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Molecular mechanisms of general anesthesia.

Son Y - Korean J Anesthesiol (2010)

Bottom Line: General anesthetics produce a widespread neurodepression in the central nervous system by enhancing inhibitory neurotransmission and reducing excitatory neurotransmission.The gamma-aminobutyric acid type A (GABA(A)) receptors are leading candidates as a primary target of general anesthetics.This review summarizes current knowledge on how anesthetics modify GABA(A) receptor function.

View Article: PubMed Central - PubMed

Affiliation: Department of Anesthesiology and Pain Medicine, Wonkwang University School of Medicine, Iksan, Korea.

ABSTRACT
General anesthetics produce a widespread neurodepression in the central nervous system by enhancing inhibitory neurotransmission and reducing excitatory neurotransmission. However, the action mechanisms of general anesthetics are not completely understood. Moreover, the general anesthetic state comprises multiple components (amnesia, unconsciousness, analgesia, and immobility), each of which is mediated by different receptors and neuronal pathways. Recently, neurotransmitter- and voltage-gated ion channels have emerged as the most likely molecular targets for general anesthetics. The gamma-aminobutyric acid type A (GABA(A)) receptors are leading candidates as a primary target of general anesthetics. This review summarizes current knowledge on how anesthetics modify GABA(A) receptor function.

No MeSH data available.


Related in: MedlinePlus

Synaptic and extrasynaptic activation of γ-aminobutyric acid subtype A (GABAA) receptors. Action potential dependent release of GABA into the synaptic cleft transiently activates GABAA receptors in the postsynaptic membrane. This generates inhibitory postsynaptic currents (IPSCs). Extrasynaptic GABAA receptors are activated by low concentrations of GABA in the extracellular space. These receptors have low desensitization rates and can produce a tonic current (continuous current). The tonic current is revealed by application of a GABAA antagonist, Bicuculline, which inhibits the current. Many general anesthetics enhance the tonic current at clinically relevant concentrations. ITonic represents the amplitude of the steady state current.
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Figure 1: Synaptic and extrasynaptic activation of γ-aminobutyric acid subtype A (GABAA) receptors. Action potential dependent release of GABA into the synaptic cleft transiently activates GABAA receptors in the postsynaptic membrane. This generates inhibitory postsynaptic currents (IPSCs). Extrasynaptic GABAA receptors are activated by low concentrations of GABA in the extracellular space. These receptors have low desensitization rates and can produce a tonic current (continuous current). The tonic current is revealed by application of a GABAA antagonist, Bicuculline, which inhibits the current. Many general anesthetics enhance the tonic current at clinically relevant concentrations. ITonic represents the amplitude of the steady state current.

Mentions: GABAA receptors clustered at postsynaptic terminals are activated by a near-saturating concentration of GABA. GABA transmits information to inhibitory synapse by generating the fast and transient inhibitory postsynaptic currents (IPSCs) (Fig. 1) [18]. For many years, enhancement of fast synaptic inhibition was widely thought to be the primary mechanism underlying the actions of many GABAergic drugs.


Molecular mechanisms of general anesthesia.

Son Y - Korean J Anesthesiol (2010)

Synaptic and extrasynaptic activation of γ-aminobutyric acid subtype A (GABAA) receptors. Action potential dependent release of GABA into the synaptic cleft transiently activates GABAA receptors in the postsynaptic membrane. This generates inhibitory postsynaptic currents (IPSCs). Extrasynaptic GABAA receptors are activated by low concentrations of GABA in the extracellular space. These receptors have low desensitization rates and can produce a tonic current (continuous current). The tonic current is revealed by application of a GABAA antagonist, Bicuculline, which inhibits the current. Many general anesthetics enhance the tonic current at clinically relevant concentrations. ITonic represents the amplitude of the steady state current.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC2908224&req=5

Figure 1: Synaptic and extrasynaptic activation of γ-aminobutyric acid subtype A (GABAA) receptors. Action potential dependent release of GABA into the synaptic cleft transiently activates GABAA receptors in the postsynaptic membrane. This generates inhibitory postsynaptic currents (IPSCs). Extrasynaptic GABAA receptors are activated by low concentrations of GABA in the extracellular space. These receptors have low desensitization rates and can produce a tonic current (continuous current). The tonic current is revealed by application of a GABAA antagonist, Bicuculline, which inhibits the current. Many general anesthetics enhance the tonic current at clinically relevant concentrations. ITonic represents the amplitude of the steady state current.
Mentions: GABAA receptors clustered at postsynaptic terminals are activated by a near-saturating concentration of GABA. GABA transmits information to inhibitory synapse by generating the fast and transient inhibitory postsynaptic currents (IPSCs) (Fig. 1) [18]. For many years, enhancement of fast synaptic inhibition was widely thought to be the primary mechanism underlying the actions of many GABAergic drugs.

Bottom Line: General anesthetics produce a widespread neurodepression in the central nervous system by enhancing inhibitory neurotransmission and reducing excitatory neurotransmission.The gamma-aminobutyric acid type A (GABA(A)) receptors are leading candidates as a primary target of general anesthetics.This review summarizes current knowledge on how anesthetics modify GABA(A) receptor function.

View Article: PubMed Central - PubMed

Affiliation: Department of Anesthesiology and Pain Medicine, Wonkwang University School of Medicine, Iksan, Korea.

ABSTRACT
General anesthetics produce a widespread neurodepression in the central nervous system by enhancing inhibitory neurotransmission and reducing excitatory neurotransmission. However, the action mechanisms of general anesthetics are not completely understood. Moreover, the general anesthetic state comprises multiple components (amnesia, unconsciousness, analgesia, and immobility), each of which is mediated by different receptors and neuronal pathways. Recently, neurotransmitter- and voltage-gated ion channels have emerged as the most likely molecular targets for general anesthetics. The gamma-aminobutyric acid type A (GABA(A)) receptors are leading candidates as a primary target of general anesthetics. This review summarizes current knowledge on how anesthetics modify GABA(A) receptor function.

No MeSH data available.


Related in: MedlinePlus