Effects of cerebral ischemia on dopamine receptors in the gerbil striatum

Araki, Tsutomu; Kato, Harubumi; Shuto, Katsuro; Fujiwara, Takehiko; Kogure, Kyuya; Itoyama, Yasuto

doi:10.1016/0014-2999(96)00227-0

Cited by 9 publications

(10 citation statements)

References 43 publications

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“…Rolipram at these doses is pharmacologically active to facilitate cAMP level by PDE-IV inhibition. These present results suggest that the hyperactivation in dopaminergic neural transmission, especially through D 1 receptors, plays a key role in the development of ischemic damages in the striatum (Araki et al, 1996;Kanai et al, 1993;Nagasawa et al, 1992a). In addition to damage due to an amount of oxidative radical forms of dopamine (e.g., 6-hydroxydopamine), the hyperactivation of the cAMP second messenger system might play an important role in the development of neuronal damage after transient ischemic insults at least in the striatum, resulting in degradation of neurons containing D 1 dopamine receptors.…”

Section: Discussionsupporting

confidence: 51%

“…Neuronal damage after transient focal ischemic insult can be detectable not only by changes in CBF, CMRO 2 , and CMRglc, but also by changes in neurotransmitter systems in the CNS (Araki et al, 1996(Araki et al, , 1997Globus et al, 1988;Kanai et al, 1993;Kruger et al, 1999;Nagasawa et al, 1992a;Nakata et al, 1997;Prehn et al, 1991Prehn et al, , 1993Semkova et al, 1998;Sette et al, 1993;Shibata et al, 1992;Slivka et al, 1988;Vera et al, 1996;Zhao et al, 2001). Neurons are anatomically and functionally integrated as a network directly (Hattori et al, 1976) or indirectly (Bunney and Aghajanian, 1976) through multisynaptic connections.…”

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confidence: 99%

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Transient Focal Ischemia Affects the cAMP Second Messenger System and Coupled Dopamine D₁ and 5-HT_1A Receptors in the Living Monkey Brain: A Positron Emission Tomography Study Using Microdialysis

Tsukada

Fukumoto

Nishiyama

et al. 2004

J Cereb Blood Flow Metab

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Using positron emission tomography (PET) and microdialysis, the present study showed that neuronal damages after transient focal ischemia was partly induced by hyperactivation of the cyclic adenosine 3',5'-monophosphate (cAMP) second messenger system through modulations of dopamine D, and serotonin 5-HT1A receptors in the living brains of cynomolgus monkeys. Occlusion of the right middle cerebral artery for 3 hours suppressed CBF in the striatum, and reperfusion induced hyperperfusion in the neocortex and striatum of the occluded side. Six hours after reperfusion, the activity of the cAMP second messenger system assayed with [11C]rolipram was significantly facilitated in the neocortex and striatum where CBF was lowered more than 40% of normal during occlusion ("ischemic" area). Seven days later, impaired dopamine D1 and 5-HT1A receptor binding, measured with [11C]SCH23390 and [carbonyl-11C]WAY-100635, respectively, was observed in the ischemic area. Microdialysis analysis revealed that the striatal dopamine level provided a transient and marked increased during occlusion and after reperfusion, whereas the cortical serotonin level transiently increased only after reperfusion, and was at an undetectable level thereafter. Administration of rolipram (0.1 and 1 mg/kg, intravenously) during occlusion facilitated reduction of dopamine D1 binding, whereas rolipram administration 6 hours after reperfusion induced a further decrease in 5-HT1A receptor binding. These results suggest that the activation of cAMP second messenger system modulated by dopamine D1 and 5-HT1A receptors could be involved in the neuronal degeneration after transient cerebral ischemic insult.

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Section: Discussionsupporting

confidence: 51%

mentioning

confidence: 99%

Transient Focal Ischemia Affects the cAMP Second Messenger System and Coupled Dopamine D₁ and 5-HT_1A Receptors in the Living Monkey Brain: A Positron Emission Tomography Study Using Microdialysis

Tsukada

Fukumoto

Nishiyama

et al. 2004

J Cereb Blood Flow Metab

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“…Przedborski et al (1991) demonstrated that perinatal hypoxic-ischemic brain injury significantly reduced DA D1 and D2 receptors in the lesioned caudate-putamen of rats. Araki et al (1996) observed that cerebral ischemia selectively reduced DA D1 receptors but not D2 receptors in the striatum associated with cell loss. It is also observed that in infants with hypoxic-ischemic brain injury, striatal D2 receptor density decreased as the severity of injury increased.…”

Section: Discussionmentioning

confidence: 96%

Hyperbaric oxygenation mitigates focal cerebral injury and reduces striatal dopamine release in a rat model of transient middle cerebral artery occlusion

Yang

Camporesi

Yang

et al. 2002

European Journal of Applied Physiology

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The usefulness of the administration of hyperbaric oxygen (HBO) in the treatment of acute focal cerebral ischemia remains debatable. A significant association exists between focal cerebral injury and an excessive release of extracellular dopamine (DA). In vivo microdialysis was used in the present study to examine the effect of HBO on DA release in the striatum during ischemia and reperfusion in rats. The histological changes occurring were also evaluated. Focal cerebral ischemia was induced by occlusion of the middle cerebral artery (MCA) using a surgically placed intraluminal filament. Control rats (n=8) were subjected to 1 h of ischemia, whilst the study rats (n=8) were in addition treated with HBO (2.8 atmospheres of absolute pressure 100% O(2)) during ischemia. Both groups were returned to breathing room air at normal pressure during reperfusion. Microdialysis samples were continuously collected at 15 min intervals at 2 microl.min(-1). The [mean (SE)] increase in release of striatal DA attained significance after 30 min of occlusion of MCA [170 (24)%], and continued to increase [268 (26)% at 45 min] reaching a peak level at 60 min [672 (59)%] before returning to the baseline level during the late reperfusion phase. There was no significant change in the level of DA in HBO treated rats during the period of ischemia. A significant reduction in edema and neuronal shrinkage were observed by histological examination in HBO treated rats when compared to the control rats. The results showed that HBO, when administered during ischemia, offered significant neuroprotection in our experimental model of transient focal cerebral ischemia in the rat. The mechanism seems to imply, at least in part, a reduced level of DA.

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“…These different sensitivities of receptor bindings to brain damage might be caused by the different stability of receptor proteins to radical reactions. Araki et al (1996) suggested that the striatopallidal neurons, which contain D 2 receptors, are relatively more resistant to transient cerebral ischemia than striatonigral neurons (D 1 receptors). As reperfusion induced radicals have been thought to be the major causes of ischemic brain damage (Morimoto et al, 1996;Wei et al, 1998), the striatopallidal neurons might also be more resistant to SNP-induced cell damage.…”

Section: Discussionmentioning

confidence: 99%

Intrastriatal microinjection of sodium nitroprusside induces cell death and reduces binding of dopaminergic receptors

Yanamoto

Hosoi

Uesaka

et al. 2003

Synapse

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Rat striatum was microinjected with 50 nmol sodium nitroprusside (SNP) and neural cell death as well as the binding of dopaminergic receptors were followed for 24 h after the infusion using TTC staining, cresyl violet staining, and quantitative autoradiography. Striatal cell death was observed 3 h after the infusion of SNP. A widespread area of cell death, including part of the cerebral cortex, was seen at 24 h after the infusion. A decrease of more than 80% in dopamine D1 receptor binding was seen in rat brain slices prepared 2 h after the infusion of SNP, whereas only a slight decrease in dopamine D2 receptor binding and almost no changes in dopamine transporter binding were observed. One day after the infusion, less than 10% of the binding of all three types of dopaminergic receptors remained in a widespread area in the infused side of the striatum and part of the cerebral cortex. Microinjection of either NOC-18 (50 nmol), another type of NO donor, or sodium cyanide (50 nmol) did not caused cell death. In addition, microinjection of FeCl2 (50 nmol) into the striatum caused cell death and reduction in dopamine D() receptor binding. These results suggest that iron-related radical reactions, but not NO itself, might have important roles on SNP-caused cell death. The current receptor binding study also indicated that dopamine D1 receptor binding is the most sensitive indicator for detection of cell death or cell damage induced by radical reactions in the rat striatum.

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Effects of cerebral ischemia on dopamine receptors in the gerbil striatum

Cited by 9 publications

References 43 publications

Transient Focal Ischemia Affects the cAMP Second Messenger System and Coupled Dopamine D₁ and 5-HT_1A Receptors in the Living Monkey Brain: A Positron Emission Tomography Study Using Microdialysis

Transient Focal Ischemia Affects the cAMP Second Messenger System and Coupled Dopamine D₁ and 5-HT_1A Receptors in the Living Monkey Brain: A Positron Emission Tomography Study Using Microdialysis

Hyperbaric oxygenation mitigates focal cerebral injury and reduces striatal dopamine release in a rat model of transient middle cerebral artery occlusion

Intrastriatal microinjection of sodium nitroprusside induces cell death and reduces binding of dopaminergic receptors

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Effects of cerebral ischemia on dopamine receptors in the gerbil striatum

Cited by 9 publications

References 43 publications

Transient Focal Ischemia Affects the cAMP Second Messenger System and Coupled Dopamine D1 and 5-HT1A Receptors in the Living Monkey Brain: A Positron Emission Tomography Study Using Microdialysis

Transient Focal Ischemia Affects the cAMP Second Messenger System and Coupled Dopamine D1 and 5-HT1A Receptors in the Living Monkey Brain: A Positron Emission Tomography Study Using Microdialysis

Hyperbaric oxygenation mitigates focal cerebral injury and reduces striatal dopamine release in a rat model of transient middle cerebral artery occlusion

Intrastriatal microinjection of sodium nitroprusside induces cell death and reduces binding of dopaminergic receptors

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Transient Focal Ischemia Affects the cAMP Second Messenger System and Coupled Dopamine D₁ and 5-HT_1A Receptors in the Living Monkey Brain: A Positron Emission Tomography Study Using Microdialysis

Transient Focal Ischemia Affects the cAMP Second Messenger System and Coupled Dopamine D₁ and 5-HT_1A Receptors in the Living Monkey Brain: A Positron Emission Tomography Study Using Microdialysis