Extracellular amino acid levels in hippocampus during pilocarpine-induced seizures

Millan, M.H.; Chapman, A. Chaston; Meldrum, Brian S.

doi:10.1016/0920-1211(93)90018-3

Cited by 108 publications

(53 citation statements)

References 34 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Microdialysis studies in humans (During and Spencer, 1993;Wilson et al, 1996) and animals (Smolders et al, 1997;Ueda et al, 2002) have shown significant elevations in extracellular glutamate during SE. On the other hand, there are also many microdialysis studies that failed to show increases in extracellular glutamate during SE (Bruhn et al, 1992;Millan et al, 1993). However it is well established that prolonged exposure to glutamate can kill neurons (Choi et al, 1987;Limbrick et al, 2003) and it has been suggested that increased glutamate in the extracellular space may account for neuronal death associated with SE (Delorenzo et al, 2005;Fountain and Lothman, 1995;Fujikawa, 2005;Wasterlain et al, 1993).…”

Section: Discussionmentioning

confidence: 99%

In vitro status epilepticus but not spontaneous recurrent seizures cause cell death in cultured hippocampal neurons

et al. 2007

View full text Add to dashboard Cite

SummaryIt is established that the majority but not all of the seizure-induced cell death is associated with status epilepticus while spontaneous recurrent seizures associated with epilepsy do not cause neuronal death. Extracellular effects and compensatory changes in brain physiology complicate assessment of neuronal death in vivo as the result of seizures. In this study we utilized a well-characterized in vitro hippocampal neuronal culture model of both continuous high-frequency epileptiform discharges (status epilepticus) and spontaneous recurrent epileptiform discharges (acquired epilepsy) to investigate the direct effects of continuous and episodic electrographic epileptiform discharges on cell death in a carefully controlled extracellular environment. The results from this study indicate that continuous high-frequency epileptiform discharges can cause neuronal death in a time-dependent manner. Episodic epileptiform seizure activity occurring for the life of the neurons in culture was not associated with increased neuronal cell death. Our data confirm observations from clinical and some animal studies that spontaneous recurrent seizures do not initiate cell death. The hippocampal neuronal culture model provides a powerful in vitro tool for carefully evaluating the effects of seizure activity alone on neuronal viability in the absence of various confounding factors and may provide new insights into the development of novel therapeutic agents to prevent neuronal injury during status epilepticus.

show abstract

Section: Discussionmentioning

confidence: 99%

In vitro status epilepticus but not spontaneous recurrent seizures cause cell death in cultured hippocampal neurons

et al. 2007

View full text Add to dashboard Cite

show abstract

“…4,5) Furthermore, a significant increase in glutamate levels has been observed in human epilepsy patients as well as in experimental models of epilepsy. [6][7][8][9][10] Excessive glutamate release and activation of the glutamate receptors induces an increase in intracellular Ca 2+ levels, subsequently triggering a cascade of cellular responses, including nitric oxide synthase (NOS) activation, enhanced oxygen free-radical production, and disturbed mitochondrial function, which ultimately causes inflammatory responses and neuronal cell death. [11][12][13][14] Thus, influencing central glutamatergic neurotransmission may provide a potential target for epilepsy treatment.…”

mentioning

confidence: 99%

Protective Effects of Bupivacaine against Kainic Acid-Induced Seizure and Neuronal Cell Death in the Rat Hippocampus

Chiu

Wang

et al. 2015

Biological & Pharmaceutical Bulletin

View full text Add to dashboard Cite

The excessive release of glutamate is a critical element in the neuropathology of epilepsy, and bupivacaine, a local anesthetic agent, has been shown to inhibit the release of glutamate in rat cerebrocortical nerve terminals. This study investigated whether bupivacaine produces antiseizure and antiexcitotoxic effects using a kainic acid (KA) rat model, an animal model used for temporal lobe epilepsy, and excitotoxic neurodegeneration experiments. The results showed that administering bupivacaine (0.4 mg/kg or 2 mg/kg) intraperitoneally to rats 30 min before intraperitoneal injection of KA (15 mg/kg) increased seizure latency and reduced the seizure score. In addition, bupivacaine attenuated KA-induced hippocampal neuronal cell death, and this protective effect was accompanied by the inhibition of microglial activation and production of proinflammatory cytokines such as interleukin (IL)-1β, IL-6, and tumor necrosis factor-α in the hippocampus. Moreover, bupivacaine shortened the latency of escaping onto the platform in the Morris water maze learning performance test. Collectively, these data suggest that bupivacaine has therapeutic potential for treating epilepsy.

show abstract

“…Furthermore, in Shetland dogs with familial idiopathic epilepsy, an increased value for glutamate and aspartate was found in the CSF (Morita et al, 2002). Large and rapid increases of extracellular glutamate and aspartate were also observed after injection of pilocarpine (Millan et al, 1993). The reduction of the extracellular aspartate and glutamate concentrations in the central nervous system is primarily achieved by excitatory amino acid transporters (EAATs) (for review see Amara and Fontana, 2002).…”

Section: Discussionmentioning

confidence: 99%

Amino acid composition of brain cysts: levels of excitatory amino acids in cyst fluid fail to predict seizures

Wieser¹,

Rudolph²,

Blau³

et al. 2003

Epilepsy Research

View full text Add to dashboard Cite

Extracellular amino acid levels in hippocampus during pilocarpine-induced seizures

Cited by 108 publications

References 34 publications

In vitro status epilepticus but not spontaneous recurrent seizures cause cell death in cultured hippocampal neurons

In vitro status epilepticus but not spontaneous recurrent seizures cause cell death in cultured hippocampal neurons

Protective Effects of Bupivacaine against Kainic Acid-Induced Seizure and Neuronal Cell Death in the Rat Hippocampus

Amino acid composition of brain cysts: levels of excitatory amino acids in cyst fluid fail to predict seizures

Contact Info

Product

Resources

About