The cataleptic state induced by ketamine: a review of the neuropharmacology of anesthesia

Winters, Wendell D.; Ferrar-Allado, Theresa; Guzmán-Flores, C; Alcaraz, Manuel

doi:10.1016/0028-3908(72)90016-0

Cited by 151 publications

(31 citation statements)

References 11 publications

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“…When the present results are considered, it should be recalled that nitrous oxide alone only in duces stage 2 anaesthesia, a stage accompanied by signs of excitation and by cataleptoid behaviour (Winters et al , 1972). One cannot expect, therefore, the metabolic (or circulatory) effects of nitrous oxide to resemble those induced by general anaesthetics of the barbiturate type, or that any ef fects elicited should involve changes of a uniform type (cf.…”

Section: Discussionmentioning

confidence: 75%

Effect of Nitrous Oxide on Local Cerebral Glucose Utilization in Rats

Ingvar

Siesjö

1982

J Cereb Blood Flow Metab

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Summary: The influence of 70-80% N20 on local local cerebral glucose utili zation (CMRg1) in the rat brain was studied with the ['4C]deoxyglucose method in minimally restrained, spontaneously breathing animals 75 min following dis continuation of halothane anaesthesia. Nitrous oxide was found to have only small effects on local CMRgl in the majority of the 25 structures analyzed. When corrections were made for a small difference in body temperature between nitrous oxide-breathing animals and those breathing air, nitrous oxide was found to significantly increase local CMRg1 in some subcortical structures by 15-25% (red nucleus, thalamus, geniculate bodies, and superior colliculus), and to decrease local CMRg1 in nucleus accumbens and sensorimotor cortex by comparable amounts. Thus, although nitrous oxide does not alter overall glu cose utilization in the brain, it differentially affects CMRg1 in some brain struc tures.

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Section: Discussionmentioning

confidence: 75%

Effect of Nitrous Oxide on Local Cerebral Glucose Utilization in Rats

Ingvar

Siesjö

1982

J Cereb Blood Flow Metab

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“…Compared with other intravenous anaesthetic agents discussed above, the 'dissociative anaesthetic' ketamine has a very different in vivo and in vitro profile of action (table 2b). Ketamine and related arylcycloalkylamines such as phencyclidine produce an atypical state of 'dissociative' anaesthesia, characterized by sedation, immobility, amnesia, marked analgesia and a feeling of dissociation from the environment, without true unconsciousness [262]. These compounds can also produce intense hallucinations that limit their clinical use, especially in adults [2].…”

Section: Intravenous Agentsmentioning

confidence: 99%

General anaesthetic actions on ligand-gated ion channels

Krasowski

Harrison

1999

Cellular and Molecular Life Sciences (CMLS)

358

275

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The molecular mechanisms of general anaesthetics have remained largely obscure since their introduction into clinical practice just over 150 years ago. This review describes the actions of general anaesthetics on mammalian neurotransmitter-gated ion channels. As a result of research during the last several decades, ligand-gated ion channels have emerged as promising molecular targets for the central nervous system effects of general anaesthetics. The last 10 years have witnessed an explosion of studies of anaesthetic modulation of recombinant ligand-gated ion channels, including recent studies which utilize chimeric and mutated receptors to identify regions of ligand-gated ion channels important for the actions of general anaesthetics. Exciting future directions include structural biology and gene-targeting approaches to further the understanding of general anaesthetic molecular mechanisms.

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“…The electrophysiological consequences of systemic administration of ketamine are complex, with some regions showing inhibition and other regions exhibiting excitation that can progress to seizure-like activity. 47,63,64 By contrast, iontophoretic application of ketamine to neurons uniformly antagonizes NMDAevoked excitatory responses. [65][66][67][68] The well documented ability of ketamine to inhibit excitatory actions of NMDA at the cellular level, and induce excitatory responses after systemic administration, suggests that the excitatory effects of ketamine result from disruption of inhibitory neural circuits (ie from disinhibition).…”

Section: Neurobiological Consequences Of Nmda Antagonist Administrationmentioning

confidence: 99%

Mechanisms of typical and atypical antipsychotic drug action in relation to dopamine and NMDA receptor hypofunction hypotheses of schizophrenia

1999

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Available evidence indicates that clozapine is the most effective antipsychotic currently used for the pharmacotherapy of schizophrenia. Unfortunately, clozapine can cause serious side effects that limit the use of the drug. The therapeutic mechanism of action of clozapine is poorly understood, and accordingly, it has been difficult to design new drugs with the advantageous therapeutic properties of clozapine. Based on hypotheses that dopaminergic and serotonergic receptor-blocking properties of clozapine account for its clinical efficacy, several novel antipsychotic drugs have been introduced recently. There is currently insufficient data to reach definitive conclusions regarding the efficacy of the newer 'atypical' antipsychotics in comparison to clozapine. However, most published studies, and general clinical impressions, suggest that none of the newer drugs are as effective as clozapine in treating patients resistant to typical antipsychotic drug therapy. The present paper briefly reviews the clinical experience with the newer 'atypical' antipsychotic drugs and then discusses clinical and preclinical data potentially relevant to mechanisms of action of clozapine in relation to the NMDA receptor hypofunction hypothesis of schizophrenia.Keywords: clozapine; olanzapine; risperidone; ziprasidone; quetiapine; antipsychotic; schizophrenia; dopamine; NMDA The introduction of clozapine for the pharmacotherapy of schizophrenia represented a significant advance in the treatment of this devastating mental illness. Clozapine is superior to typical neuroleptic drugs (eg haloperidol) in treating positive and negative symptoms, and is effective in many patients who are refractory to typical antipsychotics. [1][2][3] In addition, clozapine does not induce the extrapyramidal side effects (EPS) commonly caused by the typical agents. Because of these properties, clozapine was termed atypical and represents the prototype drug of this class. Although clozapine is the most efficacious antipsychotic currently available, serious side effects induced by the drug, including agranulocytosis, impose substantial limitations on its use. Concerted research and development efforts have been made to produce an antipsychotic drug with the therapeutic advantages of clozapine, without the properties contributing to its serious side effects. However, the specific pharmacological characteristics of clozapine that confer its therapeutic properties are poorly understood. Clozapine binds to a diverse number of neurotransmitter receptors (see Table 1) but it is unclear whether actions at specific serotonin, dopamine, or adrenergic receptors, alone or in combination, account for its clinical efficacy.A number of specific hypotheses concerning mechanisms of action of clozapine have directed drug discovery efforts and led to clinical trials of drugs with widely different receptor-binding characteristics. The clinical experience with drugs whose development was inspired by clozapine will be briefly reviewed and then actions of clozapine and other antip...

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The cataleptic state induced by ketamine: a review of the neuropharmacology of anesthesia

Cited by 151 publications

References 11 publications

Effect of Nitrous Oxide on Local Cerebral Glucose Utilization in Rats

Effect of Nitrous Oxide on Local Cerebral Glucose Utilization in Rats

General anaesthetic actions on ligand-gated ion channels

Mechanisms of typical and atypical antipsychotic drug action in relation to dopamine and NMDA receptor hypofunction hypotheses of schizophrenia

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