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  1. Article ; Online: Involvement of nitric oxide pathway in the acute anticonvulsant effect of salmon calcitonin in rats.

    Filiz, Ahmet Kemal / Karabulut, Sebahattin

    Epilepsy research

    2022  Volume 180, Page(s) 106864

    Abstract: Epilepsy is a chronic neurological disease that is thought to affect up to 1% of the world's population. Evidence suggests that salmon calcitonin (sCT) has positive effects on epileptic seizures and epileptogenesis. However, it remains unknown that ... ...

    Abstract Epilepsy is a chronic neurological disease that is thought to affect up to 1% of the world's population. Evidence suggests that salmon calcitonin (sCT) has positive effects on epileptic seizures and epileptogenesis. However, it remains unknown that whether nitric oxide (NO) pathway contributed to this antiepileptic effect of sCT. We have used the pentylenetetrazole (PTZ)-induced seizure rat model to identify the effect of sCT on seizure score, seizure-induced cognitive deficit, and the NO pathway in the brain. We found that sCT increases the first myoclonic jerk (FMJ), decreased Racine's convulsion scale (RCS), and abates seizure-induced cognitive impairment. We further demonstrated that sCT attenuated the abnormal increase of NO in the brain. These results revealed that sCT exerts an antiepileptic effect by modulating the NO pathway in the brain.
    MeSH term(s) Animals ; Anticonvulsants/pharmacology ; Anticonvulsants/therapeutic use ; Calcitonin ; Disease Models, Animal ; Electroencephalography ; Nitric Oxide ; Pentylenetetrazole/toxicity ; Rats ; Rats, Sprague-Dawley
    Chemical Substances Anticonvulsants ; Nitric Oxide (31C4KY9ESH) ; salmon calcitonin (7SFC6U2VI5) ; Calcitonin (9007-12-9) ; Pentylenetetrazole (WM5Z385K7T)
    Language English
    Publishing date 2022-01-19
    Publishing country Netherlands
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 632939-1
    ISSN 1872-6844 ; 0920-1211
    ISSN (online) 1872-6844
    ISSN 0920-1211
    DOI 10.1016/j.eplepsyres.2022.106864
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    Zs.A 2193: Show issues Location:
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  2. Article ; Online: GSK461364A suppresses proliferation of gastric cancer cells and induces apoptosis.

    Ataseven, Dilara / Taştemur, Şeyma / Yulak, Fatih / Karabulut, Sebahattin / Ergul, Mustafa

    Toxicology in vitro : an international journal published in association with BIBRA

    2023  Volume 90, Page(s) 105610

    Abstract: Polo-like kinase 1 (PLK1) is crucial in regulating cell division and has been shown to have an oncogenic function in several cancers. Since PLK1 overexpression is closely related to tumorigenesis and has been correlated with poor clinical outcomes, ... ...

    Abstract Polo-like kinase 1 (PLK1) is crucial in regulating cell division and has been shown to have an oncogenic function in several cancers. Since PLK1 overexpression is closely related to tumorigenesis and has been correlated with poor clinical outcomes, specific inhibition of PLK1 in cancer cells is a promising approach for developing new anticancer drugs. In this context, the aim of the present study was to evaluated the potential cytotoxic effects of GSK461364A, a competitive inhibitor for PLK1, in gastric cancer cell line SNU-1 cells and explored its cytotoxic mechanism. The cells were exposed to GSK461364A at different concentrations ranging from 1 to 40 μM for 24 h, and it showed considerable cytotoxicity with an IC
    MeSH term(s) Humans ; Stomach Neoplasms/drug therapy ; Cell Cycle Proteins/genetics ; Cell Cycle Checkpoints ; Apoptosis ; Antineoplastic Agents/pharmacology ; Cell Proliferation ; Cell Line, Tumor
    Chemical Substances GSK 461364A ; Cell Cycle Proteins ; Antineoplastic Agents
    Language English
    Publishing date 2023-05-05
    Publishing country England
    Document type Journal Article
    ZDB-ID 639064-x
    ISSN 1879-3177 ; 0887-2333
    ISSN (online) 1879-3177
    ISSN 0887-2333
    DOI 10.1016/j.tiv.2023.105610
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    Zs.A 2223: Show issues Location:
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  3. Article ; Online: Thiamine alleviates cognitive impairment and epileptogenesis by relieving brain inflammation in PTZ-induced kindling rat model.

    Karabulut, Sebahattin / Filiz, Ahmet Kemal / Akkaya, Recep

    Neurological research

    2022  Volume 44, Issue 10, Page(s) 902–909

    Abstract: Objective: Epileptogenesis, the process by which the brain becomes epileptic, is related to neuroinflammation, hyperexcitability cognitive deficits. Evidence suggests that improving brain inflammation can inhibit the epileptogenesis process and help the ...

    Abstract Objective: Epileptogenesis, the process by which the brain becomes epileptic, is related to neuroinflammation, hyperexcitability cognitive deficits. Evidence suggests that improving brain inflammation can inhibit the epileptogenesis process and help the emergence of new drugs for the treatment of epilepsy. Therefore, the PTZ kindling model of epilepsy was utilized to assess the neuroprotective role of thiamine in epileptogenesis.
    Methods: Male rats were exposed to PTZ-induced kindling and pretreated with low thiamine (25 mg/kg) or high thiamine (50 mg/kg). Cyclooxygenase (COX-1 and COX-2), interleukin 1-beta (IL-1β), tumor necrosis factor-alpha (TNF-α), and nuclear factor-κB (NF-κB) concentrations in the brain were analyzed using biochemical assays. Cognitive function was evaluated using the passive avoidance test.
    Results: Thiamine ameliorated epileptogenesis and enhanced the rats' performance in the passive avoidance test. Also, thiamine significantly decreased the level of neuroinflammatory mediators in the brain induced by PTZ.
    Conclusion: These results provide evidence that thiamine alleviates PTZ-induced neuroinflammation and cognitive impairments.
    MeSH term(s) Animals ; Cognitive Dysfunction/drug therapy ; Cognitive Dysfunction/etiology ; Cyclooxygenase 2 ; Encephalitis ; Epilepsy/chemically induced ; Epilepsy/drug therapy ; Kindling, Neurologic ; Male ; NF-kappa B ; Pentylenetetrazole/toxicity ; Rats ; Seizures/chemically induced ; Seizures/drug therapy ; Seizures/pathology ; Thiamine/pharmacology ; Thiamine/therapeutic use ; Tumor Necrosis Factor-alpha
    Chemical Substances NF-kappa B ; Tumor Necrosis Factor-alpha ; Cyclooxygenase 2 (EC 1.14.99.1) ; Pentylenetetrazole (WM5Z385K7T) ; Thiamine (X66NSO3N35)
    Language English
    Publishing date 2022-04-21
    Publishing country England
    Document type Journal Article
    ZDB-ID 424428-x
    ISSN 1743-1328 ; 0161-6412
    ISSN (online) 1743-1328
    ISSN 0161-6412
    DOI 10.1080/01616412.2022.2066785
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    Zs.A 1491: Show issues Location:
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  4. Article ; Online: The effect of magnesium sulfate on memory and anxiety-like behavior in a rat model: an investigation of its neuronal molecular mechanisms.

    Cetin, Ali / Ozdemir, Ercan / Golgeli, Asuman / Taskiran, Ahmet Sevki / Karabulut, Sebahattin / Ergul, Mustafa / Gumus, Erkan / Durna Dastan, Sevgi

    Neurological research

    2024  , Page(s) 1–11

    Abstract: Background: Anxiety is an adaptive response to potentially threatening conditions. Excessive and uncontrolled anxiety responses become nonadaptive and cause anxiety disorders. To better understand the anxiety-modulating effects of Mg sulfate, behavioral ...

    Abstract Background: Anxiety is an adaptive response to potentially threatening conditions. Excessive and uncontrolled anxiety responses become nonadaptive and cause anxiety disorders. To better understand the anxiety-modulating effects of Mg sulfate, behavioral test batteries in the assessment of anxiety and learning and memory functions were performed simultaneously over a time period. This study also examines the effects of Mg sulfate compared to diazepam, an anxiolytic drug with amnestic effects on anxiety-like behavior, as well as possible oxidative-nitrosative stress and hippocampal changes in male rats exposed to predator odor.
    Methods: Young adult Sprague-Dawley male rats were used. The rats were assessed using a comprehensive neurobehavioral test battery consisting of novel object recognition, open field, and successive alleys tasks. Anxiety was induced by cat odor, and diazepam and Mg were used as study drugs. Of the frontal cortex and hippocampus, the state of total oxidant and antioxidant and NO levels and histological examination of hippocampal CA1, CA2, CA3, and DG regions were performed.
    Results: Diazepam- and Mg-treated rats showed an improvement in anxiety-related behavior to predator odors. Furthermore, Mg treatment alleviated some of the increasing oxidative stress in the frontal cortex and hippocampus of rats, while diazepam treatment in particular enhanced hippocampal oxidant and antioxidant activity. In addition, brain NO increase induced by animal odor exposure or diazepam treatment was ameliorated by Mg administration.
    Conclusions: Overall, our work suggests that Mg had a partial anxiolytic effect on anxiety-like behaviors, although not as much as diazepam, and this effect varied depending on the dose. Mg treatment might counteract increased oxidative stress and elevated NO levels in the brain.
    Language English
    Publishing date 2024-05-08
    Publishing country England
    Document type Journal Article
    ZDB-ID 424428-x
    ISSN 1743-1328 ; 0161-6412
    ISSN (online) 1743-1328
    ISSN 0161-6412
    DOI 10.1080/01616412.2024.2352234
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    Zs.A 1491: Show issues Location:
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  5. Article ; Online: FGF-18 alleviates memory impairments and neuropathological changes in a rat model of Alzheimer's disease.

    Ciltas, Arzuhan Cetindag / Karabulut, Sebahattin / Sahin, Bilal / Filiz, Ahmet Kemal / Yulak, Fatih / Ozkaraca, Mustafa / Karatas, Ozhan / Cetin, Ali

    Neuropeptides

    2023  Volume 101, Page(s) 102367

    Abstract: Alzheimer's disease (AD) is a multifactorial pathology marked by amyloid beta (Aβ) accumulation, tau hyperphosphorylation, and progressive cognitive decline. Previous studies show that fibroblast growth factor 18 (FGF18) exerts a neuroprotective effect ... ...

    Abstract Alzheimer's disease (AD) is a multifactorial pathology marked by amyloid beta (Aβ) accumulation, tau hyperphosphorylation, and progressive cognitive decline. Previous studies show that fibroblast growth factor 18 (FGF18) exerts a neuroprotective effect in experimental models of neurodegeneration; however, how it affects AD pathology remains unknown. This study aimed to ascertain the impact of FGF18 on the behavioral and neuropathological changes in the rat model of sporadic AD induced by intracerebroventricular (ICV) injection of streptozotocin (STZ). The rats were treated with FGF18 (0.94 and 1.88 pmol, ICV) on the 15th day after STZ injection. Their cognitive function was assessed in the Morris water maze and passive avoidance tests for 5 days from the 16th to the 21st days. Aβ levels and histological signs of neurotoxicity were detected using the enzyme-linked immunosorbent assay (ELISA) assay and histopathological analysis of the brain, respectively. FGF18 mildly ameliorated the STZ-induced cognitive impairment; the Aβ accumulation was reduced; and the neuronal damage including pyknosis and apoptosis was alleviated in the rat brain. This study highlights the promising therapeutic potential for FGF18 in managing AD.
    MeSH term(s) Rats ; Animals ; Alzheimer Disease/metabolism ; Amyloid beta-Peptides/metabolism ; Fibroblast Growth Factors/metabolism ; Fibroblast Growth Factors/pharmacology ; Fibroblast Growth Factors/therapeutic use ; Brain/metabolism ; Memory Disorders/drug therapy ; Disease Models, Animal ; Streptozocin ; Maze Learning
    Chemical Substances fibroblast growth factor 18 ; Amyloid beta-Peptides ; Fibroblast Growth Factors (62031-54-3) ; Streptozocin (5W494URQ81)
    Language English
    Publishing date 2023-07-22
    Publishing country Netherlands
    Document type Journal Article
    ZDB-ID 9048-7
    ISSN 1532-2785 ; 0143-4179
    ISSN (online) 1532-2785
    ISSN 0143-4179
    DOI 10.1016/j.npep.2023.102367
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    Zs.A 1592: Show issues Location:
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  6. Article ; Online: Protective effects of lamotrigine and vitamin B12 on pentylenetetrazole-induced epileptogenesis in rats.

    Filiz, Ahmet Kemal / Gumus, Erkan / Karabulut, Sebahattin / Tastemur, Yasar / Taskiran, Ahmet Sevki

    Epilepsy & behavior : E&B

    2021  Volume 118, Page(s) 107915

    Abstract: Epileptogenesis is a process that includes molecular and cellular events that foster the establishment of hyperexcitable neuronal networks in the brain. Pentylenetetrazole (PTZ)-induced kindling model in rodents has added new information to the knowledge ...

    Abstract Epileptogenesis is a process that includes molecular and cellular events that foster the establishment of hyperexcitable neuronal networks in the brain. Pentylenetetrazole (PTZ)-induced kindling model in rodents has added new information to the knowledge about the pathogenesis of epilepsy and potential targets of novel antiepileptic agents. Evidence from animal and human studies suggests that oxidative and inflammatory events may play important roles in the initiation and maintaining seizure activities. Vitamin B12 has beneficial effects on the nervous system and presents pleiotropic effects with antioxidant and anti-inflammatory aspects. In the present study, we aimed to test the hypothesis that vitamin B12 and their combination with lamotrigine prevents behavioral deficits, hippocampal damage, oxidation, and proinflammatory state during epileptogenesis. Male rats were subjected to PTZ-induced epileptogenesis and pretreated with vitamin B12 (50 µg/kg) or Lamotrigine (LTG) (25 mg/kg) or B12 (50 µg/kg) + LTG (25 mg/kg). Vitamin B12 and its combination with LTG suppressed epileptogenesis and improved the performance of rats in the passive avoidance test. In addition, Vitamin B12 and its combination with LTG decreased levels of total oxidative status (TOS), oxidative stress index (OSI), interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α), and increased total antioxidant status (TAS) levels in the hippocampus and cerebral cortex. Furthermore, it reduced hippocampal neuronal damage. Current findings support the beneficial actions of vitamin B12 due to its antioxidative and anti-inflammatory properties during the course of disease.
    MeSH term(s) Animals ; Anticonvulsants/pharmacology ; Anticonvulsants/therapeutic use ; Disease Models, Animal ; Hippocampus ; Kindling, Neurologic ; Lamotrigine/therapeutic use ; Male ; Oxidative Stress ; Pentylenetetrazole/toxicity ; Rats ; Vitamin B 12/pharmacology
    Chemical Substances Anticonvulsants ; Vitamin B 12 (P6YC3EG204) ; Lamotrigine (U3H27498KS) ; Pentylenetetrazole (WM5Z385K7T)
    Language English
    Publishing date 2021-03-17
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2010587-3
    ISSN 1525-5069 ; 1525-5050
    ISSN (online) 1525-5069
    ISSN 1525-5050
    DOI 10.1016/j.yebeh.2021.107915
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    Zs.A 5289: Show issues Location:
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  7. Article ; Online: Galium aparine L. protects against acetaminophen-induced hepatotoxicity in rats.

    Sahin, Bilal / Karabulut, Sebahattin / Filiz, Ahmet Kemal / Özkaraca, Mustafa / Gezer, Arzu / Akpulat, Hüseyin Aşkın / Ataseven, Hilmi

    Chemico-biological interactions

    2022  Volume 366, Page(s) 110119

    Abstract: The toxicity of acetaminophen (N-acetyl-para-aminophenol (APAP)) is the most frequent cause of drug-induced liver damage. Galium aparine L. (GA) is traditionally used to treat jaundice. We aimed to investigate the hepatoprotective potential of GA in the ... ...

    Abstract The toxicity of acetaminophen (N-acetyl-para-aminophenol (APAP)) is the most frequent cause of drug-induced liver damage. Galium aparine L. (GA) is traditionally used to treat jaundice. We aimed to investigate the hepatoprotective potential of GA in the APAP-induced hepatic encephalopathy (HE) rat model. Qualitative phytochemical characterization of GA was performed by LC/Q-TOF/MS analysis. Wistar rats were pretreated with GA (250 and 500 mg/kg b.wt. per oral) for five days. On the 6th day, the rats were exposed to APAP (1500 mg/kg b.wt. oral gavage) and behavioral tests (open field and passive avoidance tests) were applied on the 7th and 8th days. The animals were killed, and biochemical and histopathological parameters were assessed in blood and hepatic specimens. GA pretreated rats exhibited a significant reduction in APAP-induced liver damage, evidenced by the reduction in liver necrosis and alanine aminotransferase (ALT), aspartate aminotransferase (AST), and bilirubin (BIL). GA demonstrated an anxiolytic effect, as seen in the acquisition trial and grooming behavior. The short-term memory performances of animals were not changed in all groups, suggesting that APAP intoxication did not affect hippocampal function. These results show that GA extract markedly exerts hepatoprotective activity, while its effect on hepatic encephalopathy was limited.
    MeSH term(s) Acetaminophen/toxicity ; Alanine Transaminase ; Animals ; Anti-Anxiety Agents/pharmacology ; Aspartate Aminotransferases ; Bilirubin ; Chemical and Drug Induced Liver Injury/drug therapy ; Chemical and Drug Induced Liver Injury/pathology ; Chemical and Drug Induced Liver Injury/prevention & control ; Galium ; Hepatic Encephalopathy/pathology ; Liver ; Plant Extracts/pharmacology ; Rats ; Rats, Wistar
    Chemical Substances Anti-Anxiety Agents ; Plant Extracts ; Acetaminophen (362O9ITL9D) ; Aspartate Aminotransferases (EC 2.6.1.1) ; Alanine Transaminase (EC 2.6.1.2) ; Bilirubin (RFM9X3LJ49)
    Language English
    Publishing date 2022-08-24
    Publishing country Ireland
    Document type Journal Article
    ZDB-ID 218799-1
    ISSN 1872-7786 ; 0009-2797
    ISSN (online) 1872-7786
    ISSN 0009-2797
    DOI 10.1016/j.cbi.2022.110119
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    Zs.A 686: Show issues Location:
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  8. Article: Effect of the allopregnanolone and allotetrahydrodeoxycorticosteron on spike-wave discharges in the EEG of absence epilepsy rat models.

    Karabulut, Sebahattin / Bayramov, Ruslan / Korkmaz Bayramov, Keziban / Filiz, Ahmet K / Taskiran, Ahmet S / Ozdemir, Ercan

    General physiology and biophysics

    2018  Volume 37, Issue 2, Page(s) 205–211

    Abstract: Absence epilepsy is a generalized nonconvulsive type of epilepsy that is characterized by spike-wave discharges (SWD) with a frequency of 2.5-4 Hz in the EEG. The activation of the GABAergic system in central nervous system suppresses convulsive seizures ...

    Abstract Absence epilepsy is a generalized nonconvulsive type of epilepsy that is characterized by spike-wave discharges (SWD) with a frequency of 2.5-4 Hz in the EEG. The activation of the GABAergic system in central nervous system suppresses convulsive seizures but exacerbates absence seizures. Endogenous neuroactive steroids such as 3α-hydroxy-5α-pregnan-20-one (3α,5α-THPROG; allopregnanolone) and 3α,21-dihydroxy-5α-pregnan-20-one (3α,5α-THDOC, allotetrahydrodeoxycorticosteron) are GABA-A receptor-positive allosteric modulators. Finasteride which is a 5α-reductase inhibitor can selectively block the synthesis of endogenous steroids. In this study, we compared the effects of endogenous steroids (THPROG and THDOC) on SWD by using finasteride-treated Wistar Albino Glaxo from Rijswijk (WAG/Rij) rats as a model of absence epilepsy. Wistar (WIS-THPROG and WIS-THDOC) and WAG/Rij (WAG-THPROG and WAG-THDOC) rats were divided into 4 groups (n = 8). After stereotactic surgical procedures, all rats were prepared for direct cortical EEG measurement. Following finasteride administration to each group, THPROG was administered to WIS-THPROG and WAG-THPROG groups, and THDOC to WIS-THDOC and WAG-THDOC groups intraperitoneally. While there was no any SWD activity detected in WIS-THPROG and WIS-THDOC groups, a significant increase in SWD count in WAG-THPROG (p = 0.012) and in WAG-THDOC (p = 0.012), and in SWD total duration in WAG-THPROG (p = 0.012) and WAG-THDOC groups (p = 0.011) were observed after steroid injection. No difference between the efficacy of THPROG and THDOC on absence seizures in WAG/Rij rats was observed.
    MeSH term(s) Animals ; Brain/drug effects ; Desoxycorticosterone/analogs & derivatives ; Desoxycorticosterone/pharmacology ; Disease Models, Animal ; Electroencephalography/drug effects ; Epilepsy, Absence ; Male ; Pregnanolone/pharmacology ; Rats ; Rats, Wistar
    Chemical Substances Desoxycorticosterone (40GP35YQ49) ; tetrahydrodeoxycorticosterone (4AB717DP4A) ; Pregnanolone (BXO86P3XXW)
    Language English
    Publishing date 2018-03
    Publishing country Slovakia
    Document type Journal Article
    ZDB-ID 791184-1
    ISSN 0231-5882
    ISSN 0231-5882
    DOI 10.4149/gpb_2017041
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    Zs.A 1874: Show issues Location:
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  9. Article: Wi-Fi decreases melatonin protective effect and increases hippocampal neuronal damage in pentylenetetrazole induced model seizures in rats.

    Akkaya, Recep / Gümüş, Erkan / Akkaya, Birnur / Karabulut, Sebahattin / Gülmez, Kader / Karademir, Mustafa / Taştemur, Yaşar / Taşkıran, Ahmet Şevki

    Pathophysiology : the official journal of the International Society for Pathophysiology

    2019  Volume 26, Issue 3-4, Page(s) 375–379

    Abstract: Aim: Epilepsy is a common brain disorder in which the seizures could cause a neuronal loss in the hippocampus. Oxidative stress has an important role in the pathology of epilepsy. Some studies indicate that Wi-Fi increases oxidative stress and ... ...

    Abstract Aim: Epilepsy is a common brain disorder in which the seizures could cause a neuronal loss in the hippocampus. Oxidative stress has an important role in the pathology of epilepsy. Some studies indicate that Wi-Fi increases oxidative stress and suppresses antioxidant systems. The aim of this study is to investigate the effect of Wi-Fi on melatonin anticonvulsive effect and oxidative damage in pentylenetetrazole-induced epileptic seizures in rats.
    Methods: In our study, we used 30 male Wistar Albino rats, 230-250 grams of the body weight. The animals were divided into five groups as control, saline (1 ml/kg/day olive oil for 30 days), Wi-Fi (12 h/day for 30 days), melatonin (10 mg/kg/day for 30 days) and melatonin + Wi-Fi (10 mg/kg/day +12 h/day for 30 days). In the thirtieth day, thirty minutes after the last drugs administration at the indicated doses, PTZ in 45 mg/kg was administered to induce epileptic seizure. The animals were observed for 30 min during the seizure stages (according to the Racine Scale) and first myoclonic jerk times (FMJ). Twenty-four hours after PTZ injection, brain tissues were removed for biochemical and histopathological evaluation. The hippocampal Cornu Ammonis (CA) 1, CA3 and DG (dentate gyrus) regions were histopathologically evaluated in terms of a neuronal damage in addition that oxidative stress markers (total antioxidant status (TAS), total oxidant status (TOS) and oxidative stress index (OSI)) were measured in brain tissues.
    Results: Wi-Fi was not found to affect behavioral changes associated with epilepsy (p > 0.05). However, Wi-Fi reduced anticonvulsive and antioxidant effect of melatonin (p < 0.05). Moreover, Wi-Fi increased neuronal damage in hippocampus (p < 0.05).
    Conclusion: Wi-Fi did not directly affect epileptic seizures. Nevertheless, it inhibits the positive effects of melatonin on epilepsy and it also has negative effects on hippocampal neuronal damage. These effects of Wi-Fi may occur via oxidative pathways.
    Language English
    Publishing date 2019-11-21
    Publishing country Netherlands
    Document type Journal Article
    ZDB-ID 1212740-1
    ISSN 0928-4680
    ISSN 0928-4680
    DOI 10.1016/j.pathophys.2019.11.003
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  10. Article ; Online: Effects of post-learning REM sleep deprivation on hippocampal plasticity-related genes and microRNA in mice.

    Karabulut, Sebahattin / Korkmaz Bayramov, Keziban / Bayramov, Ruslan / Ozdemir, Fadime / Topaloglu, Tugba / Ergen, Ergul / Yazgan, Kamile / Taskiran, Ahmet Sevki / Golgeli, Asuman

    Behavioural brain research

    2018  Volume 361, Page(s) 7–13

    Abstract: Sleep is essential for memory consolidation that stabilizes a memory trace. Memory consolidation includes waves of new gene expression and protein synthesis. Recently, microRNAs (miRNAs) have emerged as critical regulators of memory processes. Previous ... ...

    Abstract Sleep is essential for memory consolidation that stabilizes a memory trace. Memory consolidation includes waves of new gene expression and protein synthesis. Recently, microRNAs (miRNAs) have emerged as critical regulators of memory processes. Previous studies demonstrated that rapid eye movement (REM) sleep deprivation (REM SD) during specific time windows after training in the Morris water maze (MWM) task impairs memory consolidation. Here, we showed that the post-learning REM sleep, extending from 3 to 6 h after last training, is critical for spatial learning in the MWM task. Further, we found that the REM SD after training significantly changes the hippocampal expression of brain-derived neurotrophic factor (BDNF) mRNA; however, it causes minimal difference in the hippocampal expressions of calcium-calmodulin-dependent protein kinase II (CAMKII) and cAMP response-element-binding (CREB). In addition, it considerably affected the hippocampal expressions of miR-132, miR-182, and miR-124. In conclusion, after the MWM task, the post-learning REM sleep during specific time windows can modulate spatial memory consolidation, and its deprivation can impact the hippocampal transcriptional processes including memory-related miRNAs and mRNAs.
    MeSH term(s) Animals ; Brain-Derived Neurotrophic Factor/metabolism ; Calcium-Calmodulin-Dependent Protein Kinase Type 2/metabolism ; Cyclic AMP Response Element-Binding Protein/metabolism ; Hippocampus/metabolism ; Learning/physiology ; Male ; Maze Learning/drug effects ; Memory/physiology ; Memory Consolidation/physiology ; Mice ; Mice, Inbred BALB C ; MicroRNAs/genetics ; Neuronal Plasticity/genetics ; Neuronal Plasticity/physiology ; Sleep ; Sleep Deprivation/metabolism ; Sleep Deprivation/physiopathology ; Sleep, REM/physiology
    Chemical Substances Brain-Derived Neurotrophic Factor ; Cyclic AMP Response Element-Binding Protein ; MIRN132 microRNA, mouse ; MicroRNAs ; Mirn124 microRNA, mouse ; Mirn182 microRNA, mouse ; Calcium-Calmodulin-Dependent Protein Kinase Type 2 (EC 2.7.11.17)
    Language English
    Publishing date 2018-12-27
    Publishing country Netherlands
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 449927-x
    ISSN 1872-7549 ; 0166-4328
    ISSN (online) 1872-7549
    ISSN 0166-4328
    DOI 10.1016/j.bbr.2018.12.045
    Database MEDical Literature Analysis and Retrieval System OnLINE

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