Publications by authors named "Nurhan Enginar"

Antimuscarinic administration and food intake cause convulsions in mice and rats after fasting for 48 h or less. Increased M and M muscarinic receptor expression in brain regions during fasting, and reversal of changes by refeeding may contribute to these seizures. Since receptor expression is regulated in response to agonist stimulation, this study investigated effects of nonselective muscarinic receptor agonist oxotremorine on convulsions in fasted animals.

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Tamoxifen has been shown to reduce glutamate release from presynaptic glutamatergic nerves and reverse tolerance to morphine-induced respiratory depression. Changes in glutamatergic neurotransmission in the central nervous system contribute to morphine tolerance, dependence, and withdrawal. This study, therefore, evaluated effects of tamoxifen on development of analgesic tolerance and dependence, and brain glutamate and glutamine levels in chronic morphine administration.

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Increased opioid synthesis and release, and enhanced alpha-2 adrenoceptor signaling have been suggested to mediate repeated oxytocin-induced long-lasting effects including elevated pain threshold in rats. This study evaluated whether oxytocin pretreatment would influence development of dependence and tolerance to the nociceptive and body temperature responses to morphine and enhance effects of alpha-2 adrenergic agonist clonidine on nociceptive threshold, body temperature and morphine withdrawal signs. Rats injected subcutaneously with saline or 1 mg/kg oxytocin for 5 days were implanted with placebo or morphine pellets 24 h after the treatment period.

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Protein kinase C inhibitor tamoxifen reduces symptoms of acute mania in bipolar patients and mania-like behaviors in animals. Memory impairment and altered levels of glutamate and glutamate/glutamine ratio have been reported in mania. Tamoxifen suppresses glutamate release which plays an important role in memory.

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Objectives: Fasted rodents treated with antimuscarinics develop convulsions after refeeding. Food deprivation for 48 hr produces changes in [3H]glutamate binding suggesting glutamatergic contribution to the underlying mechanism of the seizures that are somewhat unresponsive to antiepileptics. Studies in animals and epileptic patients yielded considerable information regarding the anticonvulsant effect of the noncompetitive N-methyl-D-aspartate (NMDA) receptor antagonist ketamine.

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Prolonged or repeated seizures have been shown to cause spontaneous recurrent seizures, increased anxiety‑related behavior, locomotor hyperactivity, impaired functions of learning and memory, and neuronal damage in the hippocampus and other brain regions in animals. Mice and rats treated with antimuscarinic drugs after fasting for two days or less develop convulsions after being allowed to eat ad libitum. To address whether such behavioral and neuroanatomic changes occur following these convulsions, mice treated i.

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Treatment of fasted mice and rats with the nonselective muscarinic antagonist, scopolamine or atropine, causes convulsions after food intake. This study evaluated the effect of fasting on the expression of M and M muscarinic receptors in the brain regions, the relationship between receptor expression and seizure stages, and the muscarinic receptor subtype which plays a role in the occurrence of convulsions. Mice were grouped as allowed to eat ad lib (fed) and deprived of food for 24h (fasted).

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The antidepressant-induced reduction in immobility time in the forced swimming test may depend on memory impairment due to the drug's anticholinergic efficacy. Therefore, the present study evaluated learning and memory of the immobility response in rats after the pretest and test administrations of antidepressants having potent, comparatively lower, and no anticholinergic activities. Immobility was measured in the test session performed 24 h after the pretest session.

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Background/aim: Treating animals repeatedly with intermittent and increasing morphine doses has been suggested to allow some withdrawal during each dosing interval, which causes repeated stress. The present study aimed to test this hypothesis and assess sex-related differences in withdrawal signs and their suppression by clonidine.

Materials And Methods: Male and female rats and mice were administered with increasing doses of morphine twice daily at different dosing intervals.

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This study evaluated the effects of different doses of atropine and new antiepileptics, levetiracetam and topiramate, on the development of convulsions triggered by food intake in antimuscarinic-treated fasted animals. Mice deprived of food for 24 h and treated i.p.

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Food intake triggers convulsions in fasted BALB/c mice and Wistar albino rats treated with antimuscarinic drugs, scopolamine or atropine. Inbred strain studies have yielded considerable information regarding genetic influences on seizure susceptibility and factors contribute to epileptogenesis in rodents. This study, therefore, investigated sensitivity to antimuscarinic-induced seizures in C57BL/6J mice and Sprague-Dawley rats.

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This study evaluated the effect of intermittent administration in the development of dependence to diazepam in chronic use of the drug. Gabapentin was used to provide an anxiolytic effect on drug-free days. During a 28-day treatment schedule, rats were given diazepam (15 mg/kg) once daily continuously, or intermittently with saline or gabapentin (50 mg/kg) on days 5, 10, 15, 20, and 25.

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Biperiden is one of the most commonly abused anticholinergic drugs. This study assessed its motivational effects in the acquisition of conditioned place preference in rats. Biperiden neither produced place conditioning itself nor enhanced the rewarding effect of morphine.

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Food intake triggers convulsions in fasted mice and rats treated with antimuscarinic drugs, scopolamine or atropine. Bearing some similarities in triggering factor and manifestations of the seizures in patients with eating-evoked epilepsy, seizures in fasted animals may provide insight into the mechanism(s) of this rare and partially controlled form of reflex epilepsy.

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Food intake triggers convulsions in fasted mice and rats treated with antimuscarinic drugs, scopolamine or atropine. Most of the drugs produced anticonvulsant efficacy in these convulsions have sedative effects. Thus, the present study was performed to evaluate the contribution of sedation in the suppression of convulsions by using sedative drugs chlorpromazine, morphine, amitriptyline and diphenhydramine.

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It has been shown that mice and rats treated with antimuscarinic drugs, scopolamine or atropine, after fasting for 48 h develop convulsions soon after refeeding. The present study was performed to evaluate whether mice also develop convulsions after being deprived of food for 1-24 h. The effect of day-night fasting on the development of convulsions was also determined in 12-h deprived animals.

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The tricyclic amitriptyline and the selective serotonin reuptake inhibitor fluoxetine have distinct actions in animal models of anxiety, though both antidepressants are used against anxiety disorders. Grooming behavioural sequencing, rather than its general "activity" measures, has been suggested to measure effectively the pharmacologically induced anxiolytic and anxiogenic-like effects in rats and mice. In the present study, the acute effects of amitriptyline and fluoxetine on anxiety were re-evaluated by using an analysis algorithm in novelty-induced grooming activity in rats.

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The present study was performed to evaluate convulsions after food intake in fasted rats pretreated with scopolamine or atropine and to determine whether these convulsions respond to drugs found effective in fasted mice. Scopolamine (2.4 mg/kg) and atropine (2.

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The present study was performed to further evaluate the contribution of antimuscarinic activity and hypoglycaemia to the development of scopolamine-induced convulsions in fasted mice after food intake. The effects of anticonvulsant drugs on convulsions were also evaluated. Antimuscarinic drugs atropine (3 mg/kg) and biperiden (10 mg/kg) were given intraperitoneally (i.

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