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Article ; Online: Stiripentol inhibits spike-and-wave discharges in animal models of absence seizures: A new mechanism of action involving T-type calcium channels.

Riban, Veronique / Heulard, Isabelle / Reversat, Lucie / Si Hocine, Hakim / Verleye, Marc

2022 Volume 63, Issue 5, Page(s) 1200–1210

Abstract: Objective: Stiripentol (STP; Diacomit®) is an antiepileptic drug indicated for Dravet syndrome that has been identified as a γ-aminobutyric acid (GABAergic) positive allosteric modulator. Dravet syndrome is characterized by multiple seizure types: ... ...

Abstract	Objective: Stiripentol (STP; Diacomit®) is an antiepileptic drug indicated for Dravet syndrome that has been identified as a γ-aminobutyric acid (GABAergic) positive allosteric modulator. Dravet syndrome is characterized by multiple seizure types: generalized tonic-clonic, focal, myoclonic, and absence seizures. In addition to its antiepileptic effects on tonic-clonic seizures, STP has also been reported to reduce the frequency of atypical absence seizures in patients. Our study focused on STP potential effects on absence seizures, to better characterize its full spectrum of mechanisms of action. Methods: STP effects on absence seizures were quantified by electroencephalographic recording in two animal models: rats treated with a low dose of pentylenetetrazol (20 mg/kg ip) and rats from the WAG/Rij strain. In addition, we characterized STP effects on T-type calcium channel activity. Peak currents were recorded with manual patch clamp on cells transfected with cDNA encoding for the human isoform for Ca Results: STP administered before pentylenetetrazol almost completely abolished the generation of spike-and-wave discharges (SWDs) at the dose of 300 mg/kg. At this dose, STP also statistically significantly decreased SWD cumulated duration and number in WAG/Rij rats. Its antiepileptic effect was maintained in WAG/Rij rats, whose seizures were aggravated by the GABA agonist THIP (gaboxadol hydrochloride). Furthermore, electrophysiological recordings showed that STP inhibits T-type calcium channel peak activity, with a higher specificity for the Ca Significance: In addition to its previously characterized anticonvulsive properties, these data highlight a new mechanism of action of STP on abnormal thalamocortical activity. This strong antiabsence effect on seizures is correlated with an inhibition of T-type calcium channels. This new mechanism of action could be implicated in the specificity of STP therapeutic effects in Dravet syndrome.
MeSH term(s)	Animals ; Anticonvulsants/pharmacology ; Anticonvulsants/therapeutic use ; Calcium Channels, T-Type ; Dioxolanes ; Disease Models, Animal ; Electroencephalography ; Epilepsies, Myoclonic/drug therapy ; Epilepsy, Absence/drug therapy ; Epilepsy, Absence/genetics ; Humans ; Pentylenetetrazole/toxicity ; Rats ; Rats, Wistar ; Seizures/chemically induced ; Seizures/drug therapy
Chemical Substances	Anticonvulsants ; Calcium Channels, T-Type ; Dioxolanes ; stiripentol (R02XOT8V8I) ; Pentylenetetrazole (WM5Z385K7T)
Language	English
Publishing date	2022-03-09
Publishing country	United States
Document type	Journal Article
ZDB-ID	216382-2
ISSN	1528-1167 ; 0013-9580
ISSN (online)	1528-1167
ISSN	0013-9580
DOI	10.1111/epi.17201
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Zs.A 517: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MO 475: Show issues

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Article ; Online: In Vitro and In Vivo Neuroprotective Effects of Etifoxine in β-Amyloidinduced Toxicity Models.

Riban, Veronique / Meunier, Johann / Buttigieg, Dorothee / Villard, Vanessa / Verleye, Marc

CNS & neurological disorders drug targets

2020 Volume 19, Issue 3, Page(s) 227–240

Abstract: Aim: The aim of this study is to examine the effect of etifoxine on β-amyloid-induced toxicity models.: Background: Etifoxine is an anxiolytic compound with a dual mechanism of action; it is a positive allosteric modulator of GABAergic receptors as ... ...

Abstract	Aim: The aim of this study is to examine the effect of etifoxine on β-amyloid-induced toxicity models. Background: Etifoxine is an anxiolytic compound with a dual mechanism of action; it is a positive allosteric modulator of GABAergic receptors as well as a ligand for the 18 kDa mitochondrial Translocator Protein (TSPO). TSPO has recently raised interest in Alzheimer's Disease (AD), and experimental studies have shown that some TSPO ligands could induce neuroprotective effects in animal models. Objective: In this study, we examined the potential protective effect of etifoxine in an in vitro and an in vivo model of amyloid beta (Aβ)-induced toxicity in its oligomeric form, which is a crucial factor in AD pathologic mechanisms. Methods: Neuronal cultures were intoxicated with Aβ1-42, and the effects of etifoxine on oxidative stress, Tau-hyperphosphorylation and synaptic loss were quantified. In a mice model, behavioral deficits induced by intracerebroventricular administration of Aβ25-35 were measured in a spatial memory test, the spontaneous alternation and in a contextual memory test, the passive avoidance test. Results: In neuronal cultures intoxicated with Aβ1-42, etifoxine dose-dependently decreased oxidative stress (methionine sulfoxide positive neurons), tau-hyperphosphorylation and synaptic loss (ratio PSD95/synaptophysin). In a mice model, memory impairments were fully alleviated by etifoxine administered at anxiolytic doses (12.5-50mg/kg). In addition, markers of oxidative stress and apoptosis were decreased in the hippocampus of these animals. Conclusion: Our results have shown that in these two models, etifoxine could fully prevent neurotoxicity and pathological changes induced by Aβ. These results confirm that TSPO ligands could offer an interesting therapeutic approach to Alzheimer's disease.
MeSH term(s)	Alzheimer Disease/drug therapy ; Amyloid beta-Peptides/metabolism ; Amyloid beta-Peptides/toxicity ; Animals ; Anti-Anxiety Agents/therapeutic use ; Apoptosis/drug effects ; Disease Models, Animal ; Hippocampus/drug effects ; Male ; Mice ; Neurons/metabolism ; Neuroprotective Agents/therapeutic use ; Oxazines/therapeutic use ; Oxidative Stress/drug effects
Chemical Substances	Amyloid beta-Peptides ; Anti-Anxiety Agents ; Neuroprotective Agents ; Oxazines ; etifoxine (X24X82MX4X)
Language	English
Publishing date	2020-06-01
Publishing country	United Arab Emirates
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2228394-8
ISSN	1996-3181 ; 1871-5273
ISSN (online)	1996-3181
ISSN	1871-5273
DOI	10.2174/1871527319666200601151007
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Zs.A 5892: Show issues

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Article ; Online: Etifoxine improves sensorimotor deficits and reduces glial activation, neuronal degeneration, and neuroinflammation in a rat model of traumatic brain injury.

Simon-O'Brien, Emmanuelle / Gauthier, Delphine / Riban, Véronique / Verleye, Marc

Journal of neuroinflammation

2016 Volume 13, Issue 1, Page(s) 203

Abstract: Background: Traumatic brain injury (TBI) results in important neurological impairments which occur through a cascade of deleterious physiological events over time. There are currently no effective treatments to prevent these consequences. TBI is ... ...

Abstract	Background: Traumatic brain injury (TBI) results in important neurological impairments which occur through a cascade of deleterious physiological events over time. There are currently no effective treatments to prevent these consequences. TBI is followed not only by an inflammatory response but also by a profound reorganization of the GABAergic system and a dysregulation of translocator protein 18 kDa (TSPO). Etifoxine is an anxiolytic compound that belongs to the benzoxazine family. It potentiates GABAergic neurotransmission, either through a positive allosteric effect or indirectly, involving the activation of TSPO that leads to an increase in neurosteroids synthesis. In several models of peripheral nerve injury, etifoxine has been demonstrated to display potent regenerative and anti-inflammatory properties and to promote functional recovery. Prior study also showed etifoxine efficacy in reducing brain edema in rats. In light of these positive results, we used a rat model of TBI to explore etifoxine treatment effects in a central nervous system injury, from functional outcomes to the underlying mechanisms. Methods: Male Sprague-Dawley rats received contusion (n = 18) or sham (n = 19) injuries centered laterally to bregma over the left sensorimotor cortex. They were treated with etifoxine (50 mg/kg, i.p.) or its vehicle 30 min following injury and every day during 7 days. Rats underwent behavioral testing to assess sensorimotor function. In another experiment, injured rats (n = 10) or sham rats (n = 10) received etifoxine (EFX) (50 mg/kg, i.p.) or its vehicle 30 min post-surgery. Brains were then dissected for analysis of neuroinflammation markers, glial activation, and neuronal degeneration. Results: Brain-injured rats exhibited significant sensorimotor function deficits compared to sham-injured rats in the bilateral tactile adhesive removal test, the beam walking test, and the limb-use asymmetry test. After 2 days of etifoxine treatment, behavioral impairments were significantly reduced. Etifoxine treatment reduced pro-inflammatory cytokines levels without affecting anti-inflammatory cytokines levels in injured rats, reduced macrophages and glial activation, and reduced neuronal degeneration. Conclusions: Our results showed that post-injury treatment with etifoxine improved functional recovery and reduced neuroinflammation in a rat model of TBI. These findings suggest that etifoxine may have a therapeutic potential in the treatment of TBI.
MeSH term(s)	Animals ; Anti-Inflammatory Agents/therapeutic use ; Antigens, CD/metabolism ; Antigens, Differentiation, Myelomonocytic/metabolism ; Brain Injuries, Traumatic/complications ; Cytokines/metabolism ; Disease Models, Animal ; Encephalitis/drug therapy ; Encephalitis/etiology ; Functional Laterality/drug effects ; Gait Ataxia/drug therapy ; Gait Ataxia/etiology ; Glial Fibrillary Acidic Protein/metabolism ; Locomotion/drug effects ; Macrophages/drug effects ; Male ; Nerve Degeneration/drug therapy ; Nerve Degeneration/etiology ; Neuroglia/drug effects ; Oxazines/therapeutic use ; Psychomotor Performance/drug effects ; Rats ; Rats, Sprague-Dawley ; Recovery of Function/drug effects
Chemical Substances	Anti-Inflammatory Agents ; Antigens, CD ; Antigens, Differentiation, Myelomonocytic ; CD68 antigen, human ; Cytokines ; Glial Fibrillary Acidic Protein ; Oxazines ; etifoxine (X24X82MX4X)
Language	English
Publishing date	2016-08-26
Publishing country	England
Document type	Journal Article
ISSN	1742-2094
ISSN (online)	1742-2094
DOI	10.1186/s12974-016-0687-3
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Article: Region-specific sprouting of crossed corticofugal fibers after unilateral cortical lesions in adult mice.

Riban, Veronique / Chesselet, Marie-Françoise

Experimental neurology

2006 Volume 197, Issue 2, Page(s) 451–457

Abstract: Long considered to be limited to early development or restricted adult brain regions in mammals, axonal sprouting of spared axons into denervated brain areas now appears more widespread in the adult mammalian brain. However, its extent and mechanisms ... ...

Abstract	Long considered to be limited to early development or restricted adult brain regions in mammals, axonal sprouting of spared axons into denervated brain areas now appears more widespread in the adult mammalian brain. However, its extent and mechanisms remain poorly understood. In this study, we show that robust sprouting of corticofugal axons occurs in the dorsolateral striatum but not the red nucleus of adult mice after unilateral lesions of the sensorimotor cortex induced either by mechanical removal or by thermocoagulation of pial blood vessels. These results show that local factors are critical for axonal sprouting in adult brain. They also extend previous findings in rats to a species readily amenable to genetic analysis in order to elucidate the mechanisms of this effect.
MeSH term(s)	Animals ; Behavior, Animal ; Biotin/analogs & derivatives ; Biotin/metabolism ; Brain Injuries/physiopathology ; Cerebral Cortex/physiopathology ; Dextrans/metabolism ; Functional Laterality/physiology ; Histocytochemistry/methods ; Male ; Mice ; Mice, Inbred C57BL ; Nerve Fibers/pathology ; Nerve Fibers/physiology ; Nerve Regeneration/physiology ; Neural Pathways/physiopathology
Chemical Substances	Dextrans ; biotinylated dextran amine ; Biotin (6SO6U10H04)
Language	English
Publishing date	2006-02
Publishing country	United States
Document type	Comparative Study ; Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	207148-4
ISSN	1090-2430 ; 0014-4886
ISSN (online)	1090-2430
ISSN	0014-4886
DOI	10.1016/j.expneurol.2005.10.026
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Zs.A 184: Show issues

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Article ; Online: Gene therapy in epilepsy.

Riban, Véronique / Fitzsimons, Helen L / During, Matthew J

Epilepsia

2008 Volume 50, Issue 1, Page(s) 24–32

Abstract: Results from animal models suggest gene therapy is a promising new approach for the treatment of epilepsy. Several candidate genes such as neuropeptide Y and galanin have been demonstrated in preclinical studies to have a positive effect on seizure ... ...

Abstract	Results from animal models suggest gene therapy is a promising new approach for the treatment of epilepsy. Several candidate genes such as neuropeptide Y and galanin have been demonstrated in preclinical studies to have a positive effect on seizure activity. For a successful gene therapy-based treatment, efficient delivery of a transgene to target neurons is also essential. To this end, advances have been made in the areas of cell transplantation and in the development of recombinant viral vectors for gene delivery. Recombinant adeno-associated viral (rAAV) vectors in particular show promise for gene therapy of neurological disorders due to their neuronal tropism, lack of toxicity, and stable persistence in neurons, which results in robust, long-term expression of the transgene. rAAV vectors have been recently used in phase I clinical trials of Parkinson's disease with an excellent safety profile. Prior to commencement of phase I trials for gene therapy of epilepsy, further preclinical studies are ongoing including evaluation of the therapeutic benefit in chronic models of epileptogenesis, as well as assessment of safety in toxicological studies.
MeSH term(s)	Cell Transplantation/methods ; Embryonic Stem Cells/transplantation ; Epilepsy/genetics ; Epilepsy/therapy ; Feasibility Studies ; Galanin/genetics ; Gene Transfer Techniques ; Genes, Viral/genetics ; Genetic Therapy/methods ; Genetic Vectors/genetics ; Humans ; Neuropeptide Y/genetics
Chemical Substances	Neuropeptide Y ; Galanin (88813-36-9)
Language	English
Publishing date	2008-08-19
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	216382-2
ISSN	1528-1167 ; 0013-9580
ISSN (online)	1528-1167
ISSN	0013-9580
DOI	10.1111/j.1528-1167.2008.01743.x
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Zs.A 517: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: Environmental and genetic activation of a brain-adipocyte BDNF/leptin axis causes cancer remission and inhibition.

Cao, Lei / Liu, Xianglan / Lin, En-Ju D / Wang, Chuansong / Choi, Eugene Y / Riban, Veronique / Lin, Benjamin / During, Matthew J

Cell

2010 Volume 142, Issue 1, Page(s) 52–64

Abstract: Cancer is influenced by its microenvironment, yet broader, environmental effects also play a role but remain poorly defined. We report here that mice living in an enriched housing environment show reduced tumor growth and increased remission. We found ... ...

Abstract	Cancer is influenced by its microenvironment, yet broader, environmental effects also play a role but remain poorly defined. We report here that mice living in an enriched housing environment show reduced tumor growth and increased remission. We found this effect in melanoma and colon cancer models, and that it was not caused by physical activity alone. Serum from animals held in an enriched environment (EE) inhibited cancer proliferation in vitro and was markedly lower in leptin. Hypothalamic brain-derived neurotrophic factor (BDNF) was selectively upregulated by EE, and its genetic overexpression reduced tumor burden, whereas BDNF knockdown blocked the effect of EE. Mechanistically, we show that hypothalamic BDNF downregulated leptin production in adipocytes via sympathoneural beta-adrenergic signaling. These results suggest that genetic or environmental activation of this BDNF/leptin axis may have therapeutic significance for cancer.
MeSH term(s)	Adipocytes/metabolism ; Animals ; Brain-Derived Neurotrophic Factor/genetics ; Brain-Derived Neurotrophic Factor/metabolism ; Colonic Neoplasms/genetics ; Colonic Neoplasms/metabolism ; Colonic Neoplasms/physiopathology ; Genes, APC ; Housing, Animal ; Hypothalamus/cytology ; Hypothalamus/metabolism ; Immunocompetence ; Leptin/metabolism ; Melanoma/genetics ; Melanoma/metabolism ; Melanoma/physiopathology ; Mice ; Mice, Inbred C57BL ; Neoplastic Processes ; Random Allocation ; Receptors, Adrenergic, beta/metabolism ; Signal Transduction ; Social Environment
Chemical Substances	Brain-Derived Neurotrophic Factor ; Leptin ; Receptors, Adrenergic, beta
Language	English
Publishing date	2010-06-24
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	187009-9
ISSN	1097-4172 ; 0092-8674
ISSN (online)	1097-4172
ISSN	0092-8674
DOI	10.1016/j.cell.2010.05.029
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Zs.A 1167: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MG 58: Show issues

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Article ; Online: Biodistribution and safety assessment of AAV2-GAD following intrasubthalamic injection in the rat.

Fitzsimons, Helen L / Riban, Veronique / Bland, Ross J / Wendelken, Jennifer L / Sapan, Christine V / During, Matthew J

The journal of gene medicine

2010 Volume 12, Issue 4, Page(s) 385–398

Abstract: Background: The steps necessary to translate promising new biological therapies to the clinic are poorly documented. For gene therapy, there are unique aspects that need to be addressed in biodistribution studies. Notably, the spread of the vector ... ...

Abstract	Background: The steps necessary to translate promising new biological therapies to the clinic are poorly documented. For gene therapy, there are unique aspects that need to be addressed in biodistribution studies. Notably, the spread of the vector beyond the intended target cells or tissue may result in persistent unwanted biological activity or unpredictable biological events; thus, it is critical to evaluate the risks associated with viral vector-mediated gene transfer prior to embarking on human clinical trials. Methods: In the present study, we conducted a comprehensive assessment of vector biodistribution throughout the brain, blood and major organs of rats that had been injected via the subthalamic nucleus with recombinant adeno-associated virus (AAV) expressing glutamic acid decarboxylase (GAD). In addition, behavioral and histological analyses were also performed. Results: AAV genomes were not detected in blood or cerebrospinal fluid, and did not disseminate to organs outside of the brain in the majority of animals. In the brain, an average of 97.3% of AAV2-GAD genomes were restricted to the area of the ipsilateral subthalamic nucleus (STN). There were no discernable effects of AAV2-GAD on general health, and a behavioral assessment of the animals did not reveal any alteration in general behavior, exploration, locomotion or motor symmetry. Conclusions: The present study met Food and Drug Administration requirements, in addition to efficacy and toxicity studies in rodents and nonhuman primates, to support and supplement a Phase II clinical trial invloving the gene transfer of AAV2-GAD to the human STN for the potential therapy of Parkinson's disease.
MeSH term(s)	Animals ; Cryoultramicrotomy ; DNA Primers/genetics ; DNA, Viral/blood ; DNA, Viral/cerebrospinal fluid ; Dependovirus/metabolism ; Genetic Therapy/methods ; Genetic Vectors/administration & dosage ; Genetic Vectors/adverse effects ; Genetic Vectors/pharmacokinetics ; Glutamate Decarboxylase/metabolism ; Immunohistochemistry ; Motor Activity/drug effects ; Parkinson Disease/therapy ; Rats ; Rats, Wistar ; Reverse Transcriptase Polymerase Chain Reaction ; Subthalamus/metabolism ; Subthalamus/virology
Chemical Substances	DNA Primers ; DNA, Viral ; Glutamate Decarboxylase (EC 4.1.1.15)
Language	English
Publishing date	2010-03-29
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1458024-x
ISSN	1521-2254 ; 1099-498X
ISSN (online)	1521-2254
ISSN	1099-498X
DOI	10.1002/jgm.1449
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Zs.A 5423: Show issues

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Article: Role of endothelial nitric oxide synthase in cerebral blood flow changes during kainate seizures: a genetic approach using knockout mice.

Pereira de Vasconcelos, Anne / Riban, Véronique / Wasterlain, Claude / Nehlig, Astrid

Neurobiology of disease

2006 Volume 23, Issue 1, Page(s) 219–227

Abstract: The role of endothelial nitric oxide (NO) in the cerebrovascular response to partial seizures was investigated in mice deleted for the endothelial NO synthase gene (eNOS-/-) and in their paired wild-type (WT) congeners. Local cerebral blood flow (LCBF, ... ...

Abstract	The role of endothelial nitric oxide (NO) in the cerebrovascular response to partial seizures was investigated in mice deleted for the endothelial NO synthase gene (eNOS-/-) and in their paired wild-type (WT) congeners. Local cerebral blood flow (LCBF, quantitative [14C]iodoantipyrine method) was measured 3-6 h after unilateral kainate (KA) injection in the dorsal hippocampus; controls received saline. In WT mice, KA seizures induced a 22 to 50% LCBF increase restricted to the ipsilateral hippocampus, while significant LCBF decreases (15-33%) were noticed in 22% of the contralateral areas, i.e., the parietal cortex, amygdala and three basal ganglia areas, compared to saline-injected WT mice. In eNOS-/- mice, no LCBF increases were recorded within the epileptic focus and generalized contralateral LCBF decreases (22-46%) were noticed in 2/3 of the brain areas, compared to saline-injected eNOS-/- mice. Thus, endothelial NO is the mediator of the cerebrovascular response within the epileptic focus and participates in the maintenance of LCBF in distant areas.
MeSH term(s)	Animals ; Brain/blood supply ; Brain/drug effects ; Cerebrovascular Circulation/drug effects ; Cerebrovascular Circulation/physiology ; Excitatory Amino Acid Agonists/administration & dosage ; Injections, Intraventricular ; Kainic Acid/administration & dosage ; Mice ; Mice, Knockout ; Nitric Oxide Synthase Type I/metabolism ; Nitric Oxide Synthase Type III/deficiency ; Nitric Oxide Synthase Type III/genetics ; Seizures/chemically induced ; Seizures/enzymology
Chemical Substances	Excitatory Amino Acid Agonists ; Nitric Oxide Synthase Type I (EC 1.14.13.39) ; Nitric Oxide Synthase Type III (EC 1.14.13.39) ; Kainic Acid (SIV03811UC)
Language	English
Publishing date	2006-07
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1211786-9
ISSN	1095-953X ; 0969-9961
ISSN (online)	1095-953X
ISSN	0969-9961
DOI	10.1016/j.nbd.2006.03.002
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Zs.A 4444: Show issues

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Article: Role of nitric oxide in cerebral blood flow changes during kainate seizures in mice: genetic and pharmacological approaches.

de Vasconcelos, Anne Pereira / Bouilleret, Viviane / Riban, Véronique / Wasterlain, Claude / Nehlig, Astrid

Neurobiology of disease

2005 Volume 18, Issue 2, Page(s) 270–281

Abstract: The role of neuronal nitric oxide (NO) in the cerebrovascular response to partial seizures induced by intrahippocampal injection of kainate (KA) was investigated in mice deleted for the neuronal NO synthase gene (nNOS-/-) and in wild-type controls (WT). ... ...

Abstract	The role of neuronal nitric oxide (NO) in the cerebrovascular response to partial seizures induced by intrahippocampal injection of kainate (KA) was investigated in mice deleted for the neuronal NO synthase gene (nNOS-/-) and in wild-type controls (WT). A second group of WT mice received the nNOS inhibitor, 7-nitroindazole (WT-7NI). Local cerebral blood flow (LCBF) was measured using the quantitative (14)C-iodoantipyrine method. Within the epileptic focus, all three groups of seizing mice (WT, WT-7NI, and nNOS-/-) showed significant 26-88% LCBF increases in ipsilateral hippocampus, compared to saline-injected mice. Contralaterally to the epileptic focus, KA seizures induced a 21-47% LCBF decreases in hippocampus and limbic cortex of WT mice and in most contralateral brain structures of nNOS-/- mice, while WT-7NI mice showed no contralateral CBF change. Neuronal NO appears to be not involved in the cerebrovascular response within the epileptic focus, but may rather have a role in the maintenance of distant LCBF regulation during seizures.
MeSH term(s)	Animals ; Antipyrine/analogs & derivatives ; Antipyrine/pharmacokinetics ; Brain/metabolism ; Brain/physiopathology ; Cerebral Cortex/metabolism ; Cerebral Cortex/physiopathology ; Cerebrovascular Circulation/drug effects ; Cerebrovascular Circulation/genetics ; Convulsants ; Disease Models, Animal ; Electroencephalography ; Enzyme Inhibitors/pharmacology ; Epilepsy/chemically induced ; Epilepsy/metabolism ; Epilepsy/physiopathology ; Functional Laterality/genetics ; Hippocampus/metabolism ; Hippocampus/physiopathology ; Indazoles/pharmacology ; Kainic Acid ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Nerve Tissue Proteins/antagonists & inhibitors ; Nerve Tissue Proteins/genetics ; Nitric Oxide/physiology ; Nitric Oxide Synthase/antagonists & inhibitors ; Nitric Oxide Synthase/genetics ; Nitric Oxide Synthase Type I ; Status Epilepticus/chemically induced ; Status Epilepticus/metabolism ; Status Epilepticus/physiopathology
Chemical Substances	Convulsants ; Enzyme Inhibitors ; Indazoles ; Nerve Tissue Proteins ; Nitric Oxide (31C4KY9ESH) ; Nitric Oxide Synthase (EC 1.14.13.39) ; Nitric Oxide Synthase Type I (EC 1.14.13.39) ; Nos1 protein, mouse (EC 1.14.13.39) ; Kainic Acid (SIV03811UC) ; Antipyrine (T3CHA1B51H) ; 7-nitroindazole (UX0N37CMVH) ; iodoantipyrine (V30V6H1QX4)
Language	English
Publishing date	2005-03
Publishing country	United States
Document type	Comparative Study ; Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	1211786-9
ISSN	1095-953X ; 0969-9961
ISSN (online)	1095-953X
ISSN	0969-9961
DOI	10.1016/j.nbd.2004.09.014
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Article: High temporal resolution for in vivo monitoring of neurotransmitters in awake epileptic rats using brain microdialysis and capillary electrophoresis with laser-induced fluorescence detection.

Parrot, Sandrine / Sauvinet, Valérie / Riban, Véronique / Depaulis, Antoine / Renaud, Bernard / Denoroy, Luc

Journal of neuroscience methods

2004 Volume 140, Issue 1-2, Page(s) 29–38

Abstract: A method for high temporal resolution monitoring of five neurotransmitters, dopamine (DA), noradrenaline (NA), gamma-aminobutyric acid (GABA), glutamate (Glu), l-aspartate (L-Asp), in freely-moving rats using microdialysis and capillary electrophoresis ... ...

Abstract	A method for high temporal resolution monitoring of five neurotransmitters, dopamine (DA), noradrenaline (NA), gamma-aminobutyric acid (GABA), glutamate (Glu), l-aspartate (L-Asp), in freely-moving rats using microdialysis and capillary electrophoresis with laser-induced fluorescence detection (CE-LIFD) was developed. An on-line device, including microdialysis and derivatization with naphthalene-2,3-dicarboxaldehyde, mixes the dialysate with derivatization reagents directly in the collection tube, i.e. with no reactor. Thereafter, collected derivatized samples are analyzed off-line with an automated CE system coupled to a LIFD using a 442 nm excitation. The sampling time was limited by the minimal volume required for the analysis by the automated CE system used: neurotransmitters could be determined in 667 nl dialysates (940 nl after derivatization), i.e. in samples collected every 20 s with a flow rate of 2 microl/min. The detection limits at the dialysis probe were 3 x 10(-9), 1 x 10(-9), 1.9 x 10(-8), 4.2 x 10(-7), 2.1 x 10(-7) mol/l for DA, NA, GABA, Glu and L-Asp, respectively. The protocol was validated using in vitro/in vivo tests and the performances--repeatability, linearity, characteristics of the probes--were determined. Finally, the high temporal resolution allowed the simultaneous monitoring of these neurotransmitters in rats with genetic absence epilepsy and revealed, for the first time, increases in GABA concentrations concomitantly with the seizures, detected when our new microdialysis method was combined to electroencephalographic recordings.
MeSH term(s)	Animals ; Brain/metabolism ; Brain/physiopathology ; Brain Chemistry/physiology ; Catecholamines/analysis ; Catecholamines/metabolism ; Disease Models, Animal ; Electrodes/standards ; Electrophoresis, Capillary/methods ; Epilepsy/genetics ; Epilepsy/metabolism ; Epilepsy/physiopathology ; Epilepsy, Absence/genetics ; Epilepsy, Absence/metabolism ; Epilepsy, Absence/physiopathology ; Lasers ; Male ; Microdialysis/methods ; Microscopy, Fluorescence/instrumentation ; Microscopy, Fluorescence/methods ; Neurochemistry/instrumentation ; Neurochemistry/methods ; Neurotransmitter Agents/analysis ; Neurotransmitter Agents/metabolism ; Rats ; Rats, Sprague-Dawley ; Rats, Wistar ; Time Factors ; Wakefulness
Chemical Substances	Catecholamines ; Neurotransmitter Agents
Language	English
Publishing date	2004-12-30
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	282721-9
ISSN	1872-678X ; 0165-0270
ISSN (online)	1872-678X
ISSN	0165-0270
DOI	10.1016/j.jneumeth.2004.03.025
Database	MEDical Literature Analysis and Retrieval System OnLINE

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