Protective effects of berberine against MPTP-induced dopaminergic neuron injury through promoting autophagy in mice

2021 ◽  
Author(s):  
Han Deng ◽  
ZeGang Ma
Keyword(s):  
Dopaminergic Neurons ◽  
Dopaminergic Neuron ◽  
Protective Effects ◽  
Neuron Injury

Berberine protects dopaminergic neurons in SN of MPTP-induced mice via the enhancement of AMPK-mediated autophagy.

scholarly journals Endoplasmic Reticulum Stress Is Associated with the Mesencephalic Dopaminergic Neuron Injury in Stressed Rats

2021 ◽  
Vol 2021 ◽  
pp. 1-9
Author(s):  
Shiba Niu ◽  
Weibo Shi ◽  
Yingmin Li ◽  
Shanyong Yi ◽  
Yang Li ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
Dopaminergic Neurons ◽  
Dopaminergic Neuron ◽  
Stress Exposure ◽  
Double Immunofluorescence ◽  
Immunofluorescence Labelling ◽  
Neuron Injury ◽  
Mesencephalic Dopaminergic Neuron ◽  
Double Immunofluorescence Labelling

An increasing number of people are in a state of stress due to social and psychological pressures, which may result in mental disorders. Previous studies indicated that mesencephalic dopaminergic neurons are associated with not only reward-related behaviors but also with stress-induced mental disorders. To explore the effect of stress on dopaminergic neuron and potential mechanism, we established stressed rat models of different time durations and observed pathological changes in dopaminergic neurons of the ventral tegmental area (VTA) through HE and thionine staining. Immunohistochemistry coupled with microscopy-based multicolor tissue cytometry (MMTC) was employed to investigate the number changes of dopaminergic neurons. Double immunofluorescence labelling was used to investigate expression changes of endoplasmic reticulum stress (ERS) protein GRP78 and CHOP in dopaminergic neurons. Our results showed that prolonged stress led to pathological alteration in dopaminergic neurons of VTA, such as missing of Nissl bodies and pyknosis in dopaminergic neurons. Immunohistochemistry with MMTC indicated that chronic stress exposure resulted in a significant decrease in dopaminergic neurons. Double immunofluorescence labelling showed that the endoplasmic reticulum stress protein took part in the injury of dopaminergic neurons. Taken together, these results indicated the involvement of ERS in mesencephalic dopaminergic neuron injury induced by stress exposure.

Electroacupuncture therapy ameliorates motor dysfunction via brain-derived neurotrophic factor and glial cell line-derived neurotrophic factor in a mouse model of Parkinson's disease

2019 ◽  
Author(s):  
Malk Eun Pak ◽  
Sung Min Ahn ◽  
Da Hee Jung ◽  
Hong Ju Lee ◽  
Ki Tae Ha ◽  
...  
Keyword(s):  
Substantia Nigra ◽  
Mouse Model ◽  
Mouse Models ◽  
Neurotrophic Factor ◽  
Dopaminergic Neurons ◽  
Dopaminergic Neuron ◽  
Motor Dysfunction ◽  
Protective Effects ◽  
Neuron Loss ◽  
Dopaminergic Neuron Loss

Abstract Parkinson’s disease (PD) is characterized by dopaminergic neuron loss in the substantia nigra. However, specific sensory stimulation via electroacupuncture (EA) therapy may attenuate this loss by promoting the expression of endogenous neurotrophic factors in a manner similar to physical therapy. We investigated the potential protective effects of EA on dopaminergic neurons in a mouse model of PD and whether these effects are associated with the promotion of endogenous brain-derived neurotrophic factor (BDNF) and glial cell line-derived neurotrophic factor (GDNF). Mouse models of PD were generated using 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and 6-hydroxydopamine. Motor performance was assessed using behavioral tests, and Western blot experiments, enzyme-linked immunosorbent assays, and immunohistochemical assays were performed. In both mouse models, EA treatment ameliorated motor impairments and dopaminergic neuron loss; these changes were accompanied by increases in BDNF and GDNF. In the MPTP group, EA treatment improved motor dysfunction by attenuating dopaminergic neuron loss in the substantia nigra, similar to the effects of levodopa. EA treatment significantly upregulated BDNF and GDNF expression in both the substantia nigra and striatum. Moreover, EA treatment induced the expression of cAMP response element binding protein (CREB) as well as Akt and Pitx3 in dopaminergic neurons in the substantia nigra. However, levodopa treatment did not induce BDNF/GDNF activation or related signaling factors. Thus, EA therapy may exert protective effects on dopaminergic neurons by upregulating the expression of BDNF, GDNF, and related signaling factors, thereby improving motor function. Hence, EA may represent an effective adjuvant therapy for motor deficits in patients with PD.

Protective effects of minocycline on 3,4-methylenedioxymethamphetamine-induced neurotoxicity in serotonergic and dopaminergic neurons of mouse brain

2006 ◽  
Vol 544 (1-3) ◽  
pp. 1-9 ◽  
Author(s):  
Lin Zhang ◽  
Yukihiko Shirayama ◽  
Eiji Shimizu ◽  
Masaomi Iyo ◽  
Kenji Hashimoto
Keyword(s):  
Mouse Brain ◽  
Dopaminergic Neurons ◽  
Protective Effects

Transient High-Frequency Firing in a Coupled-Oscillator Model of the Mesencephalic Dopaminergic Neuron

2006 ◽  
Vol 95 (2) ◽  
pp. 932-947 ◽  
Author(s):  
Alexey S. Kuznetsov ◽  
Nancy J. Kopell ◽  
Charles J. Wilson
Keyword(s):  
Nmda Receptor ◽  
High Frequency ◽  
Dopaminergic Neurons ◽  
Dopaminergic Neuron ◽  
Receptor Activation ◽  
Oscillator Model ◽  
Coupled Oscillator ◽  
Depolarization Block ◽  
Nmda Receptor Activation ◽  
Coupled Oscillator Model

Dopaminergic neurons of the midbrain fire spontaneously at rates <10/s and ordinarily will not exceed this range even when driven with somatic current injection. When driven at higher rates, these cells undergo spike failure through depolarization block. During spontaneous bursting of dopaminergic neurons in vivo, bursts related to reward expectation in behaving animals, and bursts generated by dendritic application of N-methyl-d-aspartate (NMDA) agonists, transient firing attains rates well above this range. We suggest a way such high-frequency firing may occur in response to dendritic NMDA receptor activation. We have extended the coupled oscillator model of the dopaminergic neuron, which represents the soma and dendrites as electrically coupled compartments with different natural spiking frequencies, by addition of dendritic AMPA (voltage-independent) or NMDA (voltage-dependent) synaptic conductance. Both soma and dendrites contain a simplified version of the calcium-potassium mechanism known to be the mechanism for slow spontaneous oscillation and background firing in dopaminergic cells. The compartments differ only in diameter, and this difference is responsible for the difference in natural frequencies. We show that because of its voltage dependence, NMDA receptor activation acts to amplify the effect on the soma of the high-frequency oscillation of the dendrites, which is normally too weak to exert a large influence on the overall oscillation frequency of the neuron. During the high-frequency oscillations that result, sodium inactivation in the soma is removed rapidly after each action potential by the hyperpolarizing influence of the dendritic calcium-dependent potassium current, preventing depolarization block of the spike mechanism, and allowing high-frequency spiking.

scholarly journals Apelin-13 Protects Dopaminergic Neurons against Rotenone—Induced Neurotoxicity through the AMPK/mTOR/ULK-1 Mediated Autophagy Activation

2020 ◽  
Vol 21 (21) ◽  
pp. 8376
Author(s):  
Peng Chen ◽  
Youcui Wang ◽  
Leilei Chen ◽  
Ning Song ◽  
Junxia Xie
Keyword(s):  
Dopaminergic Neurons ◽  
Substantia Nigra Pars Compacta ◽  
Protective Effects ◽  
Gut Peptides ◽  
Neuroprotective Effects ◽  
Compound C ◽  
Apelin Receptor ◽  
Signaling Activation

Parkinson’s disease (PD) is characterized by the progressive loss of dopaminergic neurons in the substantia nigra pars compacta. Several brain–gut peptides are able to exert neuroprotective effects on the nigrostriatal dopaminergic system. Apelin-13 is a neuropeptide, conveying potential neuroprotective activities. However, whether, and how, apelin-13 could antagonize rotenone-induced neurotoxicity has not yet been elucidated. In the present study, rotenone-treated SH-SY5Y cells and rats were used to clarify whether apelin-13 has protective effects on dopaminergic neurons, both in vivo and in vitro. The results showed that apelin-13 could protect SH-SY5Y cells from rotenone-induced injury and apoptosis. Apelin-13 was able to activate autophagy, and restore rotenone induced autophagy impairment in SH-SY5Y cells, which could be blocked by the autophagy inhibitor 3-Methyladenine. Apelin-13 activated AMPK/mTOR/ULK-1 signaling, AMPKα inhibitor compound C, as well as apelin receptor blockage via siRNA, which could block apelin-13-induced signaling activation, autophagy activation, and protective effects, in rotenone-treated SH-SY5Y cells. These results indicated that apelin-13 exerted neuroprotective properties against rotenone by stimulating AMPK/mTOR/ULK-1 signaling-mediated autophagy via the apelin receptor. We also observed that intracerebroventricular injection of apelin-13 could alleviate nigrostriatal dopaminergic neuron degeneration in rotenone-treated rats. Our findings provide new insights into the mechanism by which apelin-13 might attenuate neurotoxicity in PD.

2.441 Nicotine provides protective effects in dopaminergic neurons via the nicotinic receptors

2007 ◽  
Vol 13 ◽  
pp. S138
Author(s):  
H. Takeuchi ◽  
T. Yanagida ◽  
K. Takata ◽  
Y. Kitamura ◽  
T. Taniguchi ◽  
...  
Keyword(s):  
Dopaminergic Neurons ◽  
Nicotinic Receptors ◽  
Protective Effects

Protective effects of fisetin and other berry flavonoids in Parkinson's disease

2017 ◽  
Vol 8 (9) ◽  
pp. 3033-3042 ◽  
Author(s):  
Pamela Maher
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Substantia Nigra ◽  
Dopaminergic Neurons ◽  
Degenerative Disease ◽  
Protective Effects

Parkinson's disease (PD) is an age-associated degenerative disease of the midbrain that results from the loss of dopaminergic neurons in the substantia nigra.

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