Depletion of norepinephrine of the central nervous system Down-regulates the blood glucose level in d-glucose-fed and restraint stress models

Park, Soo-Hyun; Kim, Sung‐Su; Lee, Jae Ryeong; Sharma, Naveen; Suh, Hwal

doi:10.1016/j.neulet.2016.02.055

Cited by 4 publications

(5 citation statements)

References 35 publications

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“…First, we examined whether continuous intravenous infusion of a glucose solution can affect RS-induced elevation of plasma catecholamine. In agreement with previous findings of the effects of RS on plasma catecholamine (Kvetnansky et al, 1992;Pajovic et al, 2006) and glucose (Park et al, 2016), exposure to RS increased plasma catecholamine and blood glucose levels in this study. Furthermore, we found that blood glucose levels after RS did not differ between groups for three doses (1%, 5% or 10%) of glucose solutions.…”

Section: Discussionsupporting

confidence: 94%

Glucose infusion suppresses acute restraint stress-induced peripheral and central sympathetic responses in rats

Yamaguchi

Kakinuma

Yakura

et al. 2022

Autonomic Neuroscience

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Section: Discussionsupporting

confidence: 94%

Glucose infusion suppresses acute restraint stress-induced peripheral and central sympathetic responses in rats

Yamaguchi

Kakinuma

Yakura

et al. 2022

Autonomic Neuroscience

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“…The blood glucose level of Dbh −/− mice was not different to that of control after fasting for 24 hr (Ste Marie & Palmiter, ). In Park's study, the blood glucose levels showed no difference compared with that of the control after d ‐glucose‐feeding for 90 min (S. H. Park et al, ). Luo, Luo, and Cincotta () found that the blood glucose levels of hamsters were similar to those of the control following 5 weeks’ infusion with NE.…”

Section: Discussionmentioning

confidence: 98%

“…However, the blood glucose level of Dbh −/− mice showed no differences compared with the control in the glucose tolerance test (Ste Marie & Palmiter, ). Park found that depleting NE at the supraspinal and spinal levels appeared to be responsible for downregulating the blood glucose levels in d ‐glucose‐fed mice (S. H. Park, Kim, Lee, Sharma, & Suh, ). These studies did not seem to support the use of NE to protect MSCs from apoptosis.…”

Section: Discussionmentioning

confidence: 99%

Norepinephrine protects against apoptosis of mesenchymal stem cells induced by high glucose

Kong

Cheng

et al. 2019

Journal Cellular Physiology

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In diabetes, the number of bone mesenchymal stem cells (MSCs) decreases and their differentiation is impaired. However, the exact mechanism is unclear. Patients with diabetes often experience sympathetic nerve injury. Norepinephrine (NE), a major mediator of the sympathetic nervous system, influences rat MSC migration in culture and in vivo. The present study aimed to investigate the effect of NE on MSCs under high glucose conditions; therefore MSCs were treated with high glucose and NE. High glucose-induced MSCs apoptosis, which was reversed by NE. To verify the effect of NE, mice underwent sympathectomy and were used to establish a diabetic model. Diabetic mice with sympathectomy had a higher apoptosis rate and higher levels of reactive oxygen species in their bone marrow-derived cells than diabetic mice without sympathectomy. High glucose inhibited p-AKT production and B-Cell CLL/ Lymphoma 2 expression, and promoted BAX and caspase-3 expression. NE reversed these effects of high glucose. An AKT inhibitor enhanced the effects of high glucose. Thus, NE had a protective effect on MSC apoptosis induced by high glucose, possibly via the AKT/BCL-2 pathway. K E Y W O R D S apoptosis, diabetes mellitus, mesenchymal stem cells, norepinephrine

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“…In the present paper, we used clonidine as a useful and well-known animal model of depression (Enginar and Eroglu, 1990; Parale and Kulkarni 1986; Park et al 2016) to investigate the antidepressant-like effect of 1MeTIQ. Clonidine is an alpha 2 adrenoceptor agonist used in clinical practice in the therapy of hypertension; however, depression is known to be a side effect of clonidine treatment.…”

Section: Discussionmentioning

confidence: 99%

“…Clonidine is an alpha 2 adrenoceptor agonist used in the treatment of hypertension. Clonidine has been shown to produce depressive behavioral effects in laboratory animals, and thus it has been suggested to be a suitable animal model of depression (Enginar and Eroğlu 1990; Lim et al 2016; Parale and Kulkarni 1986; Park et al 2016). …”

Section: Introductionmentioning

confidence: 99%

Antidepressant-Like Effect of the Endogenous Neuroprotective Amine, 1MeTIQ in Clonidine-Induced Depression: Behavioral and Neurochemical Studies in Rats

et al. 2017

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Biogenic amines such as norepinephrine, dopamine, and serotonin play a well-described role in the treatment of mood disorders especially depression. Animal models are widely used to study antidepressant-like effect in rodents; however, it should be taken into account that pharmacological models do not always answer to the complexity of the disease processes. This study verified the behavioral (forced swim test (FST), locomotor activity test) and neurochemical effects (monoamines metabolism) of a low dose of clonidine (0.1 mg/kg i.p.) which was used as an experimental model of depression. In such pharmacological model, we investigated the antidepressant-like effect of an endogenous neuroprotective amine, 1-methyl-1,2,3,4-tetrahydroisoquinoline (1MeTIQ) administered in a dose of 25 mg/kg (i.p.) before clonidine in the behavioral and neurochemical tests carried out in rats. The behavioral study has shown that clonidine produced depression in the locomotor activity test but did not cause pro-depressive effect in the FST. 1MeTIQ produced antidepressant-like effect in the FST and completely antagonized clonidine-induced sedation in the locomotor activity test. Neurochemical data demonstrated that clonidine produced a significant inhibition of monoamine metabolism in the central nervous system. The release of dopamine, noradrenaline, and serotonin as well as the rate of their metabolism were diminished in the investigated brain structures (frontal cortex, hypothalamus, and striatum). 1MeTIQ completely antagonized the clonidine-induced depression of monoaminergic systems and restored their levels to the control values. 1MeTIQ as an endogenous neuroprotective compound with a distinct antidepressant-like activity in rodents produces hope on the efficiency of antidepressant medicines for future practical clinical use.

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Depletion of norepinephrine of the central nervous system Down-regulates the blood glucose level in d-glucose-fed and restraint stress models

Cited by 4 publications

References 35 publications

Glucose infusion suppresses acute restraint stress-induced peripheral and central sympathetic responses in rats

Glucose infusion suppresses acute restraint stress-induced peripheral and central sympathetic responses in rats

Norepinephrine protects against apoptosis of mesenchymal stem cells induced by high glucose

Antidepressant-Like Effect of the Endogenous Neuroprotective Amine, 1MeTIQ in Clonidine-Induced Depression: Behavioral and Neurochemical Studies in Rats

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