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Article ; Online: Nitroglycerin enhances the propagation of cortical spreading depression: comparative studies with sumatriptan and novel kynurenic acid analogues.

Knapp, Levente / Szita, Bence / Kocsis, Kitti / Vécsei, László / Toldi, József

2017 Volume 11, Page(s) 27–34

Abstract: Background: The complex pathophysiology of migraine is not yet clearly understood; therefore, experimental models are essential for the investigation of the processes related to migraine headache, which include cortical spreading depression (CSD) and NO ...

Abstract	Background: The complex pathophysiology of migraine is not yet clearly understood; therefore, experimental models are essential for the investigation of the processes related to migraine headache, which include cortical spreading depression (CSD) and NO donor-induced neurovascular changes. Data on the assessment of drug efficacy in these models are often limited, which prompted us to investigate a novel combined migraine model in which an effective pharmacon could be more easily identified. Materials and methods: In vivo electrophysiological experiments were performed to investigate the effect of nitroglycerin (NTG) on CSD induced by KCl application. In addition, sumatriptan and newly synthesized neuroactive substances (analogues of the neuromodulator kynurenic acid [KYNA]) were also tested. Results: The basic parameters of CSDs were unchanged following NTG administration; however, propagation failure was decreased compared to the controls. Sumatriptan decreased the number of CSDs, whereas propagation failure was as minimal as in the NTG group. On the other hand, both of the KYNA analogues restored the ratio of propagation to the control level. Discussion: The ratio of propagation appeared to be the indicator of the effect of NTG. This is the first study providing direct evidence that NTG influences CSD; furthermore, we observed different effects of sumatriptan and KYNA analogues. Sumatriptan changed the generation of CSDs, whereas the analogues acted on the propagation of the waves. Our experimental design overlaps with a large spectrum of processes present in migraine pathophysiology, and it can be a useful experimental model for drug screening.
MeSH term(s)	Cortical Spreading Depression/drug effects ; Dose-Response Relationship, Drug ; Humans ; Injections, Intraperitoneal ; Kynurenic Acid/administration & dosage ; Kynurenic Acid/pharmacology ; Migraine Disorders/drug therapy ; Nitroglycerin/administration & dosage ; Nitroglycerin/pharmacology ; Sumatriptan/administration & dosage ; Sumatriptan/pharmacology ; Vasodilator Agents/administration & dosage ; Vasodilator Agents/pharmacology
Chemical Substances	Vasodilator Agents ; Sumatriptan (8R78F6L9VO) ; Nitroglycerin (G59M7S0WS3) ; Kynurenic Acid (H030S2S85J)
Language	English
Publishing date	2017
Publishing country	New Zealand
Document type	Comparative Study ; Journal Article
ZDB-ID	2451346-5
ISSN	1177-8881 ; 1177-8881
ISSN (online)	1177-8881
ISSN	1177-8881
DOI	10.2147/DDDT.S117166
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Article ; Online: Enantioselective Synthesis of 8-Hydroxyquinoline Derivative, Q134 as a Hypoxic Adaptation Inducing Agent.

Hackler, László / Gyuris, Márió / Huzián, Orsolya / Alföldi, Róbert / Szebeni, Gábor J / Madácsi, Ramóna / Knapp, Levente / Kanizsai, Iván / Puskás, László G

Molecules (Basel, Switzerland)

2019 Volume 24, Issue 23

Abstract: Hypoxia is a common feature of neurodegenerative diseases, including Alzheimer's disease that may be responsible for disease pathogenesis and progression. Therefore, the hypoxia-inducible factor (HIF)1 system, responsible for hypoxic adaptation, is a ... ...

Abstract	Hypoxia is a common feature of neurodegenerative diseases, including Alzheimer's disease that may be responsible for disease pathogenesis and progression. Therefore, the hypoxia-inducible factor (HIF)1 system, responsible for hypoxic adaptation, is a potential therapeutic target to combat these diseases by activators of cytoprotective protein induction. We have selected a candidate molecule from our cytoprotective hydroxyquinoline library and developed a novel enantioselective synthesis for the production of its enantiomers. The use of quinidine or quinine as a catalyst enabled the preparation of enantiomer-pure products. We have utilized in vitro assays to evaluate cytoprotective activity, a fluorescence-activated cell sorting (FACS) based assay measuring mitochondrial membrane potential changes, and gene and protein expression analysis. Our data showed that the enantiomers of Q134 showed potent and similar activity in all tested assays. We have concluded that the enantiomers exert their cytoprotective activity via the HIF1 system through HIF1A protein stabilization.
MeSH term(s)	Cell Line, Tumor ; Flow Cytometry ; Gene Expression Profiling ; Gene Expression Regulation/drug effects ; Humans ; Hydroxyquinolines/chemical synthesis ; Hydroxyquinolines/chemistry ; Hydroxyquinolines/pharmacology ; Hypoxia-Inducible Factor 1, alpha Subunit/chemistry ; Hypoxia-Inducible Factor 1, alpha Subunit/metabolism ; Membrane Potential, Mitochondrial/drug effects ; Oxidative Stress/drug effects ; Oxyquinoline/analogs & derivatives ; Protein Stability/drug effects ; Quinidine/chemistry ; Quinine/chemistry ; Stereoisomerism
Chemical Substances	HIF1A protein, human ; Hydroxyquinolines ; Hypoxia-Inducible Factor 1, alpha Subunit ; Oxyquinoline (5UTX5635HP) ; Quinine (A7V27PHC7A) ; Quinidine (ITX08688JL)
Language	English
Publishing date	2019-11-23
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	1413402-0
ISSN	1420-3049 ; 1431-5165 ; 1420-3049
ISSN (online)	1420-3049
ISSN	1431-5165 ; 1420-3049
DOI	10.3390/molecules24234269
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Article ; Online: Acetyl-l-carnitine restores synaptic transmission and enhances the inducibility of stable LTP after oxygen-glucose deprivation.

Kocsis, Kitti / Frank, Rita / Szabó, József / Knapp, Levente / Kis, Zsolt / Farkas, Tamás / Vécsei, László / Toldi, József

Neuroscience

2016 Volume 332, Page(s) 203–211

Abstract: Hypoxic circumstances result in functional and structural impairments of the brain. Oxygen-glucose deprivation (OGD) on hippocampal slices is a technique widely used to investigate the consequences of ischemic stroke and the potential neuroprotective ... ...

Abstract	Hypoxic circumstances result in functional and structural impairments of the brain. Oxygen-glucose deprivation (OGD) on hippocampal slices is a technique widely used to investigate the consequences of ischemic stroke and the potential neuroprotective effects of different drugs. Acetyl-l-carnitine (ALC) is a naturally occurring substance in the body, and it can therefore be administered safely even in relatively high doses. In previous experiments, ALC pretreatment proved to be effective against global hypoperfusion. In the present study, we investigated whether ALC can be protective in an OGD model. We are not aware of any earlier study in which the long-term potentiation (LTP) function on hippocampal slices was measured after OGD. Therefore, we set out to determine whether an effective ALC concentration has an effect on synaptic plasticity after OGD in the hippocampal CA1 subfield of rats. A further aim was to investigate the mechanism underlying the protective effect of this compound. The experiments revealed that ALC is neuroprotective against OGD in a dose-dependent manner, which is manifested not only in the regeneration of the impaired synaptic transmission after the OGD, but also in the inducibility and stability of the LTP. In the case of the most effective concentration of ALC (500μM), use of a phosphoinositide 3-kinase (PI3K) inhibitor (LY294002) revealed that the PI3K/Akt signaling pathway has a key role in the restoration of the synaptic transmission and plasticity reached by ALC treatment.
MeSH term(s)	Acetylcarnitine/pharmacology ; Animals ; Brain Ischemia/drug therapy ; Brain Ischemia/physiopathology ; CA1 Region, Hippocampal/drug effects ; CA1 Region, Hippocampal/physiopathology ; Chromones/pharmacology ; Dose-Response Relationship, Drug ; Enzyme Inhibitors/pharmacology ; Excitatory Postsynaptic Potentials/drug effects ; Excitatory Postsynaptic Potentials/physiology ; Glucose/deficiency ; Long-Term Potentiation/drug effects ; Long-Term Potentiation/physiology ; Male ; Morpholines/pharmacology ; Neuroprotective Agents/pharmacology ; Phosphatidylinositol 3-Kinases/antagonists & inhibitors ; Phosphatidylinositol 3-Kinases/metabolism ; Proto-Oncogene Proteins c-akt/metabolism ; Rats, Wistar ; Signal Transduction/drug effects ; Tissue Culture Techniques
Chemical Substances	Chromones ; Enzyme Inhibitors ; Morpholines ; Neuroprotective Agents ; 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one (31M2U1DVID) ; Acetylcarnitine (6DH1W9VH8Q) ; Phosphatidylinositol 3-Kinases (EC 2.7.1.-) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1) ; Glucose (IY9XDZ35W2)
Language	English
Publishing date	2016-09-22
Publishing country	United States
Document type	Journal Article
ZDB-ID	196739-3
ISSN	1873-7544 ; 0306-4522
ISSN (online)	1873-7544
ISSN	0306-4522
DOI	10.1016/j.neuroscience.2016.06.046
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Article ; Online: A simple novel technique to induce short-lasting local brain ischaemia in the rat.

Knapp, Levente / Gellért, Levente / Herédi, Judit / Kocsis, Kitti / Oláh, Gáspár / Fuzik, János / Kis, Zsolt / Vécsei, László / Toldi, József / Farkas, Tamás

Neuropathology and applied neurobiology

2014 Volume 40, Issue 5, Page(s) 603–609

Abstract: Aims: Brain ischaemia models are essential to study the pathomechanisms of stroke. Our aim was to investigate the reliability and reproducibility of our novel focal ischaemia-reperfusion model.: Methods: To induce a cortical transient ischaemic ... ...

Abstract	Aims: Brain ischaemia models are essential to study the pathomechanisms of stroke. Our aim was to investigate the reliability and reproducibility of our novel focal ischaemia-reperfusion model. Methods: To induce a cortical transient ischaemic attack, we lifted the distal middle cerebral artery (MCA) with a special hook. The early changes after 2 × 15-min occlusion were observed in the somatosensory evoked responses (SERs). The histological responses to 2 × 15-min MCA occlusion and to 30-, 45- or 60-min ischaemia were examined after a 1-day survival period by 2,3,5-triphenyltetrazolium chloride (TTC) and Fluoro Jade C (FJC) staining. Another group, with 30-min ischaemia, was analysed histologically by FJC, S100 and CD11b labelling after a 5-day survival period. Results: The amplitudes of the SERs decreased immediately at the beginning of the ischaemic period, and remained at a reduced level during the ischaemia. Reperfusion resulted in increasing SER amplitudes, but they never regained the control level. The short-lasting ischaemia did not lead to brain infarction when evaluated with TTC, but intense labelling was found with FJC. The 30-min ischaemia did not result in FJC labelling after 1 day, but marked labelling was observed after 5 days with FJC, S100 and CD11b in the cortical area supplied by the MCA. Conclusions: We present here a novel, readily reproducible method to induce focal brain ischaemia. The ischaemia-reperfusion results in noteworthy changes in the SERs and the appearance of conventional tissue damage markers. This method involves possibilities for precise blood flow regulation, and the setting of the required level of perfusion.
MeSH term(s)	Animals ; Brain Ischemia/etiology ; Brain Ischemia/pathology ; Brain Ischemia/physiopathology ; Disease Models, Animal ; Electric Stimulation ; Evoked Potentials, Somatosensory ; Infarction, Middle Cerebral Artery ; Male ; Rats ; Rats, Wistar ; Reproducibility of Results ; Somatosensory Cortex/pathology ; Somatosensory Cortex/physiopathology
Language	English
Publishing date	2014-08
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	80371-6
ISSN	1365-2990 ; 0305-1846
ISSN (online)	1365-2990
ISSN	0305-1846
DOI	10.1111/nan.12069
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Article: Effects of Blood Glutamate Scavenging on Cortical Evoked Potentials

Nagy, Dávid / Knapp, Levente / Marosi, Máté / Farkas, Tamás / Kis, Zsolt / Vécsei, László / Teichberg, Vivian I / Toldi, József

Cellular and molecular neurobiology. 2010 Oct., v. 30, no. 7

2010

Abstract: It is well known that traumatic or ischemic brain injury is followed by acute excitotoxicity caused by the presence of abnormally high glutamate (Glu) in brain fluids. It has recently been demonstrated that excess Glu can be eliminated from brain into ... ...

Abstract	It is well known that traumatic or ischemic brain injury is followed by acute excitotoxicity caused by the presence of abnormally high glutamate (Glu) in brain fluids. It has recently been demonstrated that excess Glu can be eliminated from brain into blood following the intravenous administration of oxaloacetate (OxAc), which, by scavenging blood Glu, induces an enhanced and neuroprotective brain-to-blood Glu efflux. In this study, we subjected rats to intravenous OxAc administration (i.v., 12.5, 25, and 50 mg/kg, respectively), and studied its effects on somatosensory evoked cortical potentials (EPs). Against our expectation, the amplitudes of EPs did not decrease but increased in a dose- and time-dependent manner after OxAc administration. Similar effects were observed when blood Glu scavenging was enhanced by combining OxAc (12.5 mg/kgbw) with recombinant glutamate-oxaloacetate transaminase (GOT, 0.14 nmol/100 g rat). On the basis of these results, we suggest that the changes of amplitudes of the EPs involve not only a glutamatergic but also the weakening of a GABAergic component. We cannot rule out the possibility that OxAc penetrates into the brain and improves mitochondrial functions.
Keywords	neurotoxicity
Language	English
Dates of publication	2010-10
Size	p. 1101-1106.
Publisher	Springer US
Publishing place	Boston
Document type	Article
ZDB-ID	283404-2
ISSN	0272-4340
ISSN	0272-4340
DOI	10.1007/s10571-010-9542-8
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Effects of blood glutamate scavenging on cortical evoked potentials.

Nagy, Dávid / Knapp, Levente / Marosi, Máté / Farkas, Tamás / Kis, Zsolt / Vécsei, László / Teichberg, Vivian I / Toldi, József

Cellular and molecular neurobiology

2010 Volume 30, Issue 7, Page(s) 1101–1106

Abstract	It is well known that traumatic or ischemic brain injury is followed by acute excitotoxicity caused by the presence of abnormally high glutamate (Glu) in brain fluids. It has recently been demonstrated that excess Glu can be eliminated from brain into blood following the intravenous administration of oxaloacetate (OxAc), which, by scavenging blood Glu, induces an enhanced and neuroprotective brain-to-blood Glu efflux. In this study, we subjected rats to intravenous OxAc administration (i.v., 12.5, 25, and 50 mg/kg, respectively), and studied its effects on somatosensory evoked cortical potentials (EPs). Against our expectation, the amplitudes of EPs did not decrease but increased in a dose- and time-dependent manner after OxAc administration. Similar effects were observed when blood Glu scavenging was enhanced by combining OxAc (12.5 mg/kgbw) with recombinant glutamate-oxaloacetate transaminase (GOT, 0.14 nmol/100 g rat). On the basis of these results, we suggest that the changes of amplitudes of the EPs involve not only a glutamatergic but also the weakening of a GABAergic component. We cannot rule out the possibility that OxAc penetrates into the brain and improves mitochondrial functions.
MeSH term(s)	Animals ; Aspartate Aminotransferase, Cytoplasmic/metabolism ; Brain/drug effects ; Brain/metabolism ; Evoked Potentials, Somatosensory/drug effects ; Evoked Potentials, Somatosensory/physiology ; Glutamic Acid/blood ; Hydrogen-Ion Concentration ; Male ; Oxaloacetic Acid/pharmacology ; Rats ; Rats, Wistar
Chemical Substances	Oxaloacetic Acid (2F399MM81J) ; Glutamic Acid (3KX376GY7L) ; Aspartate Aminotransferase, Cytoplasmic (EC 2.6.1.-)
Language	English
Publishing date	2010-07-06
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	283404-2
ISSN	1573-6830 ; 0272-4340
ISSN (online)	1573-6830
ISSN	0272-4340
DOI	10.1007/s10571-010-9542-8
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Article ; Online: Unexpected effects of peripherally administered kynurenic acid on cortical spreading depression and related blood-brain barrier permeability.

Oláh, Gáspár / Herédi, Judit / Menyhárt, Akos / Czinege, Zsolt / Nagy, Dávid / Fuzik, János / Kocsis, Kitti / Knapp, Levente / Krucsó, Erika / Gellért, Levente / Kis, Zsolt / Farkas, Tamás / Fülöp, Ferenc / Párdutz, Arpád / Tajti, János / Vécsei, László / Toldi, József

Drug design, development and therapy

2013 Volume 7, Page(s) 981–987

Abstract: Cortical spreading depression (CSD) involves a slowly-propagating depolarization wave in the cortex, which can appear in numerous pathophysiological conditions, such as migraine with aura, stroke, and traumatic brain injury. Neurons and glial cells are ... ...

Abstract	Cortical spreading depression (CSD) involves a slowly-propagating depolarization wave in the cortex, which can appear in numerous pathophysiological conditions, such as migraine with aura, stroke, and traumatic brain injury. Neurons and glial cells are also depolarized transiently during the phenomena. CSD is followed by a massive increase in glutamate release and by changes in the brain microcirculation. The aim of this study was to investigate the effects of two N-methyl-D-aspartate receptor antagonists, endogenous kynurenic acid (KYNA) and dizocilpine, on CSD and the related blood-brain barrier (BBB) permeability in rats. In intact animals, KYNA hardly crosses the BBB but has some positive features as compared with its precursor L-Kynurenine, which is frequently used in animal studies (KYNA cannot be metabolized to excitotoxic agents such as 3-hydroxy-L-kynurenine and quinolinic acid). We therefore investigated the possible effects of peripherally administered KYNA. Repetitive CSD waves were elicited by the application of 1 M KCl solution to the cortex. Direct current-electrocorticograms were measured for 1 hour. Four parameters of the waves were compared. Evans blue dye and fluorescent microscopy were used to study the possible changes in the permeability of the BBB. The results demonstrated that N-methyl-D-aspartate receptor antagonists can reduce the number of CSD waves and decrease the permeability of the BBB during CSD. These results suggest that KYNA itself or its derivatives may offer a new approach in the therapy of migraines.
MeSH term(s)	Animals ; Blood-Brain Barrier/metabolism ; Cortical Spreading Depression/drug effects ; Dizocilpine Maleate/pharmacology ; Electroencephalography ; Excitatory Amino Acid Antagonists/administration & dosage ; Kynurenic Acid/administration & dosage ; Kynurenic Acid/pharmacology ; Male ; Microscopy, Fluorescence ; Migraine Disorders/drug therapy ; Migraine Disorders/physiopathology ; Permeability/drug effects ; Rats ; Rats, Wistar
Chemical Substances	Excitatory Amino Acid Antagonists ; Dizocilpine Maleate (6LR8C1B66Q) ; Kynurenic Acid (H030S2S85J)
Language	English
Publishing date	2013-09-16
Publishing country	New Zealand
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2451346-5
ISSN	1177-8881 ; 1177-8881
ISSN (online)	1177-8881
ISSN	1177-8881
DOI	10.2147/DDDT.S44496
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Article ; Online: Nitroglycerin enhances the propagation of cortical spreading depression: comparative studies with sumatriptan and novel kynurenic acid analogues.

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Article ; Online: Enantioselective Synthesis of 8-Hydroxyquinoline Derivative, Q134 as a Hypoxic Adaptation Inducing Agent.

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Article ; Online: Acetyl-l-carnitine restores synaptic transmission and enhances the inducibility of stable LTP after oxygen-glucose deprivation.

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Article ; Online: A simple novel technique to induce short-lasting local brain ischaemia in the rat.

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Article: Effects of Blood Glutamate Scavenging on Cortical Evoked Potentials

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Article ; Online: Effects of blood glutamate scavenging on cortical evoked potentials.

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Article ; Online: Unexpected effects of peripherally administered kynurenic acid on cortical spreading depression and related blood-brain barrier permeability.

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