neuronal pathways in the CNS. Protein base theory of anesthesia, which focuses on ion channels, took the place of lipid-based theory in the 1980’s. There are two types of receptors, which are known to be responsible for the general anes-thetic action: neurotransmitter receptors and ion channels. Back-ground channels are also described as targets for anesthetic ac-tion. Enhancement and block of TWIK Related K+ channels (TREK), TWIK related arachidonic acid activated K+ channel (TRAAK), and TWIK related acid-sensitive K+ channels (TASK) channels have been reported at low concentrations of volatile anesthetic agents. Two-pore-domain potassium channels are protein complexes em-bedded in cell membranes. They selectively allow potassium ions to pass through the cellular membrane. These channels are also ca-pable of changing the membrane potential by means of neuronal excitability, neurotransmitters and hormone secretion. Of those channels, TASK-1 and TREK-1 are activated by volatile anesthetic agents. In this article, receptors responsible for anesthesia in CNS and their mechanism of action will be reviewed.

Özet

Genel anestezik ajanlar, nörotransmitterleri modüle ederek santral sinir sisteminde yaygın nöronal değişime neden olmaktadır. Yeni yapılan moleküler araştırmalarda anestezik ajanların etki ettiği spesifik alanlar üzerinde durulmaktadır. Hipnoz, amnezi, sedasyon santral sinir sisteminde farklı reseptör, nörotransmitter ve nöronal yolaklar aracılığıyla sağlanır. 1980'lerin başında yapılan çalışmalar sonrasında, iyon kanallarına odaklanan protein temelli anestezi te-orisi, lipid temelli anestezi teorisinin yerini almıştır. Protein temelli teoriye göre, genel anestezik etkiden sorumlu iki tip reseptör mev-cuttur; nörotransmitter reseptörler ve iyon kanalları. “Background” iyon kanalları da anestezik etki için yeni tanımlanmış hedef resep-törlerdir. İki porlu (two-pore-domain) potasyum kanallarından TWIK ilişkili K+ kanalı (TREK), TWIK ilişkili araşidonik asitle aktive K+kanalı (TRAAK), TWIK ilişkili asit duyarlı K+ kanalları (TASK) tipteki kanalların volatil ajanların düşük konsantrasyonunda güçlendiği ya da bloke olduğu bildirilmiştir. İki porlu potasyum kanalları, biyolo-jik membranlarda bulunan protein kompleksleridir. İki porlu potas-yum kanalları, potasyum iyonları için özeldir ve potasyumun hücre membranından geçmesine izin verirler. İki porlu potasyum kanal-ları, nöronal uyarılma, nörotransmitter ve hormon salınımı yoluyla, membran potansiyelindeki değişikliklerden de sorumludurlar. İki porlu potasyum kanalların TASK-1 ve TREK-1 alt tipleri volatil anes-tezik ajanlarla (örneğin, izofluran, kloroform, dietil eter) uyarılır. Bu makalede santral sinir sisteminde bulunan ve genel anesteziklerin etkisinden sorumlu reseptörler ve bunların etki mekanizmaları gözden geçirilecektir.

🔖

Cite This Article

KÖNER, Ö., TEMÜR, S., İŞBİR, T. (2020). Molecular Mechanism of General Anesthesia. Experimed, Cilt: 10 - Sayı: 3, 140–143. https://ajindex.com/articles/83703

📄 Full Text PDF Viewer

📄

PDF görüntüleyici hazırlanıyor...

References (1)

  1. Brown EN, Purdon PL, Van Dort CJ. General anesthesia and altered states of arousal: A systems. Annu Rev Neurosci 2011; 34: 601-28. [CrossRef ] 2. Bandeiras C, Serro AP, Luzyanin K, Fernandes A, Saramago B, An-esthetics interacting with lipid rafts. Eur J Pharm Sci 2013; 48: 153-65. [CrossRef ] 3. Weinrich M, Worcester DL. The actions of volatile anesthetics: a new perspective. Res Pap Acta Cryst 2018; 74: 1169-77. [CrossRef ] 4. Pavel MA, Petersen EN, Lerner RA, Hansen SB. Studies on the Mechanism of General Anesthesia. BioRxiv 2018. [CrossRef ] 5. Weinrich M, Worcester DL. Xenon and other volatile anesthetics change domain structure in model lipid raft membranes. J Phys Chem B 2013; 117: 16141-7. [CrossRef ] 6. Gray E, Karslake J, Machta BB, Veatch SL. Liquid general anesthet-ics lower critical temperatures in plasma membrane vesicles. Bio-phys J 2013; 105: 2751-9. [CrossRef ] 7. Papahadjopoulos D, Jacobson K, Poste G, Shepherd G. Effects of local anesthetics on membrane properties I changes in the fluidi-ty of phospholipid bilayers. Biochim Biophys Acta 1975; 394: 504-19. [CrossRef ] 8. Lee AG. Model for action of local anaesthetics. Nature 1976; 262: 545-8. [CrossRef ] 9. Vanderkooi JM, Landesberg R, Selick H, McDonald GG. Interaction of general anesthetics with phospholipid vesicles and biological membranes. Biochim. Biophys Acta 1977; 464: 1-18. [CrossRef ] 10. Snyder SH. Drug and neurotransmitter receptors in the brain. Sci-ence 1984; 6: 224: 22-32. [CrossRef ] 11. Keramidas A, Moorhouse AJ, Schofield PR, Barry PH. Ligand-gated ion channels: mechanisms underlying ion selectivity. Progress in Biophysics and Molecular Biology 2004; 86: 161-204. [CrossRef ] 12. Gilman AG. G proteins: Transducers of Receptor-Generated Sig-nals. Annual Review of Biochemistry 1987; 56: 615-49. [CrossRef ] 13. Bowery NG, Smart TG. GABA and glycine as neurotransmitters: a brief history. British Journal of Pharmacology 2006; 47: 109-19. [CrossRef ] 14. Rebechii MJ, Pentyala SN. Anesthetic actions on other targets: protein kinase C and guanine nucleotide binding proteins. Br Journal of Anaesthesia 2002; 89: 62-78. [CrossRef ] 15. Franks NP, Lieb WR. Molecular and cellular mechanisms of general anaesthesia. Nature 1994; 367: 607-14. [CrossRef ] 16. Mihic SJ, Ye Q, Wick MJ, Koltchine VV, Krasowski MD, Finn SE. Sites of alcohols and volatile anesthetic action on GABA (A) and glycine receptors. Nature 1997; 389; 385-9. [CrossRef ] 17. Zuo Z, De Vente J, John RA. Halothane and i