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Published on: January 7, 2014
LPS-induced oxidative stress and inflammatory reaction in the rat striatum
Karolina Noworyta-Sokołowska1, Anna Górska, Krystyna Gołembiowska
1Institute of Pharmacology, Polish Academy of Sciences, Smętna 12, PL 31-343 Kraków, Poland. nfgolemb@cyf-kr.edu.pl.
Background:
Inflammation-induced microglia activation and increased oxidative stress have been observed in neurodegenerative disorders, such as Parkinson's disease. The aim of our study was to determine the appropriate dose and route of LPS administration to study hydroxyl radical generation and extracellular level of dopamine (DA), glutamate (GLU) and adenosine (ADN) in the rat striatum as markers of DA neuron damage and glial cell activation. The effect of LPS administration on DA, DOPAC, HVA and hydroxyl radical tissue level was also examined.
Methods:
LPS was given to rats in a single dose of 10 mg/kg ip, repeatedly for 5 days in a dose of 5 mg/kg ip and intrastriatally at doses 5, 20 and 40 μg/4 μl. The extracellular level of DA, hydroxyl radical, ADN and GLU were assayed in striatal dialysates using HPLC with electrochemical, fluorescence and VIS detection, respectively.
Results:
A single ip LPS (10 mg/kg) administration increased hydroxyl radical production but did not affect extracellular DA, GLU and ADN level. Repeated ip LPS (5 × 5 mg/kg) treatment decreased extracellular level of DA, GLU, ADN and production of hydroxyl radical. LPS (5 and 10 μg) given intrastriatally increased hydroxyl radical production, extracellular GLU and ADN level from 0 to 180 min after administration, but did not influence DA level. LPS (5, 20 and 40 μg) decreased striatal DA and DOPAC content, but increased HVA and hydroxyl radical level 72 h after intrastriatal administration.
Conclusions:
Our data indicate that local intrastriatal LPS administration activates glial cells and increases production of free radicals and secretion of GLU and ADN in early phase of inflammation. The damage of DA neurons is observed 72 h after local LPS administration.
Insights
Lipopolysaccharide (LPS) administration in rats activates glial cells and increases free radical production. Intrastriatal LPS causes dopamine neuron damage 72 hours post-administration, offering insights into neuroinflammation.
Area of Science:
- Neuroscience
- Neuroinflammation
- Oxidative Stress
Background:
- Neuroinflammation and oxidative stress are implicated in neurodegenerative diseases like Parkinson's.
- Microglia activation is a key feature of these conditions.
Purpose of the Study:
- To determine optimal lipopolysaccharide (LPS) dose and route for studying hydroxyl radical generation and neurotransmitter levels.
- To investigate markers of dopamine (DA) neuron damage and glial cell activation in the rat striatum.
Main Methods:
- Rats received LPS via intraperitoneal (ip) or intrastriatal (IS) administration at varying doses and durations.
- Extracellular levels of DA, glutamate (GLU), adenosine (ADN), and hydroxyl radical were measured using High-Performance Liquid Chromatography (HPLC).
Main Results:
- Single ip LPS increased hydroxyl radical but not extracellular neurotransmitters.
- Repeated ip LPS decreased extracellular DA, GLU, ADN, and hydroxyl radical.
- Intrastriatal LPS increased hydroxyl radical, GLU, and ADN early on, with DA neuron damage observed 72 hours later.
Conclusions:
- Local intrastriatal LPS administration effectively activates glial cells and elevates free radicals, GLU, and ADN.
- Dopaminergic neuron damage is a delayed consequence of intrastriatal LPS administration, occurring at 72 hours.
