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A synaptic mechanism underlying the behavioral abnormalities induced by manganese intoxication
P Calabresi1, M Ammassari-Teule, P Gubellini
1Clinica Neurologica, Dipartemente Neuroscienze, Universita' di Roma Tor Vergata, Via di Tor Vergata 135, Rome, 00133, Italy.
Neurobiology of Disease
|July 10, 2001
Summary
Manganese (Mn) intoxication in rats caused behavioral changes without motor deficits, linked to increased brain Mn. This suggests early manganism symptoms stem from abnormal dopamine D2 receptor control on brain pathways.
Area of Science:
- Neuroscience
- Toxicology
- Neuropharmacology
Background:
- Manganese (Mn) intoxication can cause neurological deficits.
- The early stages of manganism present behavioral changes without motor impairments.
- The precise synaptic mechanisms underlying early Mn intoxication are not fully understood.
Purpose of the Study:
- To characterize a rat model of manganese intoxication.
- To investigate the neurobiological underpinnings of behavioral disinhibition in early manganism.
- To identify specific synaptic pathways affected by manganese exposure.
Main Methods:
- Induction of manganese intoxication in a rat model.
- Behavioral testing to assess motor and non-motor functions.
- Electrophysiological recordings in brain slices to analyze neuronal activity.
- Pharmacological manipulation using receptor agonists and antagonists.
Main Results:
- Manganese intoxication led to behavioral disinhibition without significant motor alterations.
- Increased brain manganese levels were observed, uncoupled from striatal lesions.
- Enhanced presynaptic D2-like dopamine receptor-mediated inhibition of corticostriatal transmission was identified.
Conclusions:
- Early manganism symptoms may result from aberrant dopaminergic control of corticostriatal pathways.
- Selective dysfunction of D2-like dopamine receptors on glutamatergic terminals is implicated.
- Understanding these synaptic mechanisms is crucial for addressing manganese intoxication progression.