11 results on '"Kortenska L"'
Search Results
2. Ketanserin reduces the postischemic EEG and behavioural changes following Endothelin-1-induced occlusion of the middle cerebral artery in conscious rats
- Author
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Moyanova Slavianka, Kortenska Lidia, Kirov Roumen, Itzev Dimitar, and Usunoff Kamen
- Subjects
cerebral ischemia ,eeg ,endothelin-1 ,ketanserin ,neurological assessment ,conscious rat ,Medicine - Published
- 2008
- Full Text
- View/download PDF
3. Effects of pinealectomy on anxiety and depressive-like behaviour in Wistar rats
- Author
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Nenchovska, Z., Kortenska, L., Stefanova, M., Alova, L., Atanasova, M., and Jana Tchekalarova
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pinealectomy ,depression ,anxiety ,serotonin - Abstract
In the present study, we aimed to investigate the influence of endogenous melatonin abolishment via pinea lectomyone motional behaviour associated with anxiety and depressive responses in male Wistar rats. Sham-operated (sham) or pinealectomised (Pin) rats were tested in the hole-board (HB) test, elevated plus maze (EPM), sucrose preference test (SCT) and forced swimming test (FST) one month (Ist trial) and three months (IInd trial) after surgery. Melatonin deficit caused a significant decrease of the head-dipping at the holes accompanied by increased time of stereotype grooming both during the Ist and the IInd trial. Pinealectomy elevated both the number of entries and the time spent on the open arms in EPM test and this effect was significant a month after the removal of the pineal gland. Sucrose preference was decreased in Pin rats compared to sham rats during the light phase in both the Ist and the IInd trial, respectively. The immobility time tested in FS was significantly increased a month after pinealectomy. The observed depressive behaviour in Pin rats was accompanied by a tendency of decreased 5-HT release from the hippocampus. Taken together, a model of melatonin deficit caused an impulsiveand depressive-like behaviour, which was evident three months after pinealectomy. Our results suggest that endogenous melatonin synthetized in the pineal gland affects these behavioural responses through a regulatory mechanism on the hippocampal 5-HT release.
4. 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
5. 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
6. 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.
7. Melatonin Supplementation Alleviates Impaired Spatial Memory by Influencing Aβ 1-42 Metabolism via γ-Secretase in the icvAβ 1-42 Rat Model with Pinealectomy.
- Author
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Georgieva I, Tchekalarova J, Nenchovska Z, Kortenska L, and Tzoneva R
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- Animals, Rats, Male, Memory Disorders drug therapy, Memory Disorders metabolism, Memory Disorders etiology, Maze Learning drug effects, Melatonin pharmacology, Melatonin metabolism, Amyloid beta-Peptides metabolism, Amyloid Precursor Protein Secretases metabolism, Spatial Memory drug effects, Disease Models, Animal, Peptide Fragments metabolism, Alzheimer Disease metabolism, Alzheimer Disease drug therapy, Pinealectomy, Hippocampus metabolism, Hippocampus drug effects
- Abstract
In the search for Alzheimer's disease (AD) therapies, most animal models focus on familial AD, which accounts for a small fraction of cases. The majority of AD cases arise from stress factors, such as oxidative stress, leading to neurological changes (sporadic AD). Early in AD progression, dysfunction in γ-secretase causes the formation of insoluble Aβ
1-42 peptides, which aggregate into senile plaques, triggering neurodegeneration, cognitive decline, and circadian rhythm disturbances. To better model sporadic AD, we used a new AD rat model induced by intracerebroventricular administration of Aβ1-42 oligomers (icvAβ1-42 ) combined with melatonin deficiency via pinealectomy (pin). We validated this model by assessing spatial memory using the radial arm maze test and measuring Aβ1-42 and γ-secretase levels in the frontal cortex and hippocampus with ELISA. The icvAβ1-42 + pin model experienced impaired spatial memory and increased Aβ1-42 and γ-secretase levels in the frontal cortex and hippocampus, effects not seen with either icvAβ1-42 or the pin alone. Chronic melatonin treatment reversed memory deficits and reduced Aβ1-42 and γ-secretase levels in both structures. Our findings suggest that our icvAβ1-42 + pin model is extremely valuable for future AD research.- Published
- 2024
- Full Text
- View/download PDF
8. Predatory Odor Exposure as a Potential Paradigm for Studying Emotional Modulation of Memory Consolidation-The Role of the Noradrenergic Transmission in the Basolateral Amygdala.
- Author
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Peshev B, Ivanova P, Krushovlieva D, Kortenska L, Atanasova D, Rashev P, Lazarov N, and Tchekalarova J
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- Animals, Male, Rats, Cyclic AMP Response Element-Binding Protein metabolism, Propranolol pharmacology, Memory Consolidation physiology, Memory Consolidation drug effects, Basolateral Nuclear Complex metabolism, Basolateral Nuclear Complex physiology, Basolateral Nuclear Complex drug effects, Odorants, Norepinephrine metabolism, Hippocampus metabolism, Hippocampus physiology, Hippocampus drug effects, Emotions physiology, Emotions drug effects, Rats, Wistar
- Abstract
The pivotal role of the basolateral amygdala (BLA) in the emotional modulation of hippocampal plasticity and memory consolidation is well-established. Specifically, multiple studies have demonstrated that the activation of the noradrenergic (NA) system within the BLA governs these modulatory effects. However, most current evidence has been obtained by direct infusion of synthetic NA or beta-adrenergic agonists. In the present study, we aimed to investigate the effect of endogenous NA release in the BLA, induced by a natural aversive stimulus (coyote urine), on memory consolidation for a low-arousing, hippocampal-dependent task. Our experiments combined a weak object location task (OLT) version with subsequent mild predator odor exposure (POE). To investigate the role of endogenous NA in the BLA in memory modulation, a subset of the animals (Wistar rats) was treated with the non-selective beta-blocker propranolol at the end of the behavioral procedures. Hippocampal tissue was collected 90 min after drug infusion or after the OLT test, which was performed 24 h later. We used the obtained samples to estimate the levels of phosphorylated CREB (pCREB) and activity-regulated cytoskeleton-associated protein (Arc)-two molecular markers of experience-dependent changes in neuronal activity. The result suggests that POE has the potential to become a valuable behavioral paradigm for studying the interaction between BLA and the hippocampus in memory prioritization and selectivity.
- Published
- 2024
- Full Text
- View/download PDF
9. Protective Effect of the Novel Melatonin Analogue Containing Donepezil Fragment on Memory Impairment via MT/ERK/CREB Signaling in the Hippocampus in a Rat Model of Pinealectomy and Subsequent Aβ 1-42 Infusion.
- Author
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Tchekalarova J, Ivanova P, Krushovlieva D, Kortenska L, and Angelova VT
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- Rats, Animals, Donepezil pharmacology, Pinealectomy, Hippocampus metabolism, Amyloid beta-Peptides metabolism, Memory Disorders drug therapy, Memory Disorders etiology, Melatonin pharmacology, Melatonin therapeutic use, Alzheimer Disease drug therapy, Peptide Fragments
- Abstract
A reduction in melatonin function contributes to the acceleration of Alzheimer's disease (AD), and understanding the molecular processes of melatonin-related signaling is critical for intervention in AD progression. Recently, we synthesized a series of melatonin analogues with donepezil fragments and tested them in silico and in vitro. In this study, one of the most potent compounds, 3c , was evaluated in a rat model of pinealectomy (pin) followed by icvAβ
1-42 infusion. Melatonin was used as the reference drug. Treatment with melatonin and 3c (10 mg/kg, i.p. for 14 days) had a beneficial effect on memory decline and the concomitant increase in hippocampal Aβ1-42 and pTAU in the pin+icvAβ1-42 rats. Melatonin supplementation facilitated non-amyloidogenic signaling via non-receptor (histone deacetylase sirtuin 1, SIRT1) and receptor-related signaling (MT/ERK/CREB). The hybrid 3c analogue up-regulated the MT1A and MT2B receptors, pERK and pCREB. Our results strongly support the hypothesis that melatonin-related analogues may become a promising drug candidate for Alzheimer's disease therapy.- Published
- 2024
- Full Text
- View/download PDF
10. Sex-Dependent Effects of Piromelatine Treatment on Sleep-Wake Cycle and Sleep Structure of Prenatally Stressed Rats.
- Author
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Tchekalarova J, Kortenska L, Marinov P, and Ivanova N
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- Animals, Circadian Rhythm physiology, Electroencephalography, Female, Indoles, Male, Pregnancy, Pyrans pharmacology, Rats, Receptors, Melatonin, Sleep physiology, Brain-Derived Neurotrophic Factor pharmacology, Melatonin pharmacology, Melatonin therapeutic use
- Abstract
Prenatal stress (PNS) impairs the circadian rhythm of the sleep/wake cycle. The melatonin (MT) analogue Piromelatine (Pir) was designed for the treatment of insomnia. The present study aimed to explore effects of Pir on circadian rhythmicity, motor activity, and sleep structure in male and female rats with a history of prenatal stress (PNS). In addition, we elucidated the role of MT receptors and brain-derived neurotrophic factor (BDNF) to ascertain the underlying mechanism of the drug. Pregnant rats were exposed to different stressors from day seven until birth. Piromelatine (20 mg/kg/day/14 days) was administered to young adult offspring. Home-cage locomotion, electroencephalographic (EEG) and electromyographic (EMG) recordings were conducted for 24 h. Offspring treated with vehicle showed sex-and phase-dependent disturbed circadian rhythm of motor activity and sleep/wake cycle accompanied by elevated rapid eye movement (REM) pattern and theta power and diminished non-rapid eye movement (NREM) sleep and delta power. While Pir corrected the PNS-induced impaired sleep patterns, the MT receptor antagonist luzindol suppressed its effects in male and female offspring. In addition, Pir increased the BDNF expression in the hippocampus in male and female offspring with PNS. Our findings suggest that the beneficial effect of Pir on PNS-induced impairment of sleep/wake cycle circadian rhythm and sleep structure is exerted via activation of MT receptors and enhanced BDNF expression in the hippocampus in male and female offspring.
- Published
- 2022
- Full Text
- View/download PDF
11. Impact of Melatonin Deficit on Emotional Status and Oxidative Stress-Induced Changes in Sphingomyelin and Cholesterol Level in Young Adult, Mature, and Aged Rats.
- Author
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Tchekalarova J, Nenchovska Z, Kortenska L, Uzunova V, Georgieva I, and Tzoneva R
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- Animals, Emotions, Oxidative Stress, Rats, Sphingomyelins, Melatonin pharmacology, Pineal Gland physiology, Pineal Gland surgery
- Abstract
The pineal gland regulates the aging process via the hormone melatonin. The present report aims to evaluate the effect of pinealectomy (pin) on behavioral and oxidative stress-induced alterations in cholesterol and sphingomyelin (SM) levels in young adult, mature and aging rats. Sham and pin rats aged 3, 14 and 18 months were tested in behavioral tests for motor activity, anxiety, and depression. The ELISA test explored oxidative stress parameters and SM in the hippocampus, while total cholesterol was measured in serum via a commercial autoanalyzer. Mature and aged sham rats showed low motor activity and increased anxiety compared to the youngest rats. Pinealectomy affected emotional responses, induced depressive-like behavior, and elevated cholesterol levels in the youngest rats. However, removal of the pineal gland enhanced oxidative stress by diminishing antioxidant capacity and increasing the MDA level, and decreased SM level in the hippocampus of 14-month-old rats. Our findings suggest that young adult rats are vulnerable to emotional disturbance and changes in cholesterol levels resulting from melatonin deficiency. In contrast, mature rats with pinealectomy are exposed to an oxidative stress-induced decrease in SM levels in the hippocampus.
- Published
- 2022
- Full Text
- View/download PDF
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