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Lāsma Ļauberte

Latvijas Organiskās Sintēzes Institūts

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Nikolajs Sjakste

University of Latvia

Ivars Kalvinsh

Latvijas Organiskās Sintēzes Institūts

Dainuvı̄te Meirena

Latvijas Organiskās Sintēzes Institūts

Maija Dzintare

Latvian Academy of Sport Education

ЛБ

Л. Баумане

Latvijas Organiskās Sintēzes Institūts

Jelena Sharipova

Kazan State Medical University

Tatjana Sjakste

University of Latvia

Ivars Kalviņš

Latvijas Organiskās Sintēzes Institūts

Jeļizaveta Sokolovska

University of Latvia

Liga Zvejniece

Latvijas Organiskās Sintēzes Institūts

Cooperative Institutions

Latvijas Organiskās Sintēzes Institūts

University of Latvia

Institute of Organic Synthesis

Riga Stradiņš University

Latvian Academy of Sciences

Latvian Biomedical Research and Study Centre

Institut Jacques Monod

Pauls Stradiņš Clinical University Hospital

Riga East University Hospital

Université Paris Cité

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Changes in GLUT1 expression under metformin treatment in rat models of severe and mild stretozotocin diabetes mellitus

13th European Congress of Endocrinology (2011)

Jeļizaveta Sokolovska Sergejs Isajevs Olga Sugoka Jelena Sharipova Lāsma Ļauberte

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Effects of gamma-Butyrobetaine and Mildronate on Nitric Oxide Production in Lipopolysaccharide-Treated Rats

Pharmacology & Toxicology (2004)

Nikolajs Sjakste Л. Баумане Jean‐Luc Boucher Maija Dzintare Dainuvı̄te Meirena

10.1111/j.1742-7843.2004.pto940108.x

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Citations (8)

Mildronate positively affects compensation of diabetes in streptozotocin rats and alters iNOS gene expression in rat tissues

11th European Congress of Endocrinology (2009)

Jeļizaveta Sokolovska Ivars Kalvinsh Jelena Sharipova Lāsma Ļauberte Nikolajs Sjakste

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Effects of γ‐Butyrobetaine and Mildronate on Nitric Oxide Production in Lipopolysaccharide‐Treated Rats

Basic & Clinical Pharmacology & Toxicology (2004)

Nikolajs Sjakste Л. Баумане Jean‐Luc Boucher Maija Dzintare Dainuvı̄te Meirena

Abstract: Production of nitric oxide was measured in lipopolysaccharide‐treated rats (10 mg/kg, 4 hr) using the electron paramagnetic resonance method. As compared to the control animals, the nitric oxide level in liver of lipopolysaccharide‐treated rats increased from 27.6±4.7 to 1485±129 ng/g tissue, in heart from 4.8±0.7 to 271±26 ng/g tissue, in blood from 33.6±12.4 to 638±136 ng/g tissue, in kidney from 3.3±0.5 to 356±31 ng/g tissue, in brain cortex from 46.0±3.4 to 227±27 ng/g tissue, in cerebellum from 27.7±2.6 to 218±30 ng/g tissue, and in testes from 13.8±1.1 to 86±8 ng/g tissue. Administration of the antiischaemic drug, mildronate (120 mg/kg) caused a significant twofold decrease of the nitric oxide level in brain cortex and cerebellum 1 hr after drug administration. Its natural analogue γ‐butyrobetaine (30 mg/kg) triggered a twofold decrease of the nitric oxide concentration in all studied tissues 30 min. after the administration. Nitric oxide reached the initial level 2 hr later. Neither mildronate nor γ‐butyrobetaine could inhibit the inducible nitric oxide synthase in vitro . Analogues of γ‐butyrobetaine appear to be prospective drugs for the treatment of circulatory complications of sepsis.

10.1111/j.1742-7843.2004.pto_940108.x

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Reduced GFAP Expression in Bergmann Glial Cells in the Cerebellum of Sigma-1 Receptor Knockout Mice Determines the Neurobehavioral Outcomes after Traumatic Brain Injury

International Journal of Molecular Sciences (2021)

Gundega Stelfa Edijs Vavers Baiba Švalbe Rinalds Serzants Anna Miteniece

Neuroprotective effects of Sigma-1 receptor (S1R) ligands have been observed in multiple animal models of neurodegenerative diseases. Traumatic brain injury (TBI)-related neurodegeneration can induce long-lasting physical, cognitive, and behavioral disabilities. The aim of our study was to evaluate the role of S1R in the development of neurological deficits after TBI. Adult male wild-type CD-1 (WT) and S1R knockout (S1R-/-) mice were subjected to lateral fluid percussion injury, and behavioral and histological outcomes were assessed for up to 12 months postinjury. Neurological deficits and motor coordination impairment were less pronounced in S1R-/- mice with TBI than in WT mice with TBI 24 h after injury. TBI-induced short-term memory impairments were present in WT but not S1R-/- mice 7 months after injury. Compared to WT animals, S1R-/- mice exhibited better motor coordination and less pronounced despair behavior for up to 12 months postinjury. TBI induced astrocyte activation in the cortex of WT but not S1R-/- mice. S1R-/- mice presented a significantly reduced GFAP expression in Bergmann glial cells in the molecular layer of the cerebellum compared to WT mice. Our findings suggest that S1R deficiency reduces TBI-induced motor coordination impairments by reducing GFAP expression in Bergmann glial cells in the cerebellum.

Sigma-1 Receptor

Knockout mouse

Motor coordination

10.3390/ijms222111611

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Genetic inactivation of the sigma-1 chaperone protein results in decreased expression of the R2 subunit of the GABA-B receptor and increased susceptibility to seizures

Neurobiology of Disease (2020)

Edijs Vavers Baiba Zvejniece Gundega Stelfa Baiba Švalbe Kārlis Vilks

There is a growing body of evidence demonstrating the significant involvement of the sigma-1 chaperone protein in the modulation of seizures. Several sigma-1 receptor (Sig1R) ligands have been demonstrated to regulate the seizure threshold in acute and chronic seizure models. However, the mechanism by which Sig1R modulates the excitatory and inhibitory pathways in the brain has not been elucidated. The aim of this study was to compare the susceptibility to seizures of wild type (WT) and Sig1R knockout (Sig1R-/-) mice in intravenous pentylenetetrazol (PTZ) and (+)-bicuculline (BIC) infusion-induced acute seizure and Sig1R antagonist NE-100-induced seizure models. To determine possible molecular mechanisms, we used quantitative PCR, Western blotting and immunohistochemistry to assess the possible involvement of several seizure-related genes and proteins. Peripheral tissue contractile response of WT and Sig1R-/- mice was studied in an isolated vasa deferentia model. The most important finding was the significantly decreased expression of the R2 subunit of the GABA-B receptor in the hippocampus and habenula of Sig1R-/- mice. Our results demonstrated that Sig1R-/- mice have decreased thresholds for PTZ- and BIC-induced tonic seizures. In the NE-100-induced seizure model, Sig1R-/- animals demonstrated lower seizure scores, shorter durations and increased latency times of seizures compared to WT mice. Sig1R-independent activities of NE-100 included downregulation of the gene expression of iNOS and GABA-A γ2 and inhibition of KCl-induced depolarization in both WT and Sig1R-/- animals. In conclusion, the results of this study indicate that the lack of Sig1R resulted in decreased expression of the R2 subunit of the GABA-B receptor and increased susceptibility to seizures. Our results confirm that Sig1R is a significant molecular target for seizure modulation and warrants further investigation for the development of novel anti-seizure drugs.

Pentylenetetrazol

Sigma-1 Receptor

Seizure threshold

Knockout mouse

10.1016/j.nbd.2020.105244

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Citations (15)

Drastic increase in nitric oxide content in rat brain under halothane anesthesia revealed by EPR method

Biochemical Pharmacology (1999)

Nikolajs Sjakste Л. Баумане Dainuvı̄te Meirena Lāsma Ļauberte Maija Dzintare

Chloral hydrate

10.1016/s0006-2952(99)00281-6

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Citations (35)

[Role of nitric oxide (NO) in the mechanism of anesthetic action].

PubMed (2001)

Nikolajs Sjakste Maija Dzintare Л. Баумане Dainuvı̄te Meirena Lāsma Ļauberte

Published reports on modifications of nitric oxide (NO) synthase (NOS) activity and NO production in the brain during development of anesthesia induced by the most common inhalational (halothane, isoflurane, sevoflurane, enflurane) and intravenous (ketamine, barbiturates, propofol, etomidate) anesthetics are reviewed. According to a popular universally acknowledged hypothesis, inhibition of NOS activity and blockade of NO neurotransmitter function are important steps in the mechanism of action of anesthetics. There are data which confirm the validity of this hypothesis for all above-listed drugs, but there are also data which disagree with it. Some scientists find that anesthesia has no effect on NOS activity and NO production, others found that the enzyme activity and NOS gene expression increased under the effect of anesthesia. Published reports and authors' data on a drastic increase of NO content in the cerebral cortex in halothane anesthesia are discussed. The effects of narcotics on NO-mediated changes in vascular tone are analyzed.

Etomidate

Enflurane

Mechanism of Action

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Citations (3)

Involvement of Nitric Oxide Production in the Mildronate Mechanism of Action

Pharmacology communications (2002)

Maija Dzintare Л. Баумане Dainuvı̄te Meirena Lāsma Ļauberte Ivars Kalvinsh

Mechanism of Action

10.1080/10604450213832

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