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Abstract
The neural mechanisms behind anesthetic-induced behavioral
changes such as loss of consciousness, amnesia, and analgesia,
are widely dispersed within the central nervous system CNS. For
example, blockade at the level of the spinal cord can provide
analgesia and immobility in response to noxious reflexes, but only
interventions within the brain can bring about amnesia and
hypnosis. (Kennedy, Norman. 2005)
In past decades research has been focused on molecular and
cellular targets and actions of general anesthesia. At these
microscopic levels, accumulating evidence suggests that general
anesthetics act on multiple neuronal membrane proteins that
function as ion channels and neurotransmitter receptors.
(Hemmings et al., 2005)
Much research has focused on ligand gated ion channels
(LGICs) as targets of general anesthetics. Since the 1980s,
gamma-amino-butyric acid type A (GABAA) chloride channels,
particularly, have emerged as promising molecular targets of
general anesthetics. GABAA receptors are known to regulate
anxiety, vigilance, memory, and muscle tension. GABAergic
neurons and interneurons are ubiquitously expressed throughout
the central nervous system CNS. (Tepper et al., 2004)
Many general anesthetics, intravenous as well as most of the
volatile anesthetics, have been shown to allosterically modulate
GABAA chloride channels, resulting in potentiation of inhibitory
synaptic transmission. GABAA receptors are therefore likely to
English Summary
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play an important role in the CNS depression associated with most
general anesthetics.