Effects of phencyclidine on excitatory amino acid activation of spinal interneurones in the cat

Lodge, David; Anis, Nabil A.

doi:10.1016/0014-2999(82)90022-x

Cited by 149 publications

(73 citation statements)

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“…An important element of several of these theoretical positions is that NMDA receptor hypofunction (NRH) produced by any mechanism can be psychotogenic. This has renewed interest in the clinical effects of NMDA glutamate receptor antagonists.Ketamine and phencyclidine (PCP) are non-competitive NMDA glutamate receptor antagonists (Zukin and Zukin 1979;Vincent et al 1979;Lodge and Anis 1982;Lodge et al 1987) which can produce a transient state of NRH in the brain. Early investigators characterized a PCP-induced clinical syndrome of schizophrenia-like Received March 18, 1998; revised June 19, 1998; accepted June 29, 1998.…”

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confidence: 99%

“…Ketamine and phencyclidine (PCP) are non-competitive NMDA glutamate receptor antagonists (Zukin and Zukin 1979;Vincent et al 1979;Lodge and Anis 1982;Lodge et al 1987) which can produce a transient state of NRH in the brain. Early investigators characterized a PCP-induced clinical syndrome of schizophrenia-like symptoms, including hallucinations, delusions, idiosyncratic and illogical thinking, poverty of speech and thought, agitation, disturbances of emotion, affect, withdrawal, decreased motivation, and dissociation (Johnstone et al 1959;Luby et al 1959;Rosenbaum et al 1959;Luby et al 1962;Corssen and Domino 1966;Bakker and Amini 1961;Davies and Beech 1960;Domino and Luby 1981).…”

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Ketamine-Induced NMDA Receptor Hypofunction as a Model of Memory Impairment and Psychosis

Newcomer

Farber

Jevtović-Todorović

et al. 1999

Neuropsychopharmacology

541

350

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Considerable research interest has recently been focused on the role of glutamate and related neural circuitry in the neurobiology of schizophrenia. The results of these investigations have emphasized hypofunction of glutamatergic neurons and/or the N-methyl-D-aspartate (NMDA) glutamate receptor (Tsai et al. 1995;Kim et al. 1980aKim et al. , 1980bSherman et al. 1991;Deutsch et al. 1989;Javitt and Zukin 1991;Olney 1988a;Olney 1988b;Olney and Farber 1995). An important element of several of these theoretical positions is that NMDA receptor hypofunction (NRH) produced by any mechanism can be psychotogenic. This has renewed interest in the clinical effects of NMDA glutamate receptor antagonists.Ketamine and phencyclidine (PCP) are non-competitive NMDA glutamate receptor antagonists (Zukin and Zukin 1979;Vincent et al. 1979;Lodge and Anis 1982;Lodge et al. 1987) which can produce a transient state of NRH in the brain. Early investigators characterized a PCP-induced clinical syndrome of schizophrenia-like Received March 18, 1998; revised June 19, 1998; accepted June 29, 1998. N EUROPSYCHOPHARMACOLOGY 1999 -VOL . 20 , NO . 2 NMDA Receptor Hypofunction Induced Memory Decrease 107 symptoms, including hallucinations, delusions, idiosyncratic and illogical thinking, poverty of speech and thought, agitation, disturbances of emotion, affect, withdrawal, decreased motivation, and dissociation (Johnstone et al. 1959;Luby et al. 1959;Rosenbaum et al. 1959;Luby et al. 1962;Corssen and Domino 1966;Bakker and Amini 1961;Davies and Beech 1960;Domino and Luby 1981). This PCP-induced syndrome can be indistinguishable from acute presentations of schizophrenia (Yesavage and Freeman 1978;Erard et al. 1980). Ketamine, a PCP analog still used in human anesthesia, has been reported to cause reactions similar to but not as severe as those caused by PCP, including brief, reversible "positive" and "negative" schizophrenia-like symptoms (Krystal et al. 1994;Malhotra et al. 1996). Both PCP and ketamine can exacerbate psychosis in schizophrenia Luby et al. 1962;Lahti et al. 1995a;Lahti et al. 1995b;Malhotra et al. 1997).Declarative, explicit or secondary memory and learning deficits in patients with schizophrenia occur early in the course of the illness and are quantitatively large compared with deficits in other differentiated elements of cognitive performance, showing stability "on" versus "off" antipsychotic medication and over repeated testing (Gruzelier et al. 1988;Saykin et al. 1991Saykin et al. , 1994Cannon et al. 1994). Clinical and preclinical investigations suggest the hypothesis that changes in NMDA glutamate receptor activity in patients with schizophrenia may be causally related to memory impairments found in this disorder. Relevant to this hypothesis, the activation of post-synaptic NMDA receptors is important for the induction of the activity-dependent synaptic modification called long-term potentiation (LTP) (Bliss and Collingridge 1993;Collingridge and Bliss 1995), and hippocampal LTP has been postulated to underlie cert...

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Ketamine-Induced NMDA Receptor Hypofunction as a Model of Memory Impairment and Psychosis

Newcomer

Farber

Jevtović-Todorović

et al. 1999

Neuropsychopharmacology

541

350

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“…Non competitive NMDA antagonists include the disso ciative anaesthetics ketamine and phencyclidine (PCP) (Lodge and Anis, 1982), IT-opiates and mor phinans (such as dextrorphan) (Church et aI., 1985;Choi et aI., 1987), and the anticonvulsant MK801 (Sircar et aI., 1987;Wong et aI., 1988). These ap pear to have a common site of action related to the ion channel.…”

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Protection by NMDA Antagonists against Selective Cell Loss following Transient Ischaemia

Swan¹,

Meldrum²

1990

J Cereb Blood Flow Metab

159

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“…ketamine, nitrous oxide (N 2 O) and xenon. 9,10 Dexmedetomidine is the exception to these mechanisms. The drug is a potent α 2 -adrenergic receptor agonist that has eight times higher affinity for the α 2 -adrenergic receptor than clonidine.…”

Section: Mechanism Of Action Of Anaesthetics On the Brainmentioning

confidence: 99%

Anaesthesia and the developing brain

Prozesky

2014

Southern African Journal of Anaesthesia and Analgesia

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Increasing concern about the effect of anaesthesia on the infant and young child is being raised by healthcare practitioners, as well as the public. Immature neurons exposed to anaesthesia may lead to apoptosis and long-term neurobehavioural deficits in animals. The majority of anaesthetic agents work by influencing the gamma-aminobutyric acid or N-methyl-D-aspartate receptors and may induce animal neuroapoptosis. The search for neuroprotective strategies to reverse or counteract the effect of anaesthesia has not been very successful so far. Dexmedetomidine is an α 2 -adrenergic receptor and may have neuroprotective effects. Available human studies have failed to prove any long-term neurobehavioural deficiencies caused by anaesthetic exposure. Large international prospective studies are currently underway that may change the practice of paediatric and obstetric anaesthesiologists in the future.

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Effects of phencyclidine on excitatory amino acid activation of spinal interneurones in the cat

Cited by 149 publications

References 1 publication

Ketamine-Induced NMDA Receptor Hypofunction as a Model of Memory Impairment and Psychosis

Ketamine-Induced NMDA Receptor Hypofunction as a Model of Memory Impairment and Psychosis

Protection by NMDA Antagonists against Selective Cell Loss following Transient Ischaemia

Anaesthesia and the developing brain

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