Experimental studies of remarkable monoamine releases and neural resistance to the transient ischemia and reperfusion

Yoshimoto, Kanji; Namera, Akira; Arima, Yasunobu; Nagao, Tsuneatsu; Saji, Hiroh; Takasaka, Tomokazu; Uemura, Takeshi; Watanabe, Yoshihisa; Ueda, Seinosuke; Nagao, Masataka

doi:10.1016/j.pathophys.2014.08.005

Cited by 6 publications

(4 citation statements)

References 22 publications

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“…In recent years, a growing number of studies have indicated the involvement of dopaminergic systems in stroke modulation (Gower and Tiberi, 2018). The results of microdialysis of the present study demonstrated that cerebral ischemia induced a robust and transient release of DA extracellularly in the striatum, which is consistent with previous studies (Globus et al, 1988;Tsukada et al, 2004;Li et al, 2010;Yoshimoto et al, 2014). Moreover, the dynamic variations of DOPAC and HVA were consistent with that reported previously (Globus et al, 1988).…”

Section: Discussionsupporting

confidence: 92%

Neuroprotective Effects of Salidroside on Cerebral Ischemia/Reperfusion-Induced Behavioral Impairment Involves the Dopaminergic System

et al. 2019

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Salidroside, a phenylpropanoid glycoside, is the main bioactive component of Rhodiola rosea L. Salidroside has prominent anti-stroke effects in cerebral ischemia/reperfusion models. However, the underlying mechanisms of its actions are poorly understood. This study examined the anti-stroke effects of salidroside in middle cerebral artery occlusion (MCAO)-induced rat model of stroke and its potential mechanisms involving the dopaminergic system. Salidroside administration increased the levels of dopamine (DA), homovanillic acid (HVA), and 3,4-dihydroxyphenylacetic acid (DOPAC) in the ipsilateral striatum after induction of transient ischemia, which were assessed using microdialysis with high-performance liquid chromatography coupled with electrochemical detection (HPLC-ECD). Furthermore, treatment with salidroside ameliorated neurobehavioral impairment, assessed with the modified neurological severity scores (mNSS), the balance beam test, and the foot fault test. Moreover, enzyme-linked immunosorbent assay (ELISA) suggested that MCAO-induced reduction in monoamine oxidase (MAO) was inhibited by salidroside. Immunohistochemical and immunofluorescence analyses revealed high level of tyrosine hydroxylase (TH) in the ipsilateral striatal caudate putamen (CPu) after cerebral ischemia/ reperfusion, which could be further elevated by salidroside. In addition, salidroside could reverse the decreased immunoreactivity of TH in the substantia nigra pars compacta (SNpc). These results suggest that the anti-stroke effects of salidroside in MCAO-induced cerebral ischemia/reperfusion may involve the modulation of monoamine metabolism in the striatum and SNpc, which may be related to the function of the dopaminergic system in the rat brain.

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Section: Discussionsupporting

confidence: 92%

Neuroprotective Effects of Salidroside on Cerebral Ischemia/Reperfusion-Induced Behavioral Impairment Involves the Dopaminergic System

et al. 2019

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“…Excessive neurotransmitter release is strongly associated with the neuronal damage and death upon cerebral ischemic damage [ 62 , 63 ]. It has been shown that NMDA receptors are overstimulated due to excessive glutamate release [ 64 , 65 ], and other monoamine neurotransmitters such as DA, serotonin (5-HT) [ 66 , 67 ] and NA [ 68 , 69 ] are released upon cerebral ischemia and play roles in ischemic damage. A previous study in gerbils showed that the regional turnover of homovanillic acid (HA)/DA increased 15 min after 1 h of bilateral brain ischemia [ 70 ].…”

Section: Discussionmentioning

confidence: 99%

What is the protective effect of preischemic kisspeptin-10 administration against ischemia/reperfusion injury of striatum on mice?

Akkaya¹,

Sümer²,

Kutlu³

et al. 2022

Turkish Journal of Medical Sciences

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Background/aim Kisspeptin is a neuropeptide with a primary role on the onset of puberty and has beneficial effects on ischemia/reperfusion (I/R) injury. In this study, we aimed to investigate the effect of kisspeptin administration on striatal I/R injury in mice. Material and methods Forty adult C57/BL6 mice were randomly divided into four groups: Sham, Kisspeptin, I/R, and I/R + Kisspeptin groups. The groups were administered with either physiological saline (Sham and I/R groups) or kisspeptin (Kisspeptin and I/R + Kisspeptin groups) intraperitoneally 40 min before the operation. A microdialysis probe was placed in the right striatum according to stereotaxic coordinates. During the experimental period, artificial cerebrospinal fluid was passed through the micropump. Then, transient cerebral ischemia was established by compressing both common carotid arteries with an aneurysm clip for 15 min and animals were reperfused for 2 h. Throughout the process of microdialysis (before, during and after I/R period), samples were collected to measure dopamine (DA), noradrenaline (NA), and 3,4-dihydroxyphenylglycine (DHPG) at intervals of 20 min continuously. At the end of the reperfusion period, the animals were decapitated, striatum was dissected, half of the animals were used for oxidative stress analyses (reduced glutathione, glutathione S-transferase (GST), superoxide dismutase (SOD), malondialdehyde (MDA), and the other half were used for histopathology analyses. Results Number of glial cells was significantly increased in kisspeptin-administered groups. DA levels in ischemic animals were decreased by kisspeptin administration (p < 0.0001). NA levels were reduced in animals administered with kisspeptin without I/R injury (p < 0.05). DHPG levels reduced during the reperfusion period in ischemic animals (p < 0.05). Kisspeptin did not exhibit a significant antioxidant activity in the ischemic animals, while GST and SOD levels were reduced in the I/R + kisspeptin group compared to the kisspeptin group (p < 0.05). Conclusion Our results suggest that kisspeptin may be regulating the neurotransmitter release and metabolism, as well as inflammatory response in brain upon I/R injury.

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“…It is well recognized that the excessive releases of GLu can provoke enzymatic process leading to irreversible neuronal injury (Guyot et al, 2001 ; Li and Yan, 2010 ). Some evidences indicate that the excessive release of DA and 5-HT may involve the generation of cytotoxic free radicals and aggravate excitotoxicity of excitatory amino acid (Cadet et al, 2000 ; Yoshimoto et al, 2014 ). It has been reported that the pretreatment of puerarin could attenuate glutamate-induced cell injury in a dose-dependent manner (Zhu et al, 2016 ).…”

Section: Resultsmentioning

confidence: 99%

Brain Pharmacokinetics and the Pharmacological Effects on Striatal Neurotransmitter Levels of Pueraria lobata Isoflavonoids in Rat

et al. 2017

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Isoflavonoids are putatively active components of Pueraria lobata and has been demonstrated prominent neuro-protection effect against cerebrovascular disorders, hypertension or Parkinson's disease (PD). However, the molecular basis for the beneficial effect of Pueraria lobata on nervous systems has not been well revealed. The present study aims to assess striatum exposure to main active isoflavonoids and changes of striatal extracellular neurotransmitters levels in rat brain after intravenous administration of Pueraria lobata isoflavonoids extracts (PLF), to further elucidate its' substantial bases for neuro activities. Fifteen rats were divided into 3 groups (five rats in each group) to receive a dose of PLF at 80 or 160 mg/kg or normal saline (vehicle), respectively. An LC-MS/MS method was employed to determine the concentrations of five main isoflavonoids and multiple neurotransmitters in microdialysate from striatal extracellular fluid (ECF) of the rats. The exposed quantities of puerarin (PU), 3′-methoxypuerarin (MPU), daidzein-8-C-apiosyl-(1-6)-glucoside (DAC), and 3′-hydroxypuerarin (HPU) in striatum were dose-dependent. The content of daidzein (DAZ) was too low to be detected in all dialysate samples through the experiment. Optimal dose PLF (80 mg/kg) promoted DA metabolism and inhibited 5-HT metabolism. No obvious change in the level of GLu was determined. The concentration of GABA presented a temporary decline firstly and then a gradual uptrend followed by a further downtrend. Higher dose (160 mg/kg) PLF could enhance the metabolism of both DA and 5-HT, and lower the extracellular level of GLu, without changing GABA concentrations, which might result in alleviation on excitatory toxicity under conditions, such as ischemia. The results infer that different dose of PLF should be chosen to achieve appropriate neurochemical modulation effects under conditions, such as hypertension or ischemia/stroke. These findings may significantly contribute to a better understanding of the neuroprotective effect of Pueraria lobata and provide new insights into its application toward neuro-degenerative diseases in the future.

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Experimental studies of remarkable monoamine releases and neural resistance to the transient ischemia and reperfusion

Cited by 6 publications

References 22 publications

Neuroprotective Effects of Salidroside on Cerebral Ischemia/Reperfusion-Induced Behavioral Impairment Involves the Dopaminergic System

Neuroprotective Effects of Salidroside on Cerebral Ischemia/Reperfusion-Induced Behavioral Impairment Involves the Dopaminergic System

What is the protective effect of preischemic kisspeptin-10 administration against ischemia/reperfusion injury of striatum on mice?

Brain Pharmacokinetics and the Pharmacological Effects on Striatal Neurotransmitter Levels of Pueraria lobata Isoflavonoids in Rat

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