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GÜLHAN, REZZAN

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GÜLHAN

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REZZAN

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1997 - 19983
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End date: 1999 × Start date: 1997 ×

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    Low dose MK-801 protects against iron-induced oxidative changes in a rat model of focal epilepsy
    (1998) YALÇIN, AHMET SUHA; Küçükkaya, B.; Aker, R.; Yüksel, M.; Onat, F.; Yalçin, A. S.
    We have used chemiluminescence measurements to examine the relationship between free radical formation and excitotoxicity in a post-traumatic epilepsy model. For this purpose, seven days after injecting iron in rat brain cortices, we measured luminol- and lucigenin-enhanced chemiluminescence in different brain regions (ipsilateral cortex, contralateral cortex, hypothalamus and hippocampus). In all brain regions (except contralateral cortices) both luminol- and lucigenin-enhanced chemiluminescence were increased in iron-injected group compared to saline-injected control group. These increases returned to control values in iron-injected rats pretreated with MK-801. Our results suggest that both free radicals and excitatory amino acids play important roles in the development of post-traumatic epilepsy and that MK-801 has protective effects against iron-induced chemiluminescence formation.
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    Effect of brain acetylcholine depletion on bicuculline-induced cardiovascular and locomotor responses
    (GORDON BREACH SCI PUBL LTD, 1997) GÜLHAN, REZZAN; Tellioglu, T; Aker, R; Oktay, S; Onat, F
    Both GABAergic and cholinergic systems are involved in central cardiovascular regulation. Previous studies have shown that GABA(A) receptor antagonists cause increases in blood pressure, heart rate and locomotor activity. In this study, we examined the role of the depletion of brain acetylcholine on the cardiovascular responses and locomotor activity induced by bicuculline methiodide in conscious Sprague-Dawley rats. The doses of 0.3 and 0.5 nmol of intracerebroventricular bicuculline methiodide produced increases in blood pressure, heart rate and locomotor activity. The dose of 18 nmol of hemicholinium-3 to deplete brain acetylcholine was given intracerebroventricularly one hour prior to bicuculline methiodide. The presser responses to bicuculline methiodide in animals pretreated with the hemicholinium-3 were higher than those seen in saline-pretreated groups, bur locomotor activity and heart rate responses to bicuculline methiodide remained unchanged in hemicholinium-3 pretreatment group. On the other hand, high dose of bicuculline methiodide (0.5 nmol) caused convulsions in some animals pretreated with hemicholinium-3 whereas bicuculline methiodide, alone, did nor cause any seizure activity. In conclusion, it seems likely that endogenous brain acetylcholine could be a modulator of GABA(A) receptor-mediated blood pressure control.
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    Effect of muscimol on cholinomimetic-induced cardiovascular responses in rats
    (1998) ONAT, FİLİZ; Onat, F.; Tellioğlu, T.; Aker, R.; Gören, Z.; Iskender, E.; Oktay, S.
    Brain acetylcholine and gamma-aminobutyric acid (GABA) are both involved in the regulation of central cardiovascular control. Despite data from anatomical and electrophysiological experiments characterizing the interaction between central GABAergic and cholinergic neurotransmission, the potential significance of this interaction in central cardiovascular regulation remains unknown. The purpose of this study was to determine whether activation of GABA(A) receptors by intracerebroventricular or intrahypothalamic administration of muscimol affects the cholinergic agonist-induced cardiovascular responses. All experiments were performed in conscious, Sprague-Dawley rats instrumented with a guide cannula for drug injection and iliac arterial catheters for direct measurement of mean arterial pressure and heart rate. Administration of a cholinergic agonist, carbachol, either intracerebroventricularly or into the dorsomedial hypothalamic nucleus, produced a significant increase in mean arterial pressure, whereas injection of carbachol into the posterior hypothalamic nucleus caused a slight elevation in blood pressure. Pretreatment with muscimol 10 min before administration of carbachol prevented the carbachol-evoked blood pressure changes. On the other hand, carbachol produced variable changes in heart rate, depending on the site of injection. In [3H]quinuclydinyl benzilate binding experiments, muscimol did not displace the muscarinic radioligand from its binding sites, suggesting that it does not exert any direct antagonistic activity at muscarinic receptors. These results suggest that the dorsomedial hypothalamic nucleus is a potential site of action for microinjected carbachol and that the GABAergic system has an inhibitory influence on cholinergic neurons involved in blood pressure regulation.