Effects of diazepam on extracellular brain neurotransmitters in pilocarpine-induced seizures in rats

Khan, Ghous M.; Smolders, Ilse Julia; Lindekens, Hilde; Manil, Jacqueline; Ebinger, Guy; Michotte, Yvette

doi:10.1016/s0014-2999(99)00209-5

Cited by 48 publications

(18 citation statements)

References 46 publications

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“…In vivo microdialysis results revealed that changes of [Glu] EXT and [GABA] EXT do not reflect synaptic activity by necessity, rather supported a regulatory role for astrocytes. There is evidence suggesting the contribution of altered [Glu] EXT and [GABA] EXT in pathomechanisms including ischemia [57][58] and epilepsy [59][60][61][62][63][64] as well as in sleep and waking [69][70]. These data clearly demonstrate that more attention has to be paid for the nonsynaptic communication through the extracellular space under physiological and pathological conditions.…”

Section: Discussionmentioning

confidence: 81%

“…Results from microdialysis studies monitoring [Glu] EXT and [GABA] EXT during epileptic seizures, however, did not substantiate the theory of unbalanced GABA/Glu ratio ( Table 1). [59][60][61][62][63][64]. Increased [Glu] EXT enhances [GABA] EXT via mGluRs localised to interneurons [5].…”

Section: Epileptic Seizuresmentioning

confidence: 99%

“…Thus, changes of [Glu] EXT depend on the method applied for seizure-induction except for kainate-induced seizures [60,[66][67]. Pilocarpine and 4-aminopyridine (4-AP) consistently produced elevation of [Glu] EXT [59][60][61][62][63][64]. In contrast, seizures evoked by inhibition of GABAa receptor-mediated responses did not elevate [Glu] EXT [12,[39][40].…”

Section: In Vivo Microdialysis Data Showed Concurrent Increases Of Bomentioning

confidence: 99%

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Extracellular Level of GABA and Glu: In Vivo Microdialysis-HPLC Measurements

Nyitrai¹,

Kékesi²,

Juhász

2006

CTMC

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In spite of several studies showing specific physiological functions of changes in the extracellular level of the major excitatory and inhibitory transmitters, Glu and GABA within the brain ([Glu](EXT), [GABA](EXT)) the exact origin (neuronal vs. astroglial, synaptic vs. extrasynaptic) of Glu and GABA present in dialysate samples is still a matter of debate. For better understanding the significance of in vivo microdialysis data, here we discuss methodological details and problems in addition to regulation of [Glu](EXT) and [GABA](EXT). Changes in [Glu](EXT) and [GABA](EXT) under pathological conditions such as ischemia and epilepsy are also reviewed. Based on recent in vivo microdialysis data we argue that ambient [Glu](EXT) and [GABA](EXT)may have a functional role. It is suggested that specific changes in concentrations of Glu and GABA in dialysate samples together with their alterations independent of neuronal activity indicate the involvement of Glu and GABA in the information processing of the brain as essential signaling molecules of nonsynaptic transmission as well. Since various drugs are able to interfere with extrasynaptic signals in vivo, studying the extracellular cell-to-cell communication of brain cells represents a new aspect to improve drugs modulating Gluergic as well as GABAergic neurotransmission.

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Section: Discussionmentioning

confidence: 81%

Section: Epileptic Seizuresmentioning

confidence: 99%

Section: In Vivo Microdialysis Data Showed Concurrent Increases Of Bomentioning

confidence: 99%

See 1 more Smart Citation

Extracellular Level of GABA and Glu: In Vivo Microdialysis-HPLC Measurements

Nyitrai¹,

Kékesi²,

Juhász

2006

CTMC

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“…In choosing between GABAergic, serotonergic, and NMDA antagonist mechanisms for means of elevation of extracellular dopamine, GABAergic mechanisms are the least likely to be responsible because the benzodiazepine positive modulators generally have no effect, or decrease extracellular dopamine in limbic striatum when systemically administered (Finlay et al 1992;Murai et al 1994;Khan et al 1999). We have investigated the impact of NMDA antagonists on striatal dopamine in a different group of awake monkeys, and seen small increases in extracellular dopamine in response to a moderately high sub-anesthetic dose (5 mg/kg) of the non-competitive antagonist ketamine (Adams et al 2002).…”

Section: Discussionmentioning

confidence: 99%

Dose-dependent effect of ethanol on extracellular dopamine in mesolimbic striatum of awake rhesus monkeys: comparison with cocaine across individuals

Bradberry

2002

Psychopharmacology

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“…Enhanced dopamine activity in the kainate model of epilepsy N Ando et al Second, seizure activity transiently elevated extracellular DA levels at various brain sites, including the hippocampus, striatum, nucleus accumbens, and prefrontal cortex (Strecker and Moneta, 1994;Dazzi et al, 1997;Smolders et al, 1997;Khan et al, 1999;Becker et al, 2000). Furthermore, the seizure-induced elevation of DA release could be enhanced if seizures were induced repeatedly (Strecker and Moneta, 1994;Dazzi et al, 1997;Becker et al, 2000).…”

Section: Seizure-induced Pathological Sensitization Of the Da Systemmentioning

confidence: 99%

Enhancement of Central Dopaminergic Activity in the Kainate Model of Temporal Lobe Epilepsy: Implication for the Mechanism of Epileptic Psychosis

Ando

Morimoto

Watanabe

et al. 2004

Neuropsychopharmacol

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There is an increased incidence of schizophrenia-like psychosis in temporal lobe epilepsy (TLE), and several risk factors have been implicated, including the duration of epilepsy and temporal lobe neuropathology. To investigate the biological mechanism of epileptic psychosis, we examined alterations of central dopaminergic systems in the kainate model of TLE. In adult rats, kainate was microinjected into the left amygdala to induce status epilepticus. An indirect dopamine agonist methamphetamine (MAP, 2 mg/kg, i.p.) was administered before and 1 month after the kainate treatment. MAP-induced locomotor activity was significantly enhanced in the kainate group compared with the baseline (pre-kainate) level, which was antagonized by pretreatment with haloperidol. The enhancement of locomotor activity in the kainate group was significantly correlated with the density of hippocampal CA1 neurons. Although the basal extracellular dopamine concentration was significantly lower in the striatum in the kainate group than in the control group (5.5 vs 39.2 fmol/20-min sample), the maximal concentration following MAP administration did not differ between the two groups. These results clearly demonstrate that hypersensitivity of the dopamine systems develops in the chronic phase of the kainate-induced TLE model, which may be responsible for the mechanism of epileptic psychosis.

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Effects of diazepam on extracellular brain neurotransmitters in pilocarpine-induced seizures in rats

Cited by 48 publications

References 46 publications

Extracellular Level of GABA and Glu: In Vivo Microdialysis-HPLC Measurements

Extracellular Level of GABA and Glu: In Vivo Microdialysis-HPLC Measurements

Dose-dependent effect of ethanol on extracellular dopamine in mesolimbic striatum of awake rhesus monkeys: comparison with cocaine across individuals

Enhancement of Central Dopaminergic Activity in the Kainate Model of Temporal Lobe Epilepsy: Implication for the Mechanism of Epileptic Psychosis

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