Lead intoxication induces noradrenaline depletion, motor nonmotor disabilities, and changes in the firing pattern of subthalamic nucleus neurons

M. Sabbar, C. Delaville, P. De Deurwaerdère, A. Benazzouz, N. Lakhdar-Ghazal
Neuroscience. 2012-05-01; 210: 375-383
DOI: 10.1016/j.neuroscience.2012.02.026

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Lead intoxication has been suggested as a high risk factor for the development of
Parkinson disease. However, its impact on motor and nonmotor functions and the
mechanism by which it can be involved in the disease are still unclear. In the
present study, we studied the effects of lead intoxication on the following: (1)
locomotor activity using an open field actimeter and motor coordination using the
rotarod test, (2) anxiety behavior using the elevated plus maze, (3)
“depression-like” behavior using sucrose preference test, and (4) subthalamic
nucleus (STN) neuronal activity using extracellular single unit recordings. Male
Sprague-Dawley rats were treated once a day with lead acetate or sodium acetate
(20 mg/kg/d i.p.) during 3 weeks. The tissue content of monoamines was used to
determine alteration of these systems at the end of experiments. Results show
that lead significantly reduced exploratory activity, locomotor activity and the
time spent on the rotarod bar. Furthermore, lead induced anxiety but not
“depressive-like” behavior. The electrophysiological results show that lead
altered the discharge pattern of STN neurons with an increase in the number of
bursting and irregular cells without affecting the firing rate. Moreover, lead
intoxication resulted in a decrease of tissue noradrenaline content without any
change in the levels of dopamine and serotonin. Together, these results show for
the first time that lead intoxication resulted in motor and nonmotor behavioral
changes paralleled by noradrenaline depletion and changes in the firing activity
of STN neurons, providing evidence consistent with the induction of atypical
parkinsonian-like deficits.

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