Activation of Dopamine D4 Receptors Is Protective Against Hypoxia/Reoxygenation-Induced Cell Death in HT22 Cells

Shimada, Saori; Hirabayashi, Mioko; Ishige, Kumiko; Kosuge, Yasuhiro; Kihara, Taro; Ito, Yoshihisa

doi:10.1254/jphs.10134fp

Cited by 21 publications

(18 citation statements)

References 29 publications

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“…In the present study, duloxetine and DOV 216,303 were able to decrease extracellular BDNF levels in undifferentiated murine HT22 hippocampal neuronal cells, which are known to express the serotonin transporter, the dopamine, and norepinephrine receptors (Heiser et al 2002; Schmidt et al 2001; Shimada et al 2010). As we expected an increase in BDNF release after antidepressant treatment, this indicates that, as in astrocytes, similar factors are of relevance in determining the net effect of an antidepressant on neuronal BDNF signaling.…”

Section: Discussionmentioning

confidence: 52%

Differential BDNF Responses of Triple Versus Dual Reuptake Inhibition in Neuronal and Astrocytoma Cells as well as in Rat Hippocampus and Prefrontal Cortex

et al. 2012

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Monoamine reuptake inhibitors increase brain-derived neurotrophic factor (BDNF) activity, and this growth factor is regarded as an interesting target for developing new antidepressant drugs. The aims of this study were to evaluate whether monoaminergic reuptake inhibition increases BDNF in vivo and in vitro as predicted by the neurotrophic hypothesis of depression, and whether triple reuptake inhibition has a superior BDNF response compared to dual reuptake inhibition. Twenty-one days of oral treatment (30 mg/kg) with the dual serotonin/noradrenaline reuptake inhibitor duloxetine or the triple serotonin/noradrenaline/dopamine reuptake inhibitor DOV 216,303 restored BDNF protein levels in the rat hippocampus, which were initially decreased due to injection stress. The prefrontal cortex contained increased BDNF levels only after DOV 216,303 treatment. In vitro, neither duloxetine nor DOV 216,303 altered intracellular BDNF levels in murine HT22 neuronal cells. In contrast, BDNF release was more effectively decreased following treatment with DOV 216,303 in these cells. In rat C62B astrocytomas, both antidepressants increased intracellular BDNF levels at their highest nontoxic concentration. C62B astrocytomas did not release BDNF, even after antidepressant treatment. Increased BDNF levels support the neurotrophic hypothesis of depression, but our findings do not clearly evidence that the BDNF response after triple reuptake inhibitors is more effective than after dual reuptake inhibitors. Moreover, the data suggest that the role of BDNF in neurons and astrocytes is complex and likely depends on factors including specificity of cell types in different brain regions, cell–cell interactions, and different mechanisms of action of antidepressants used.

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Section: Discussionmentioning

confidence: 52%

Differential BDNF Responses of Triple Versus Dual Reuptake Inhibition in Neuronal and Astrocytoma Cells as well as in Rat Hippocampus and Prefrontal Cortex

et al. 2012

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“…To mimic in vivo ischemia reperfusion (I/R) injury, we utilized an established hypoxia-reoxygenation (H/R) protocol that induces membrane injury to cultured HT22 neuron cells [16]. Leakage of lactate dehydrogenase (LDH) from the cell interior into the extracellular solution was used as an index of H/R-induced injury to HT22 cells.…”

Section: Resultsmentioning

confidence: 99%

MG53 permeates through blood-brain barrier to protect ischemic brain injury

et al. 2016

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Ischemic injury to neurons represents the underlying cause of stroke to the brain. Our previous studies identified MG53 as an essential component of the cell membrane repair machinery. Here we show that the recombinant human (rh)MG53 protein facilitates repair of ischemia-reperfusion (IR) injury to the brain. MG53 rapidly moves to acute injury sites on neuronal cells to form a membrane repair patch. IR-induced brain injury increases permeability of the blood-brain-barrier, providing access of MG53 from blood circulation to target the injured brain tissues. Exogenous rhMG53 protein can protect cultured neurons against hypoxia/reoxygenation-induced damages. Transgenic mice with increased levels of MG53 in the bloodstream are resistant to IR-induced brain injury. Intravenous administration of rhMG53, either prior to or after ischemia, can effectively alleviate brain injuries in rats. rhMG53-mediated neuroprotection involves suppression of apoptotic neuronal cell death, as well as activation of the pro-survival RISK signaling pathway. Our data indicate a physiological function for MG53 in the brain and suggest that targeting membrane repair or RISK signaling may be an effective means to treat ischemic brain injury.

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“…However, the D4R antagonist L-745,870 has been reported to decrease the vulnerability of neuronal and non-neuronal cells to oxidative stress-induced apoptosis [135]. By contrast, the activation of D4R has been reported to protect against hypoxia/reoxygenation-induced oxidative stress and cell death in HT22 cells derived from mouse hippocampal neurons [136]. In addition, the protective effects of dopamine and D4R agonist on glutamate-induced ROS production were antagonized by a D4R antagonist [137].…”

Section: Renal Dopamine Receptor Regulation Of Oxidative Stressmentioning

confidence: 99%

Renal Dopamine Receptors, Oxidative Stress, and Hypertension

Cuevas

Villar

José

et al. 2013

IJMS

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Dopamine, which is synthesized in the kidney, independent of renal nerves, plays an important role in the regulation of fluid and electrolyte balance and systemic blood pressure. Lack of any of the five dopamine receptor subtypes (D1R, D2R, D3R, D4R, and D5R) results in hypertension. D1R, D2R, and D5R have been reported to be important in the maintenance of a normal redox balance. In the kidney, the antioxidant effects of these receptors are caused by direct and indirect inhibition of pro-oxidant enzymes, specifically, nicotinamide adenine dinucleotide phosphate, reduced form (NADPH) oxidase, and stimulation of anti-oxidant enzymes, which can also indirectly inhibit NADPH oxidase activity. Thus, stimulation of the D2R increases the expression of endogenous anti-oxidants, such as Parkinson protein 7 (PARK7 or DJ-1), paraoxonase 2 (PON2), and heme oxygenase 2 (HO-2), all of which can inhibit NADPH oxidase activity. The D5R decreases NADPH oxidase activity, via the inhibition of phospholipase D2, and increases the expression of HO-1, another antioxidant. D1R inhibits NADPH oxidase activity via protein kinase A and protein kinase C cross-talk. In this review, we provide an overview of the protective roles of a specific dopamine receptor subtype on renal oxidative stress, the different mechanisms involved in this effect, and the role of oxidative stress and impairment of dopamine receptor function in the hypertension that arises from the genetic ablation of a specific dopamine receptor gene in mice.

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Activation of Dopamine D4 Receptors Is Protective Against Hypoxia/Reoxygenation-Induced Cell Death in HT22 Cells

Cited by 21 publications

References 29 publications

Differential BDNF Responses of Triple Versus Dual Reuptake Inhibition in Neuronal and Astrocytoma Cells as well as in Rat Hippocampus and Prefrontal Cortex

Differential BDNF Responses of Triple Versus Dual Reuptake Inhibition in Neuronal and Astrocytoma Cells as well as in Rat Hippocampus and Prefrontal Cortex

MG53 permeates through blood-brain barrier to protect ischemic brain injury

Renal Dopamine Receptors, Oxidative Stress, and Hypertension

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