In Parkinson's disease, degeneration of substantia nigra dopaminergic neurons is accompanied by damage on other neuronal systems. A severe denervation is for example seen in the locus coerulean noradrenergic system. Little is known about the relation between noradrenergic and dopaminergic degeneration, and the effects of noradrenergic denervation on the function of the dopaminergic neurons of substantia nigra are not fully understood. In this study, N-(2-chloroethyl)-N-ethyl-2-bromobenzylamine (DSP4) was injected in rats, whereafter behavior, striatal KCl-evoked dopamine and glutamate releases, and immunohistochemistry were monitored at 3 days, 3 months, and 6 months. Quantification of dopamine-beta-hydroxylase-immunoreactive nerve fiber density in the cortex revealed a tendency towards nerve fiber regeneration at 6 months. To sustain a stable noradrenergic denervation throughout the experimental timeline, the animals in the 6-month time point received an additional DSP4 injection (2 months after the first injection). Behavioral examinations utilizing rotarod revealed that DSP4 reduced the time spent on the rotarod at 3 but not at 6 months. KCl-evoked dopamine release was significantly increased at 3 days and 3 months, while the concentrations were normalized at 6 months. DSP4 treatment prolonged both time for onset and reuptake of dopamine release over time. The dopamine degeneration was confirmed by unbiased stereology, demonstrating significant loss of tyrosine hydroxylase-immunoreactive neurons in the substantia nigra. Furthermore, striatal glutamate release was decreased after DSP4. In regards of neuroinflammation, reactive microglia were found over the substantia nigra after DSP4 treatment. In conclusion, long-term noradrenergic denervation reduces the number of dopaminergic neurons in the substantia nigra and affects the functionality of the nigrostriatal system. Thus, locus coeruleus is important for maintenance of nigral dopaminergic neurons.

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.neuint.2019.104551DOI Listing

Publication Analysis

Top Keywords

substantia nigra
24
dopaminergic neurons
16
noradrenergic denervation
12
neurons substantia
12
nigra dopaminergic
8
kcl-evoked dopamine
8
days months
8
nerve fiber
8
dopamine release
8
dsp4 treatment
8

Similar Publications

Altered Nigral Amide Proton Transfer Imaging Signal Concordant With Motor Asymmetry in Parkinson's Disease: A Multipool CEST MRI Study.

NMR Biomed

February 2025

Department of Radiology, Beijing Hospital, National Center of Gerontology, Institute of Geriatric Medicine, Chinese Academy of Medical Sciences, Beijing, China.

Asymmetry is a natural characteristic of Parkinson's disease (PD), which can be used to distinguish PD from atypical parkinsonism. Chemical exchange saturation transfer (CEST) has demonstrated value in reflecting the subtle changes related to neuron loss and abnormal protein accumulation in PD but has not been used to investigate asymmetry in PD. This study aimed to examine asymmetrical changes in the mesencephalic nucleus of PD patients with motor asymmetry using four-pool CEST analysis and to explore the relationship between imaging asymmetry and motor asymmetry.

View Article and Find Full Text PDF

Background: Parkinson's disease (PD) and multiple system atrophy (MSA) are classified as α-synucleinopathies and are primarily differentiated by their clinical phenotypes. Delineating these diseases based on their specific α-synuclein (α-Syn) proteoform pathologies is crucial for accurate antemortem biomarker diagnosis. Newly identified α-Syn pathologies in PD raise questions about whether MSA exhibits a similar diversity.

View Article and Find Full Text PDF

[Parkin deletion affects PINK1/Parkin-mediated mitochondrial autophagy to exacerbate neuroinflammation and accelerate progression of Parkinson's disease in mice].

Nan Fang Yi Ke Da Xue Xue Bao

December 2024

Anhui Provincial Center for Neural Regeneration Technology and New Medical Materials Engineering Research, Bengbu Medical University, Bengbu 233000, China.

Objectives: To investigate the role of mitochondrial autophagy disorder caused by deletion of E3 ubiquitin ligase Parkin in neuroinflammation in a mouse model of MPTP-induced Parkinson's disease (PD).

Methods: Wild-type (WT) male C57BL/6 mice and Parkin mice were given intraperitoneal injections with MPTP or PBS for 5 consecutive days, and the changes in motor behaviors of the mice were observed using open field test. The effects of Parkin deletion on PD development and neuroinflammation were evaluated using immunofluorescence and Western blotting.

View Article and Find Full Text PDF

Mechanism of S100A9-mediated astrocyte activation via TLR4/NF-κB in Parkinson's disease.

Int Immunopharmacol

December 2024

Laboratory of Neurodegenerative Diseases and Neuroinjury Diseases, Wuxi School of Medicine, Jiangnan University, Wuxi, Jiangsu 214122, China; MOE Medical Basic Research Innovation Center for Gut Microbiota and Chronic Diseases, Wuxi School of Medicine, Jiangnan University, Wuxi, Jiangsu 214122, China. Electronic address:

Astrocyte-mediated neuroinflammation plays a key role in Parkinson's disease (PD) progression. The proinflammatory protein S100A9 is linked to various neurodegenerative diseases, but its involvement in astrocyte activation in PD remains unclear. Here, we investigate the role of S100A9 in astrocyte-mediated neuroinflammation in PD.

View Article and Find Full Text PDF

Background: Identifying Parkinson's disease (PD) during its initial phases presents considerable hurdles for clinicians.

Purpose: To examine the feasibility and efficacy of a machine learning model based on quantitative multiparametric magnetic resonance imaging (MRI) features in identifying early-stage PD.

Methods: We recruited 33 participants, including 19 with early-stage PD, 14 with advanced-stage PD and 20 healthy control subjects.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!