A single pretreatment with MK-801 or cocaine enhances their locomotor stimulant effects in rats

O’Neill, Michael F.; Sanger, Graham J

doi:10.1016/s0006-8993(99)01580-2

Cited by 11 publications

(7 citation statements)

References 29 publications

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“…Low doses of NMDA antagonists produce hyperlocomotion in rats. High doses of NMDA antagonists induce stereotypies and repetitive nonfunctional behaviors in rats which are still apparent hours after application (O'Neill and Sanger, 1999). Furthermore, subchronic application of NMDA-antagonists to rats elicits negative symptoms of psychosis produced by an enduring hypoglutaminergic state (Olney and Farber, 1995).…”

Section: Discussionmentioning

confidence: 99%

A single application of MK801 causes symptoms of acute psychosis, deficits in spatial memory, and impairment of synaptic plasticity in rats

et al. 2007

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Schizophrenia is mostly a progressive psychiatric illness. Although cognitive changes in chronic schizophrenia have been investigated, little is known about the consequences of a single psychotic episode on memory mechanisms and formation. We investigated changes in hippocampal long-term potentiation (LTP) and spatial memory in a rat model of an acute psychotic episode. Application of NMDA receptor antagonists, such as MK801 (dizolcilpine) in rats, have been shown to give rise to an acute and short-lasting behavioral state, which mirrors many symptoms of schizophrenia. Furthermore, NMDA antagonist-intake in humans elicits symptoms of schizophrenia such as hallucinations, delusions, and affective blunting. We therefore treated animals with a single systemic injection of MK801 (5 mg/kg). Increased stereotypy, locomotion, and ataxia were evident immediately after MK801-treatment, with effects disappearing within 24 h. MK801-treatment caused a disruption of prepulse inhibition of the acoustic startle reflex, 1 day but not 7 or 28 days after treatment. These effects were consistent with the occurrence of an acute psychotic episode. LTP was profoundly impaired in freely moving rats 7 days after MK801 application. Four weeks after treatment, a slight recovery of LTP was seen, however marked deficits in long-term spatial memory were evident. These data suggest that treatment with MK801 to generate an acute psychotic episode in rats, gives rise to grave disturbances in synaptic plasticity and is associated with lasting impairments with the ability to form spatial memory.

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Section: Discussionmentioning

confidence: 99%

A single application of MK801 causes symptoms of acute psychosis, deficits in spatial memory, and impairment of synaptic plasticity in rats

et al. 2007

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“…A similar effect of repeated cocaine treatment has been found in rats (Pan et al, 1991), but has not, to the best of our knowledge, been associated with degree of cocaine sensitization. Because sensitization to cocaine can be seen after even a single pretreatment (O'Neill and Sanger, 1999), changes in pharmacokinetics may not be of primary importance when considering whether sensitization develops or not. However, it could play a role in the increasing magnitude of sensitization seen with multiple drug exposures (Kalivas and Duffy, 1990;Roy et al, 1978).…”

Section: Discussionmentioning

confidence: 99%

Cross‐Sensitization Between the Locomotor Stimulant Effects of Ethanol and Those of Morphine and Cocaine in Mice

Lessov

Phillips

2003

Alcoholism Clin & Exp Res

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“…Studies from our laboratory found that in rats, a single dose of ketamine (2.5 mg/kg) resulted in sustained antidepressant effects lasting approximately one week (Maeng et al, 2008). Another study found that a single pretreatment dose with the NMDA antagonist MK-801 induced a lasting sensitivity to the second administration of the same agent four, seven, or 14 days later (O’Neill and Sanger, 1999). Interestingly, antidepressant-like behavioral responses were observed in mice lacking interneuronal NMDA receptors, supporting the notion that NMDA antagonism is not the only mechanism involved in ketamine’s rapid antidepressant effects (Pozzi et al, 2014).…”

Section: Ampa and Nmda Receptors: Specific Findings In Mood Disordmentioning

confidence: 99%

New targets for rapid antidepressant action

Machado‐Vieira

Henter

Zarate

2017

Progress in Neurobiology

125

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Current therapeutic options for major depressive disorder (MDD) and bipolar disorder (BD) are associated with a lag of onset that can prolong distress and impairment for patients, and their antidepressant efficacy is often limited. All currently approved antidepressant medications for MDD act primarily through monoaminergic mechanisms. Glutamate is the major excitatory neurotransmitter in the central nervous system, and glutamate and its cognate receptors are implicated in the pathophysiology of MDD, and in the development of novel therapeutics for this disorder. The rapid and robust antidepressant effects of the N-methyl-D-aspartate (NMDA) antagonist ketamine were first observed in 2000. Since then, other NMDA receptor antagonists have been studied in MDD. Most have demonstrated relatively modest antidepressant effects compared to ketamine, but some have shown more favorable characteristics. This article reviews the clinical evidence supporting the use of novel glutamate receptor modulators with direct affinity for cognate receptors: 1) non-competitive NMDA receptor antagonists (ketamine, memantine, dextromethorphan, AZD6765); 2) subunit (GluN2B)-specific NMDA receptor antagonists (CP-101,606/traxoprodil, MK-0657); 3) NMDA receptor glycine-site partial agonists (GLYX-13); and 4) metabotropic glutamate receptor (mGluR) modulators (AZD2066, RO4917523/basimglurant). We also briefly discuss several other theoretical glutamate receptor targets with preclinical antidepressant-like efficacy that have yet to be studied clinically; these include α-amino-3-hydroxyl-5-methyl-4-isoxazoleproprionic acid (AMPA) agonists and mGluR2/3 negative allosteric modulators. The review also discusses other promising, non-glutamatergic targets for potential rapid antidepressant effects, including the cholinergic system (scopolamine), the opioid system (ALKS-5461), corticotropin releasing factor (CRF) receptor antagonists (CP-316,311), and others.

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A single pretreatment with MK-801 or cocaine enhances their locomotor stimulant effects in rats

Cited by 11 publications

References 29 publications

A single application of MK801 causes symptoms of acute psychosis, deficits in spatial memory, and impairment of synaptic plasticity in rats

A single application of MK801 causes symptoms of acute psychosis, deficits in spatial memory, and impairment of synaptic plasticity in rats

Cross‐Sensitization Between the Locomotor Stimulant Effects of Ethanol and Those of Morphine and Cocaine in Mice

New targets for rapid antidepressant action

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