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Behavioral effects of intra-nigral microinjections of manganese chloride: interaction with nitric oxide
S Ponzoni1, F S Guimarães, E A Del Bel
1Physiology Department, State University of Londrina, PR, Brazil. ponza@sercomtel.com.br
Abstract:
1. Microinjection of manganese chloride (MnCl2) into the rat substantia nigra pars compacta (SNc) induces a neurodegenerative process manifested by apomorphine-induced rotational behavior. Manganese intoxication produces a parkinsonism-like phenotype in humans. 2. In addition to motor control the substantia nigra has also been proposed to be related to epilepsy and emotional behavior. 3. Although nitric oxide (NO) participation in neurodegenerative processes is still questioned, neurons stained for NAPDH-diaphorase, a marker of NO-producing cells, are spared in several experimental neuronal lesions. Additionally, NO has also been suggested to participate in motor control. 4. The objective of this study was to analyze the effects of MnCl2-induced nigral degeneration in audiogenic seizure susceptibility, anxiety and motor activity. We also analyzed if NO synthesis inhibition (N(G)-nitro-L-arginine 25 mg/Kg twice a day for 4 days) modifies MnCl2-induced neurodegenerative process. 5. MnCl2 (50 microg) microinjection into the SNc caused a statistical significant higher number of apomorphine (0.75 mg/kg s.c.)-induced rotations. No sensitization to audiogenic seizure was found but the lesion induced an increase of open arm exploration in the elevated plus maze, suggesting an anxiolytic effect. 6. The MnCl2-nigral lesion was accompanied by an increased number of NADPH-d positive neurons in the ipsilateral SNc and striatum (both sides). NO synthesis inhibition potentiated the MnCl2-nigral lesion and reversed the NADPH-d cell number increase. 7. The present results show that MnCl2-nigral lesion can influence emotional behavior and suggest that NO may modify the progression of manganese-induced degenerative process.
Insights
Manganese chloride (MnCl2) in the substantia nigra pars compacta (SNc) caused parkinsonism-like motor deficits and anxiety reduction in rats. Nitric oxide (NO) synthesis inhibition worsened this manganese-induced neurodegeneration.
Area of Science:
- Neuroscience
- Neurotoxicology
- Behavioral Neuroscience
Background:
- The substantia nigra pars compacta (SNc) is crucial for motor control, but also implicated in emotional behavior and epilepsy.
- Manganese chloride (MnCl2) induces parkinsonism-like symptoms in rats and humans.
- The role of nitric oxide (NO) in neurodegeneration and motor control is debated, though NO-producing neurons are often spared in lesions.
Purpose of the Study:
- To investigate MnCl2-induced nigral degeneration effects on seizure susceptibility, anxiety, and motor activity.
- To determine if inhibiting NO synthesis alters the MnCl2-induced neurodegenerative process.
Main Methods:
- Microinjection of MnCl2 into the rat SNc to induce neurodegeneration.
- Assessment of motor activity using apomorphine-induced rotations.
- Evaluation of anxiety using the elevated plus maze.
- Analysis of audiogenic seizure susceptibility.
- Inhibition of NO synthesis using N(G)-nitro-L-arginine.
Main Results:
- MnCl2 microinjection significantly increased apomorphine-induced rotations, indicating motor deficits.
- No change in seizure susceptibility was observed, but an anxiolytic effect (increased open arm exploration) was noted.
- MnCl2 lesions increased NADPH-diaphorase (NO-producing) neurons, an effect reversed by NO synthesis inhibition, which also potentiated the lesion.
Conclusions:
- MnCl2-induced nigral degeneration affects motor control and emotional behavior (anxiety).
- Nitric oxide (NO) appears to play a modulatory role in the progression of manganese-induced neurodegeneration.
- NO synthesis inhibition exacerbates MnCl2-induced nigral damage.
