15 results on '"Mitreva R"'
Search Results
2. Pharmacological activation of metabotropic glutamate receptor subtype 4 is protective against focal transient ischemia
- Author
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Bernabucci, M., Mastroiacovo, F., Moyanova, S., Kortenska, L., Mitreva, R., Ngomba, R. T., Battaglia, Giuseppe, Bruno, Valeria Maria Gloria, and Nicoletti, Ferdinando
- Published
- 2009
3. ENDOTHELIN-1-INDUCED CEREBRAL ISCHEMIA: EFFECTS OF KETANSERIN AND MK-801 ON LIMB PLACING IN RATS
- Author
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MOYANOVA, S., primary, KORTENSKA, L., additional, and MITREVA, R., additional
- Published
- 2007
- Full Text
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4. Gender differences in diabetes mellitus-induced behavioural changes in wistar and spontaneously hypertensive rats
- Author
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Petrov, K., Daniela Pechlivanova, Tchekalarova, J., Nenchovska, Z., Mitreva, R., and Stoynev, A.
5. Age-dependence of sensorimotor and cerebral electroencephalographic asymmetry in rats subjected to unilateral cerebrovascular stroke
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Moyanova, S. G., Mitreva, R. G., Kortenska, L. V., Nicoletti, F., Ngomba, R.T., Moyanova, S. G., Mitreva, R. G., Kortenska, L. V., Nicoletti, F., and Ngomba, R.T.
- Abstract
Background: The human population mostly affected by stroke is more than 65Â years old. This study was designed to meet the recommendation that models of cerebral ischemia in aged animals are more relevant to the clinical setting than young animal models. Until now the majority of the pre-clinical studies examining age effects on stroke outcomes have used rats of old age. Considering the increasing incidence of stroke among younger than old human population, new translational approaches in animal models are needed to match the rejuvenation of stroke. A better knowledge of alterations in stroke outcomes in middle-aged rats has important preventive and management implications providing clues for future investigations on effects of various neuroprotective and neurorestorative drugs against cerebrovascular accidents that may occur before late senescence. Methods: We evaluated the impact of transient focal ischemia, induced by intracerebral unilateral infusion of endothelin-1 (Et-1) near the middle cerebral artery of conscious rats, on volume of brain damage and asymmetry in behavioral and electroencephalographic (EEG) output measures in middle-aged (11-12Â month-old) rats. Results: We did not find any age-dependent difference in the volume of ischemic brain damage three days after Et-1 infusion. However, age was an important determinant of neurological and EEG outcomes after stroke. Middle-aged ischemic rats had more impaired somatosensory functions of the contralateral part of the body than young ischemic rats and thus, had greater left-right reflex/sensorimotor asymmetry. Interhemispheric EEG asymmetry was more evident in middle-aged than in young ischemic rats, and this could tentatively explain the behavioral asymmetry.Conclusions: With a multiparametric approach, we have validated the endothelin model of ischemia in middle-aged rats. The results provide clues for future studies on mechanisms underlying plasticity after brain damage and motivate investigations of nov
6. Age-dependence of sensorimotor and cerebral electroencephalographic asymmetry in rats subjected to unilateral cerebrovascular stroke
- Author
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Moyanova, S. G., Mitreva, R. G., Kortenska, L. V., Nicoletti, F., Ngomba, R.T., Moyanova, S. G., Mitreva, R. G., Kortenska, L. V., Nicoletti, F., and Ngomba, R.T.
- Abstract
Background: The human population mostly affected by stroke is more than 65Â years old. This study was designed to meet the recommendation that models of cerebral ischemia in aged animals are more relevant to the clinical setting than young animal models. Until now the majority of the pre-clinical studies examining age effects on stroke outcomes have used rats of old age. Considering the increasing incidence of stroke among younger than old human population, new translational approaches in animal models are needed to match the rejuvenation of stroke. A better knowledge of alterations in stroke outcomes in middle-aged rats has important preventive and management implications providing clues for future investigations on effects of various neuroprotective and neurorestorative drugs against cerebrovascular accidents that may occur before late senescence. Methods: We evaluated the impact of transient focal ischemia, induced by intracerebral unilateral infusion of endothelin-1 (Et-1) near the middle cerebral artery of conscious rats, on volume of brain damage and asymmetry in behavioral and electroencephalographic (EEG) output measures in middle-aged (11-12Â month-old) rats. Results: We did not find any age-dependent difference in the volume of ischemic brain damage three days after Et-1 infusion. However, age was an important determinant of neurological and EEG outcomes after stroke. Middle-aged ischemic rats had more impaired somatosensory functions of the contralateral part of the body than young ischemic rats and thus, had greater left-right reflex/sensorimotor asymmetry. Interhemispheric EEG asymmetry was more evident in middle-aged than in young ischemic rats, and this could tentatively explain the behavioral asymmetry.Conclusions: With a multiparametric approach, we have validated the endothelin model of ischemia in middle-aged rats. The results provide clues for future studies on mechanisms underlying plasticity after brain damage and motivate investigations of nov
7. Protective role for type 4 metabotropic glutamate receptors against ischemic brain damage
- Author
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Moyanova, S. G., Mastroiacovo, F., Kortenska, L. V., Mitreva, R. G., Fardone, E., Santolini, I., Sobrado, M., Battaglia, G., Bruno, V., Nicoletti, F., Ngomba, R. T., Moyanova, S. G., Mastroiacovo, F., Kortenska, L. V., Mitreva, R. G., Fardone, E., Santolini, I., Sobrado, M., Battaglia, G., Bruno, V., Nicoletti, F., and Ngomba, R. T.
- Abstract
We examined the influence of type 4 metabotropic glutamate (mGlu4) receptors on ischemic brain damage using the permanent middle cerebral artery occlusion (MCAO) model in mice and the endothelin-1 (Et-1) model of transient focal ischemia in rats. Mice lacking mGlu4 receptors showed a 25 to 30 increase in infarct volume after MCAO as compared with wild-type littermates. In normal mice, systemic injection of the selective mGlu4 receptor enhancer, N-phenyl-7-(hydroxyimino)cyclopropabchromen-1a-caboxamide (PHCCC; 10 mg/kg, subcutaneous, administered once 30 minutes before MCAO), reduced the extent of ischemic brain damage by 35 to 45. The drug was inactive in mGlu4 receptor knockout mice. In the Et-1 model, PHCCC administered only once 20 minutes after ischemia reduced the infarct volume to a larger extent in the caudate/putamen than in the cerebral cortex. Ischemic rats treated with PHCCC showed a faster recovery of neuronal function, as shown by electrocorticographic recording and by a battery of specific tests, which assess sensorimotor deficits. These data indicate that activation of mGlu4 receptors limit the development of brain damage after permanent or transient focal ischemia. These findings are promising because selective mGlu4 receptor enhancers are under clinical development for the treatment of Parkinson's disease and other central nervous system disorders. © 2011 ISCBFM All rights reserved.
8. Chronic Piromelatine Treatment Alleviates Anxiety, Depressive Responses and Abnormal Hypothalamic-Pituitary-Adrenal Axis Activity in Prenatally Stressed Male and Female Rats.
- Author
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Ivanova N, Nenchovska Z, Atanasova M, Laudon M, Mitreva R, and Tchekalarova J
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- Animals, Anxiety, Corticosterone, Female, Humans, Indoles, Male, Pituitary-Adrenal System, Pregnancy, Pyrans, Rats, Rats, Sprague-Dawley, Receptors, Glucocorticoid, Stress, Psychological, Hypothalamo-Hypophyseal System, Prenatal Exposure Delayed Effects
- Abstract
The prenatal stress (PNS) model in rodents can induce different abnormal responses that replicate the pathophysiology of depression. We applied this model to evaluate the efficacy of piromelatine (Pir), a novel melatonin analog developed for the treatment of insomnia, in male and female offspring. Adult PNS rats from both sexes showed comparable disturbance associated with high levels of anxiety and depressive responses. Both males and females with PNS demonstrated impaired feedback inhibition of the hypothalamic-pituitary-adrenal (HPA) axis compared to the intact offspring and increased glucocorticoid receptors in the hippocampus. However, opposite to female offspring, the male PNS rats showed an increased expression of mineralocorticoid receptors in the hippocampus. Piromelatine (20 mg/kg, i.p., for 21 days injected from postnatal day 60) attenuated the high anxiety level tested in the open field, elevated plus-maze and light-dark test, and depressive-like behavior in the sucrose preference and the forced swimming tests in a sex-specific manner. The drug reversed to control level stress-induced increase of plasma corticosterone 120 min later in both sexes. Piromelatine also corrected to control level the PNS-induced alterations of corticosteroid receptors only in male offspring. Our findings suggest that the piromelatine treatment exerts beneficial effects on impaired behavioral responses and dysregulated HPA axis in both sexes, while it corrects the PNS-induced changes in the hippocampal corticosteroid receptors only in male offspring., (© 2021. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.)
- Published
- 2022
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9. Endurance training exerts time-dependent modulation on depressive responses and circadian rhythms of corticosterone and BDNF in the rats with pinealectomy.
- Author
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Tchekalarova J, Atanasova M, Ivanova N, Boyadjiev N, Mitreva R, and Georgieva K
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- Animals, Depression psychology, Depression therapy, Endurance Training psychology, Exercise Test methods, Exercise Test psychology, Male, Motor Activity physiology, Physical Conditioning, Animal methods, Physical Conditioning, Animal psychology, Pineal Gland metabolism, Pineal Gland surgery, Pinealectomy psychology, Rats, Rats, Wistar, Time Factors, Brain-Derived Neurotrophic Factor metabolism, Circadian Rhythm physiology, Corticosterone metabolism, Depression metabolism, Endurance Training methods, Pinealectomy methods
- Abstract
Pinealectomy can cause a disturbance in emotional status and circadian rhythms of the endocrine and metabolic functions in the body. Endurance training is considered a part of the complex therapy of dysfunctions driven by changes in circadian dynamics of many physiological indicators. In the present study, we aimed to study the effect of endurance training on depressive behavior induced by pinealectomy in rat. We tested the hypothesis that endurance training can have a beneficial impact on depressive behavior induced by pinealectomy in rat via correction of desynchronized circadian rhythms of corticosterone secretion in plasma and brain-derived neurothrophic factor (BDNF) in the hippocampus. The continuous exercise program attenuated depressive responses characterized by the disrupted diurnal rhythm of home-cage motor activity, anhedonia in the sucrose preference test, decreased grooming in the splash test, and despair-like behavior in the forced swimming test of rats with pinealectomy to values resembling those of sham-treated controls. Parallel to the observed positive effect on the emotional status, exercise training diminished total plasma corticosterone levels and corrected its flattened pattern. While the melatonin deficiency did not affect the fluctuations of the BDNF levels, the exercise program induced a considerable and time-dependent increase in its level. These findings suggest that the antidepressant-like effect of endurance training might be mediated via correction of the disturbed circadian rhythm of corticosterone release and enhancement of hippocampal BDNF levels in rats with pinealectomy. Therefore, this alternative mode might have a potential therapeutic application in a subpopulation of people characterized by a melatonin deficiency., Competing Interests: Declaration of Competing Interest The authors have no conflicts of interest to declare., (Copyright © 2020 Elsevier Inc. All rights reserved.)
- Published
- 2020
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10. Agomelatine treatment corrects symptoms of depression and anxiety by restoring the disrupted melatonin circadian rhythms of rats exposed to chronic constant light.
- Author
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Tchekalarova J, Stoynova T, Ilieva K, Mitreva R, and Atanasova M
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- Animals, Anxiety blood, Behavior, Animal drug effects, Corticosterone blood, Depression blood, Male, Rats, Acetamides pharmacology, Acetamides therapeutic use, Anxiety prevention & control, Circadian Rhythm drug effects, Depression prevention & control, Lighting adverse effects, Melatonin blood, Sleep Phase Chronotherapy methods
- Abstract
Desynchronization of circadian rhythms is a hallmark of depression. The antidepressant agomelatine, which is an MT
1 /MT2 melatonin receptor agonist/5-HT2C serotonin receptor antagonist has advantages compared to the selective serotonin reuptake inhibitors as a circadian phase-shifting agent. The present study was designed to explore whether agomelatine is able to have an antidepressant effect on rats exposed to chronic constant light (CCL) for 6 weeks. Focus is also placed on whether this activity affects diurnal rhythms of depressive-like symptoms and is associated with restoration of impaired circadian rhythms in plasma melatonin and corticosterone. We report that CCL induced a depressive-like symptoms associated with decreased grooming in the splash test during the subjective light/inactive phase. Anhedonia-like deficit in the saccharine preference test and increased immobility in the forced swimming test were both detected during the subjective dark/active phase. The disturbed emotional fluctuations due to CCL were corrected by agomelatine treatment (40 mg/kg, i.p. for 3 weeks). Agomelatine also restored novelty-induced hypophagia, which reflects an anxiety state, during the subjective Light and Dark phase, respectively, in rats exposed to CCL. Parallel to the observed positive influence on behavior, this melatonin analogue restored impaired circadian patterns of plasma melatonin but not that of corticosterone. These findings demonstrated the antidepressant-like effect of agomelatine in rats exposed to CCL possibly exerted via correction of melatonin rhythms and are suggestive of the therapeutic potential of this drug in a subpopulation of people characterized by a melatonin deficit., (Copyright © 2018 Elsevier Inc. All rights reserved.)- Published
- 2018
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11. Long-Term Treatment with Losartan Attenuates Seizure Activity and Neuronal Damage Without Affecting Behavioral Changes in a Model of Co-morbid Hypertension and Epilepsy.
- Author
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Tchekalarova JD, Ivanova N, Atanasova D, Pechlivanova DM, Lazarov N, Kortenska L, Mitreva R, Lozanov V, and Stoynev A
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- Animals, Disease Models, Animal, Hypertension complications, Losartan administration & dosage, Male, Rats, Rats, Inbred SHR, Seizures complications, Seizures physiopathology, Status Epilepticus chemically induced, Behavior, Animal drug effects, Hippocampus drug effects, Hypertension physiopathology, Losartan pharmacology, Neurons drug effects, Seizures drug therapy
- Abstract
Over the last 10 years, accumulated experimental and clinical evidence has supported the idea that AT1 receptor subtype is involved in epilepsy. Recently, we have shown that the selective AT1 receptor antagonist losartan attenuates epileptogenesis and exerts neuroprotection in the CA1 area of the hippocampus in epileptic Wistar rats. This study aimed to verify the efficacy of long-term treatment with losartan (10 mg/kg) after kainate-induced status epilepticus (SE) on seizure activity, behavioral and biochemical changes, and neuronal damage in a model of co-morbid hypertension and epilepsy. Spontaneous seizures were video- and EEG-monitored in spontaneously hypertensive rats (SHRs) for a 16-week period after SE. The behavior was analyzed by open field, elevated plus maze, sugar preference test, and forced swim test. The levels of serotonin in the hippocampus and neuronal loss were estimated by HPLC and hematoxylin and eosin staining, respectively. The AT1 receptor antagonism delayed the onset of seizures and alleviated their frequency and duration during and after discontinuation of treatment. Losartan showed neuroprotection mostly in the CA3 area of the hippocampus and the septo-temporal hilus of the dentate gyrus in SHRs. However, the AT1 receptor antagonist did not exert a substantial influence on concomitant with epilepsy behavioral changes and decreased 5-HT levels in the hippocampus. Our results suggest that the antihypertensive therapy with an AT1 receptor blocker might be effective against seizure activity and neuronal damage in a co-morbid hypertension and epilepsy.
- Published
- 2016
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12. Long-term intracerebroventricular infusion of angiotensin II after kainate-induced status epilepticus: Effects on epileptogenesis, brain damage, and diurnal behavioral changes.
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Ivanova NM, Atanasova D, Pechlivanova DM, Mitreva R, Lazarov N, Stoynev AG, and Tchekalarova JD
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- Angiotensin II administration & dosage, Animals, Anticonvulsants administration & dosage, CA1 Region, Hippocampal pathology, Disease Models, Animal, Infusions, Intraventricular, Kainic Acid toxicity, Male, Neuroprotective Agents administration & dosage, Rats, Rats, Wistar, Status Epilepticus chemically induced, Angiotensin II pharmacology, Anticonvulsants pharmacology, Behavior, Animal drug effects, CA1 Region, Hippocampal drug effects, Circadian Rhythm drug effects, Kainic Acid pharmacology, Neuroprotective Agents pharmacology, Spatial Memory drug effects, Status Epilepticus drug therapy
- Abstract
Our previous studies revealed that Angiotensin (Ang) II has anticonvulsant effects in acute seizure models. However, data on its role in experimental models of epilepsy are missing. In the present study, we tested whether posttreatment with Ang II after kainate (KA)-induced status epilepticus (SE) can affect epileptogenesis, concomitant behavioral changes, and brain damage. The Wistar rats were intracerebroventricularly infused via osmotic mini-pumps with Ang II (1.52μg/μl/day for 28days) after SE. Spontaneous motor seizures (SMS) were video-recorded for up to three months. Locomotor activity, anxiety, and depression-like behavior were evaluated during the last week of drug infusion, while spatial memory was assessed during the 3rd month after SE. Angiotensin II decreased the latency for onset of the first SMS and increased the frequency of SMS two months after SE. The continuous peptide infusion exacerbated the KA-induced hyperactivity and caused depression-like behavior. The reduced anxiety of KA-treated rats was alleviated by Ang II exposure. The KA-induced deficit in the hippocampal-dependent spatial memory was not influenced by Ang II. However, Ang II partially prevented the neuronal damage in the hippocampus, specifically in the CA1 area. The role of AT1 and AT2 receptor activation in the effects of the octapeptide is discussed., (Copyright © 2015 Elsevier Inc. All rights reserved.)
- Published
- 2015
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13. Antiepileptogenic and neuroprotective effects of losartan in kainate model of temporal lobe epilepsy.
- Author
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Tchekalarova JD, Ivanova NM, Pechlivanova DM, Atanasova D, Lazarov N, Kortenska L, Mitreva R, Lozanov V, and Stoynev A
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- Angiotensin II Type 1 Receptor Blockers therapeutic use, Animals, Male, Random Allocation, Rats, Rats, Wistar, Treatment Outcome, Anticonvulsants therapeutic use, Epilepsy, Temporal Lobe chemically induced, Epilepsy, Temporal Lobe drug therapy, Kainic Acid toxicity, Losartan therapeutic use, Neuroprotective Agents therapeutic use
- Abstract
Recently, we have shown that the blockade of AT1 receptor might be useful as an adjuvant treatment strategy for the prevention of oxidative stress and neurotoxicity caused by status epilepticus (SE) in rats. The purpose of the present study was to further assess the efficacy of long-term treatment with losartan (10mg/kg), the selective AT1 receptor antagonist, during kainate (KA)-induced epileptogenesis in Wistar rats. Losartan treatment started after onset of SE and continued for 4weeks. The rats were video- and EEG-recorded for 3months. Locomotor activity, anxiety and depressive-like behavior were evaluated 9weeks after SE, when all rats had developed chronic epileptic state. Neuronal damage in hippocampus was analyzed by hematoxylin while serotonin (5-HT) levels in hippocampus by HPLC. AT1 receptor antagonism increased the latent seizure-free period and decreased the frequency of spontaneous motor seizures. Losartan positively affected epilepsy-provoked behavioral changes, including impulsivity, low anxiety level and depression in a phase-dependent manner and restored the changes in diurnal fluctuation of motor activity. Losartan exerted neuroprotection selectively in the CA1 area of the hippocampus in the KA-treated rats and lowered the 5-HT levels both in normal and abnormal conditions. Our findings suggest that the AT1 receptor antagonist exerts disease-modifying effects during KA-induced epileptogenesis and neuronal damage in CA1 hippocampal area, attenuated some of the behavioral changes and restored diurnal variability in locomotor activity., (Copyright © 2014 Elsevier Inc. All rights reserved.)
- Published
- 2014
- Full Text
- View/download PDF
14. Treatment with melatonin after status epilepticus attenuates seizure activity and neuronal damage but does not prevent the disturbance in diurnal rhythms and behavioral alterations in spontaneously hypertensive rats in kainate model of temporal lobe epilepsy.
- Author
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Petkova Z, Tchekalarova J, Pechlivanova D, Moyanova S, Kortenska L, Mitreva R, Popov D, Markova P, Lozanov V, Atanasova D, Lazarov N, and Stoynev A
- Subjects
- Animals, Antioxidants pharmacology, Blood Pressure drug effects, Body Weight drug effects, Brain drug effects, Circadian Rhythm drug effects, Disease Models, Animal, Epilepsy, Temporal Lobe chemically induced, Exploratory Behavior drug effects, Food Preferences drug effects, Kainic Acid toxicity, Male, Maze Learning drug effects, Melatonin pharmacology, Rats, Rats, Inbred SHR, Serotonin metabolism, Swimming psychology, Time Factors, Antioxidants therapeutic use, Behavior, Animal drug effects, Brain pathology, Epilepsy, Temporal Lobe drug therapy, Epilepsy, Temporal Lobe physiopathology, Melatonin therapeutic use
- Abstract
Melatonin is involved in the control of circadian and seasonal rhythmicity, possesses potent antioxidant activity, and exerts a neuroprotective and anticonvulsant effect. Spontaneously hypertensive rats (SHRs) are widely accepted as an experimental model of essential hypertension with hyperactivity, deficient sustained attention, and alterations in circadian autonomic profiles. The purpose of the present study was to determine whether melatonin treatment during epileptogenesis can prevent the deleterious consequences of status epilepticus (SE) in SHRs in the kainate (KA) model of temporal lobe of epilepsy (TLE). Spontaneous recurrent seizures (SRSs) were EEG- and video-recorded during and after the treatment protocol. Melatonin (10mg/kg diluted in drinking water, 8weeks) increased the seizure-latent period, decreased the frequency of SRSs, and attenuated the circadian rhythm of seizure activity in SHRs. However, melatonin was unable to affect the disturbed diurnal rhythms and behavioral changes associated with epilepsy, including the decreased anxiety level, depression, and impaired spatial memory. Melatonin reduced neuronal damage specifically in the CA1 area of the hippocampus and piriform cortex and decreased hippocampal serotonin (5-HT) levels both in control and epileptic SHRs. Although long-term melatonin treatment after SE shows a potential to attenuate seizure activity and neuronal loss, it is unable to restore epilepsy-associated behavioral abnormalities in SHRs., (Copyright © 2013 Elsevier Inc. All rights reserved.)
- Published
- 2014
- Full Text
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15. Prophylactic treatment with melatonin after status epilepticus: effects on epileptogenesis, neuronal damage, and behavioral changes in a kainate model of temporal lobe epilepsy.
- Author
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Tchekalarova J, Petkova Z, Pechlivanova D, Moyanova S, Kortenska L, Mitreva R, Lozanov V, Atanasova D, Lazarov N, and Stoynev A
- Subjects
- Analysis of Variance, Animals, Chromatography, High Pressure Liquid, Depression etiology, Electroencephalography, Excitatory Amino Acid Agonists toxicity, Exploratory Behavior drug effects, Hippocampus drug effects, Hippocampus metabolism, Hippocampus pathology, Hyperkinesis etiology, Kainic Acid toxicity, Kaplan-Meier Estimate, Male, Maze Learning drug effects, Neurons pathology, Rats, Rats, Wistar, Serotonin metabolism, Status Epilepticus chemically induced, Status Epilepticus drug therapy, Sucrose administration & dosage, Swimming, Time Factors, Central Nervous System Depressants therapeutic use, Depression prevention & control, Hyperkinesis prevention & control, Melatonin therapeutic use, Status Epilepticus complications
- Abstract
Melatonin is a potent antioxidant which showed anticonvulsant activities both in experimental and clinical studies. In the present study, we examined the effect of melatonin treatment (10mg/kg/day, diluted in drinking water, 8 weeks) during epileptogenesis on the consequences of a kainate (KA)-induced status epilepticus (SE) in rats. Melatonin increased the latency in the appearance of spontaneous recurrent seizures (SRSs) and decreased their frequency only during the treatment period. The behavioral alterations associated with hyperactivity, depression-like behavior during the light phase, and deficits in hippocampus-dependent working memory were positively affected by melatonin treatment in rats with epilepsy. Melatonin reduced the neuronal damage in the CA1 area of the hippocampus and piriform cortex and recovered the decrease of hippocampal serotonin (5-HT) level in rats with epilepsy. Taken together, long-term melatonin treatment after SE was unable to suppress the development of epileptogenesis. However, it showed a potential in reducing some of the deleterious alterations that develop during the chronic epileptic state in a diurnal phase-dependent mode., (Copyright © 2013 Elsevier Inc. All rights reserved.)
- Published
- 2013
- Full Text
- View/download PDF
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