How has molecular pharmacology contributed to our understanding of the mechanism(s) of general anesthesia?

Little, H.J.

doi:10.1016/0163-7258(95)02030-6

Cited by 52 publications

(23 citation statements)

References 171 publications

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“…As with several volatile anesthetics [16], nitrogen at pressure of 3 MPa may cause its sedative action by modifying neurotransmission systems in the central nervous system, in particular the nigrostriatal dopaminergic pathway. Indeed, acute exposure to 3 MPa nitrogen disrupts excitatory glutamatergic input to dopaminergic neurons by affecting glutamate release into the SNc, without altering NMDA receptors [7].…”

Section: Introductionmentioning

confidence: 99%

Mechanism of Action of Nitrogen Pressure in Controlling Striatal Dopamine Level of Freely Moving Rats is Changed by Recurrent Exposures to Nitrogen Narcosis

et al. 2011

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In rats, a single exposure to 3 MPa nitrogen induces change in motor processes, a sedative action and a decrease in dopamine release in the striatum. These changes due to a narcotic effect of nitrogen have been attributed to a decrease in glutamatergic control and the facilitation of GABAergic neurotransmission involving NMDA and GABA(A) receptors, respectively. After repeated exposure to nitrogen narcosis, a second exposure to 3 MPa increased dopamine levels suggesting a change in the control of the dopaminergic pathway. We investigated the role of the nigral NMDA and GABA(A) receptors in changes in the striatal dopamine levels. Dopamine-sensitive electrodes were implanted into the striatum under general anesthesia, together with a guide-cannula for drug injections into the SNc. Dopamine level was monitored by in vivo voltammetry. The effects of NMDA/GABA(A) receptor agonists (NMDA/muscimol) and antagonists (AP7/gabazine) on dopamine levels were investigated. Rats were exposed to 3 MPa nitrogen before and after five daily exposures to 1 MPa. After these exposures to nitrogen narcosis, gabazine, NMDA and AP7 had no effect on the nitrogen-induced increase in dopamine levels. By contrast, muscimol strongly enhanced the increase in dopamine level induced by nitrogen. Our findings suggest that repeated nitrogen exposure disrupted NMDA receptor function and decreased GABAergic input by modifying GABA(A) receptor sensitivity. These findings demonstrated a change in the mechanism of action of nitrogen at pressure.

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Section: Introductionmentioning

confidence: 99%

Mechanism of Action of Nitrogen Pressure in Controlling Striatal Dopamine Level of Freely Moving Rats is Changed by Recurrent Exposures to Nitrogen Narcosis

et al. 2011

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“…For example, many anesthetics, such as halothane, enflurane, fentanyl, morphine, barbital, and propofol, inhibit carotid body excitation [85]. These anesthetic agents are known to influence various ion channels [85][86][87][88]. It is most likely that anesthetics also affect ion channels in the glomus cell and in the chemoreceptor afferent nerve endings.…”

Section: Anesthetic Agentsmentioning

confidence: 99%

“…I have give the following examples: vecuronium inhibits carotid body excitation by blocking nAChRs in the carotid body; continuous infusion of dopamine inhibits carotid body excitation possibly by acting on D2 receptors in the carotid body; and benzodiazepines inhibit carotid body excitation by activating GABA A receptors in the carotid body. In clinical settings, these agents are usually used with other anesthetics that have various effects on ion channels and other neurotransmitter receptors [85][86][87][88]92,93]. It is known that halothane, enflurane, fentanyl, morphine, barbital, and propofol inhibit carotid body excitation [85].…”

Section: Summary and Clinical Implicationsmentioning

confidence: 99%

Neurotransmission in the carotid body and anesthesia

Shirahata

2002

Journal of Anesthesia

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“…Little 61 explica que a ação das sinapses inibitórias pode ser aumentada ou diminuída pelos anestésicos.…”

Section: Duldqd *Reer %Ud] 3hor Frqvwdqwh Dsrlr Dx[tolr Lqfhqwlyr 3runclassified

“…Exemplificando, os barbituratos e alguns anestésicos voláteis aumentam a ação dessas sinapses 61 . Entretanto, não é possível identificar um local-alvo crítico no cérebro que seja responsável por todos os fenômenos da anestesia, já que, quando em altas concentrações, os anestésicos afetam todas as funções cerebrais, desde o controle motor até a regulação da respiração 60 .…”

Section: Duldqd *Reer %Ud] 3hor Frqvwdqwh Dsrlr Dx[tolr Lqfhqwlyr 3runclassified

Perfil de citocinas inflamatórias em indivíduos submetidos a procedimentos cirúrgicos utilizando propofol ou isoflurano

Mazoti¹

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How has molecular pharmacology contributed to our understanding of the mechanism(s) of general anesthesia?

Cited by 52 publications

References 171 publications

Mechanism of Action of Nitrogen Pressure in Controlling Striatal Dopamine Level of Freely Moving Rats is Changed by Recurrent Exposures to Nitrogen Narcosis

Mechanism of Action of Nitrogen Pressure in Controlling Striatal Dopamine Level of Freely Moving Rats is Changed by Recurrent Exposures to Nitrogen Narcosis

Neurotransmission in the carotid body and anesthesia

Perfil de citocinas inflamatórias em indivíduos submetidos a procedimentos cirúrgicos utilizando propofol ou isoflurano

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