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Evaluation of Hemisphere Lateralization with Bilateral Local Field Potential Recording in Secondary Motor Cortex of Mice
Published on: July 31, 2019
In mice, production of plasma IL-1 and IL-6 in response to MPTP is related to behavioral lateralization
Yan-Qin Shen1, Guillaume Hebert, Yun Su
1Department of Microbiology and Immunology, Shantou University Medical College, 22 Xinling Road, Shantou 515031, Guangdong, PR China.
Abstract:
1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) induces dopaminergic neuron death in substantia nigra and dopamine loss in striatum, similar to those observed in Parkinson disease. Given MPTP can also induce alterations in brain cytokines and in peripheral immune parameters, we hypothesize that MPTP can induce an elevation of plasma cytokines. We have previously shown that cytokine production depends on behavioral lateralization in certain conditions. Therefore, we further postulate that the MPTP-induced plasma cytokines are related to behavioral lateralization. To answer these questions, C57BL/6J male mice, selected for paw preference, were injected with 25 mg/kg MPTP ip for five consecutive days and were decapitated at day 1, day 3, or day 14 after the last injection. Striatal DA and DOPAC concentration were measured by HPLC and plasma levels of IL-1beta and IL-6 were quantified by ELISA. The results showed that after MPTP treatment, striatal DA content was dramatically decreased, IL-1beta levels increased on day 3, while IL-6 levels increased on day 14. Interestingly, behavioral lateralization influenced DA/DOPAC ratio as well as plasma IL-1beta and IL-6 levels. In left-pawed mice, MPTP induced a higher decrease of DA/DOPAC ratio than in right-pawed mice. The increase of IL-1beta was observed in left-pawed but not in right-pawed mice. The elevation of IL-6 was higher in right-pawed mice than in left-pawed mice. These results have clearly demonstrated our hypotheses, that MPTP can induce increase of plasma IL-1beta and IL-6 levels in mice, and this effect is shaped by behavioral lateralization.
Insights
1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) increases plasma cytokines IL-1beta and IL-6 in mice. This MPTP-induced cytokine elevation is influenced by behavioral lateralization, impacting dopamine levels and immune responses.
Area of Science:
- Neuroscience
- Immunology
- Pharmacology
Background:
- 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) is a neurotoxin that causes dopaminergic neuron death, mimicking Parkinson disease pathology.
- MPTP exposure affects both central nervous system cytokines and peripheral immune parameters.
- Previous research indicates that cytokine production can be influenced by behavioral lateralization.
Purpose of the Study:
- To investigate whether MPTP administration elevates plasma cytokine levels in mice.
- To determine if MPTP-induced plasma cytokine changes are associated with behavioral lateralization.
- To examine the relationship between MPTP, dopamine levels, and behavioral lateralization.
Main Methods:
- C57BL/6J male mice, selected for paw preference, received daily MPTP injections (25 mg/kg) for five consecutive days.
- Mice were euthanized at 1, 3, or 14 days post-injection.
- Striatal dopamine (DA) and DOPAC concentrations were measured using High-Performance Liquid Chromatography (HPLC).
- Plasma levels of Interleukin-1 beta (IL-1beta) and Interleukin-6 (IL-6) were quantified via Enzyme-Linked Immunosorbent Assay (ELISA).
Main Results:
- MPTP treatment significantly decreased striatal DA content.
- Plasma IL-1beta levels increased by day 3, while IL-6 levels elevated by day 14 post-MPTP injection.
- Behavioral lateralization modulated the MPTP effects: left-pawed mice showed a greater decrease in the DA/DOPAC ratio, increased IL-1beta, and lower IL-6 elevation compared to right-pawed mice.
Conclusions:
- MPTP administration leads to increased plasma levels of IL-1beta and IL-6 in mice.
- The observed elevation in plasma cytokines following MPTP exposure is significantly shaped by the animal's behavioral lateralization.
- These findings suggest a complex interplay between neurotoxicity, immune response, and lateralization in the context of Parkinson disease models.
