Stimulating effect of erythropoietin on the release of dopamine and acetylcholine from the rat brain slice

Yamamoto, Masahiro; Koshimura, Kunio; Kawaguchi, Mikiko; Sohmiya, Motoi; Murakami, Yoshio; Kato, Yuzuru

doi:10.1016/s0304-3940(00)01441-5

Cited by 55 publications

(39 citation statements)

References 12 publications

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“…EPO in-vitro has also been observed to exert neurotrophic effect on cholinergic and other neurons (Tabira et al, 1995). In addition erythropoietin has also been found to exert stimulatory effect on the release of dopamine and acetylcholine in rat brain slices (Yamamoto et al, 2000). Many studies have also implicated potential anti-oxidative (Genc et al, 2004;Signore et al, 2006;Xue et al, 2007;Wang et al, 2009) actions of EPO.…”

Section: Discussionmentioning

confidence: 99%

Effects of Erythropoietin on Memory Deficits and Brain Oxidative Stress in the Mouse Models of Dementia

Kumar

Jaggi

Singh

2010

Korean J Physiol Pharmacol

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The present study was undertaken to explore the potential of erythropoietin in memory deficits of mice. Memory impairment was produced by scopolamine (0.5 mg/kg, i.p.) and intracerebroventricular streptozotocin (i.c.v STZ, 3 mg/kg, 10 μl, 1 st and 3 rd day) in separate groups of animals. Morris watermaze test was employed to assess learning and memory. The levels of brain thio-barbituric acid reactive species (TBARS) and reduced glutathione (GSH) were estimated to assess degree of oxidative stress. Brain acetylcholinesterase enzyme (AChE) activity was also measured. Scopolamine/streptozotocin administration induced significant impairment of learning and memory in mice as indicated by marked decrease in Morris water-maze performance. Scopolamine/streptozotocin administration also produced a significant enhancement of brain AChE activity and brain oxidative stress (an increase in TBARS and a decrease in GSH) levels. Treatment of erythropoietin (500 and 1,000 IU/Kg i.p.) significantly reversed scopolamine-as well as streptozotocin-induced learning and memory deficits along with attenuation of those-induced rise in brain AChE activity and brain oxidative stress levels. It may be concluded that erythropoietin exerts a beneficial effect in memory deficits of mice possibly through its multiple actions including potential anti-oxidative effect.

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Section: Discussionmentioning

confidence: 99%

Effects of Erythropoietin on Memory Deficits and Brain Oxidative Stress in the Mouse Models of Dementia

Kumar

Jaggi

Singh

2010

Korean J Physiol Pharmacol

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“…Neonatal rEpo after HI brain injury also was shown recently to preserve adult hippocampal CA1 neuron counts and provide lasting protection against spatial memory deficits (38). rEpo has also been shown to stimulate DA release from the striatum (39), and exposure to HI has been shown to affect both DA receptor expression and DA reuptake transporter expression (3,40). EpoR was identified recently on adult DA neurons (41).…”

Section: Epo Protects Dopaminergic Neuronsmentioning

confidence: 99%

Erythropoietin Protects Dopaminergic Neurons and Improves Neurobehavioral Outcomes in Juvenile Rats after Neonatal Hypoxia-Ischemia

2005

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Brain injury as a result of hypoxia-ischemia remains a common cause of morbidity and mortality in neonates. No effective therapy is currently available. The hematopoietic cytokine erythropoietin (Epo) provides neuroprotection in many adult models of brain injury and is currently being investigated as a therapeutic agent for human stroke and spinal cord injury. We tested the hypothesis that recombinant Epo (rEpo) would improve neurobehavioral outcomes after neonatal hypoxic-ischemic brain injury. Postnatal day 7 rats underwent right common carotid artery occlusion followed by a 90-min exposure to 8% oxygen. Rats were subsequently treated with rEpo or placebo. Sensory neglect and apomorphine-induced rotation were measured at P27 and P28. Rats were killed at P30, blood was drawn, and the brains were perfusion-fixed for histology and immunohistochemistry. No differences in gross brain injury between rEpo and placebotreated rats were found. Neonatal rEpo treatment protected dopamine neurons as indicated by the preservation of tyrosine hydroxylase-positive cells in the substantia nigra pars compacta and ventral tegmental area. rEpo treatment also improved functional outcomes by reducing sensory neglect and preventing the rotational asymmetry seen in control animals. No differences in hematocrit, white blood cell counts, neutrophil counts, or platelet counts were measured. We observed that rEpo treatment protected mesencephalic dopamine neurons and reduced the degree of behavioral asymmetries at 4 wk of life. On the basis of these findings, we conclude that further studies investigating the safety and efficacy of high-dose rEpo as a neuroprotective strategy are indicated in neonatal models of hypoxic-ischemic brain injury. Abbreviations ADHD, attention-deficit/hyperactivity disorder DA, dopamine Epo, erythropoietin EpoR, erythropoietin receptor HI, hypoxia-ischemia P, postnatal day rEpo, recombinant Epo SNpc, substantia nigra pars compacta TH, tyrosine hydroxylase VTA, ventral tegmental area Perinatal exposure to hypoxia-ischemia (HI) produces brain injury that is a significant source of morbidity and mortality for preterm and term neonates. Neonatal HI exposure initiates a multifactorial cascade that can persist for days, producing injury to multiple brain regions with corresponding motor, behavioral, and cognitive impairments. Although there are currently no effective therapies to ameliorate hypoxic-ischemic brain injury, several useful rodent models of neonatal brain injury are available. Using 7-d-old (P7) rat pups, which are comparable to near-term humans in brain maturity (1), the technique entails unilateral ligation of the common carotid artery and subsequent exposure of the animals to hypoxia (Rice-Vannucci model) (2). This procedure produces permanent unilateral brain injury in multiple regions, with specific impact on the basal ganglia including decreases in striatal dopamine (DA) receptors and increases in striatal DA transporters (3,4). Disruption of dopaminergic neurotransmission is suspect for several de...

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“…EPO receptors are also located in rat and mouse brain endothelial cells (23). A number of in vitro studies suggest that EPO may preserve cellular function during hypoglycaemia (8)(9)(10). A study by Miskowiak et al (24,25) has demonstrated that high-dose EPO treatment modulates neural processing in healthy adults and may improve cognitive function.…”

Section: Discussionmentioning

confidence: 99%

“…In vitro studies suggest that EPO may preserve cellular function during hypoglycaemia (8)(9)(10). Low EPO levels may be associated with more pronounced cerebral dysfunction during hypoglycaemia than higher levels in people with type 1 diabetes (1).…”

Section: Introductionmentioning

confidence: 99%

Erythropoietin and vascular endothelial growth factor as risk markers for severe hypoglycaemia in type 1 diabetes

Kristensen¹,

Pedersen‐Bjergaard²,

Schalkwijk³

et al. 2010

European Journal of Endocrinology

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Objective: Circulating erythropoietin (EPO) and vascular endothelial growth factor (VEGF) increase during hypoglycaemia and may represent protective hormonal counter-regulatory responses. We tested the hypothesis that low levels of EPO and VEGF are associated with a higher frequency of severe hypoglycaemia in a cohort of patients with type 1 diabetes. Design: Prospective observational follow-up study. Methods: Totally 219 patients with type 1 diabetes (41% females, age 46G13 years (meanGS.D.), duration of diabetes 21G12 years, and HbAlc 8.5G1.1%) were followed in a 1-year observational study. Plasma EPO and serum VEGF levels were measured at baseline with ELISA. Events of severe hypoglycaemia defined by third party assistance were recorded and validated in telephone interviews within 24 h. Results: Totally 235 episodes of severe hypoglycaemia (1.1 episodes per patient-year) were reported by 82 patients (37%). At baseline, plasma EPO was 8.6 (3.1-34.3) U/l (median (range)), and serum VEGF was 52.2 (6.6-337) pg/ml. The levels of EPO and VEGF were not associated with frequency of severe and mild hypoglycaemia. The levels of EPO were not associated with age, sex, duration of diabetes, body mass index, HbAlc, C-peptide level or hypoglycaemia awareness status. The levels of VEGF were positively associated with age and female sex. Conclusions: Although several studies suggest that VEGF and EPO may affect brain function during hypoglycaemia, this study does not support random VEGF or EPO levels to determine future risk of severe hypoglycaemia in people with type 1 diabetes.

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Stimulating effect of erythropoietin on the release of dopamine and acetylcholine from the rat brain slice

Cited by 55 publications

References 12 publications

Effects of Erythropoietin on Memory Deficits and Brain Oxidative Stress in the Mouse Models of Dementia

Effects of Erythropoietin on Memory Deficits and Brain Oxidative Stress in the Mouse Models of Dementia

Erythropoietin Protects Dopaminergic Neurons and Improves Neurobehavioral Outcomes in Juvenile Rats after Neonatal Hypoxia-Ischemia

Erythropoietin and vascular endothelial growth factor as risk markers for severe hypoglycaemia in type 1 diabetes

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