Normal Spatial Memory Following Postseizure Treatment with Ketamine: Selective Damage Attenuates Memory Deficits in Brain-Damaged Rodents

Santi, S. A.; Cook, Lisa L.; Persinger, Michael A.; O'Connor, Rodney P.

doi:10.3109/00207450109149757

Cited by 22 publications

(7 citation statements)

References 21 publications

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“…In the present study we investigated the effects of status epilepticus induced by the administration of lithium and pilocarpine to adult rats on phosphorylation of the NMDA receptor. Although the initiation of seizure activity in this model involves the activation of muscarinic cholinergic receptors, NMDA receptors are subsequently activated and have been implicated in SE‐induced neuronal cell death (Fujikawa 1995; Rice and DeLorenzo 1998), epileptogenesis (Rice and DeLorenzo 1998) and learning impairment (Santi et al . 2001; Stewart and Persinger 2001).…”

Section: Discussionmentioning

confidence: 99%

Changes in phosphorylation of the NMDA receptor in the rat hippocampus induced by status epilepticus

Niimura

Moussa

Bissoon

et al. 2005

Journal of Neurochemistry

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Systemic administration of pilocarpine preceded by lithium induces status epilepticus (SE) that results in neurodegeneration and may lead to the development of spontaneous recurrent seizures. We investigated the effect of Li/pilocarpine-induced SE on phosphorylation of the NMDA receptor in rat hippocampus. Phosphorylation of NR1 by PKC on Ser890 was decreased to 45% of control values immediately following 1 h of SE. During the first 3 h following the termination of SE, phosphorylation of Ser890 increased 4-fold before declining to control values by 24 h. Phosphorylation of NR1 by PKA was also depressed relative to controls immediately following SE and transiently increased above control values upon the termination of SE. SE was accompanied by a general increase in tyrosine phosphorylation of hippocampal proteins that lasted for several hours following the termination of seizures. Tyrosine phosphorylation of the NR2A and NR2B subunits of the NMDAR increased 3-4-fold over control values during SE, continued to increase during the first hour following SE and then declined to control levels by 24 h. SE resulted in the activation of Src and Pyk2 associated with the postsynaptic apparatus, suggesting a role for these enzymes in the SEinduced increase in tyrosine phosphorylation. Changes in phosphorylation of the NMDA receptor may play a role in the pathophysiological consequences of SE.

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Section: Discussionmentioning

confidence: 99%

Changes in phosphorylation of the NMDA receptor in the rat hippocampus induced by status epilepticus

Niimura

Moussa

Bissoon

et al. 2005

Journal of Neurochemistry

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“…However, even in these conditions, ketamine may still offer some functional benefits . In an experimental model of SE in rats (lithium–pilocarpine), functional improvements linked to the administration of ketamine have recently been reported: when administered quickly in the first half‐an‐hour, it could very efficiently spare cognition despite the fact that brain damage was still histologically evidenced especially within the entorhinal cortices and amygdalohippocampal area .…”

Section: Ketamine An Effective Treatment Of Seizures: Experimental Ementioning

confidence: 99%

“…Animal species ments linked to the administration of ketamine have recently been reported: when administered quickly in the first half-anhour, it could very efficiently spare cognition despite the fact that brain damage was still histologically evidenced especially within the entorhinal cortices and amygdalohippocampal area [129][130][131][132].…”

Section: Modelmentioning

confidence: 99%

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Treatment of Status Epilepticus with Ketamine, Are we There yet?

et al. 2013

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Status epilepticus (SE), a neurological emergency both in adults and in children, could lead to brain damage and even death if untreated. Generalized convulsive SE (GCSE) is the most common and severe form, an example of which is that induced by organophosphorus nerve agents. First- and second-line pharmacotherapies are relatively consensual, but if seizures are still not controlled, there is currently no definitive data to guide the optimal choice of therapy. The medical community seems largely reluctant to use ketamine, a noncompetitive antagonist of the N-methyl-d-aspartate glutamate receptor. However, a review of the literature clearly shows that ketamine possesses, in preclinical studies, antiepileptic properties and provides neuroprotection. Clinical evidences are scarcer and more difficult to analyze, owing to a use in situations of polytherapy. In absence of existing or planned randomized clinical trials, the medical community should make up its mind from well-conducted preclinical studies performed on appropriate models. Although potentially active, ketamine has no real place for the treatment of isolated seizures, better accepted drugs being used. Its best usage should be during GCSE, but not waiting for SE to become totally refractory. Concerns about possible developmental neurotoxicity might limit its pediatric use for refractory SE.

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“…Ketamine is a noncompetitive NMDA antagonist that can serve both neuroprotective and anticonvulsant roles. 57 Animal models have suggested a benefit in RSE 58 ; however, the effect of ketamine may be time dependent, with this agent becoming more effective after 60 minutes of seizure activity. 59 Clinical experience is limited to a few case reports.…”

Section: Refractory Status Epilepticusmentioning

confidence: 99%

Status Epilepticus

Manno

2011

The Neurohospitalist

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Status epilepticus is a neurological emergency that is commonly encountered by the neurohospitalist. Successful treatment depends upon the recognition of prolonged seizure activity and the acute mobilization of available resources. Pharmacologic treatment regimens have been shown to decrease the time needed for successful control of seizures and have provided for the rapid administration of anticonvulsant medications. Treatment strategies have evolved so that clinicians can administer effective doses of medication by whatever routes of administration are immediately available. Traditional algorithms for the treatment of status epilepticus have used a stepwise approach to the administration of first-, second-, and third-order medications. More recent options have included aggressive anesthetic doses of medications while second-line medications are being titrated.

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Normal Spatial Memory Following Postseizure Treatment with Ketamine: Selective Damage Attenuates Memory Deficits in Brain-Damaged Rodents

Cited by 22 publications

References 21 publications

Changes in phosphorylation of the NMDA receptor in the rat hippocampus induced by status epilepticus

Changes in phosphorylation of the NMDA receptor in the rat hippocampus induced by status epilepticus

Treatment of Status Epilepticus with Ketamine, Are we There yet?

Status Epilepticus

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