Anesthesia and analgesia
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Anesthesia and analgesia · Nov 2011
The toxic effects of s(+)-ketamine on differentiating neurons in vitro as a consequence of suppressed neuronal Ca2+ oscillations.
In the immature brain, neuronal Ca2+ oscillations are present during a time period of high plasticity and regulate neuronal differentiation and synaptogenesis. In this study we examined the long-term blockade of hippocampal Ca2+ oscillations, the role of the N-methyl-D-aspartate (NMDA) receptors and the effects of S(+)-ketamine on neuronal synapsin expression. ⋯ Neuronal Ca2+ oscillations mediate neuronal differentiation and synaptogenesis via activating CaMKII. By acting via the NMDA receptor, S(+)-ketamine exerts its toxic effect through the suppression of neuronal Ca2+ oscillations, down-regulation of the CaMKII, and consecutively reduced synaptic integrity.
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Anesthesia and analgesia · Nov 2011
Case ReportsCase report: Anti-N-methyl-D-aspartate receptor encephalitis and its anesthetic implications.
We describe the anesthetic management and implications of 2 patients with anti-N-methyl-D-aspartate (NMDA) receptor encephalitis. Anti-NMDA receptor encephalitis is a neurological disorder caused by production of antibodies to the NMDA receptor. ⋯ It is important to understand the pharmacologic interactions these anesthetics have with a disabled NMDA receptor while preparing an anesthetic plan for patients with anti-NMDA receptor encephalitis. Symptoms of the disease such as psychosis, paroxysmal sympathetic hyperactivity, and central hypoventilation pose risks to the induction and maintenance of anesthesia in these patients.
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Anesthesia and analgesia · Nov 2011
GABAergic excitotoxicity injury of the immature hippocampal pyramidal neurons' exposure to isoflurane.
Certain anesthetics exhibit neurotoxicity in the brains of immature but not mature animals. γ-Aminobutyric acid (GABA), the primary inhibitory neurotransmitter in the adult brain, is excitatory on immature neurons via its action at the GABAA receptor, depolarizing the membrane potential and inducing a cytosolic Ca2+ increase ([Ca2+]i), because of a reversed transmembrane chloride gradient. Recent experimental data from several rodent studies have demonstrated that exposure to isoflurane during an initial phase causes neuronal excitotoxicity and apoptosis. GABAA receptor-mediated synaptic voltage-dependent calcium channels' (VDCCs) overactivation and Ca2+ influx are involved in these neural changes. ⋯ Isoflurane-mediated enhancement of GABA-triggered [Ca2+]i release results from membrane depolarization with subsequent activation of VDCCs and further Ca2+-induced Ca2+ release from the ryanodine-sensitizing Ca2+ store. An increase in [Ca2+]i, caused by activation of the GABAA receptor and opening of VDCCs, is necessary for isoflurane-induced calcium overload of immature rat hippocampal neurons, which may be involved in the mechanism of an isoflurane-induced neurotoxic effect in the developing rodent brain.