The effect of lead, restraint stress or their co-exposure on the movement disorders incidence in male mice

Ali Hosseini-Sharifabad , Sara Naghibzadeh, Valiollah Hajhashemi

Abstract


Lead is known as an environmental contaminant with neurotoxic properties. In addition, people experience different types of chronic stress, especially in developing countries. It has been established that lead   or stress causes structural and physiological damages to the neural pathway like dopaminergic connections. Nevertheless, the effect of lead and restraint stress on movement behaviors when are experienced together has not been studied yet. In this study, male albino mice were randomly divided into different groups (n = 6). Lead acetate was daily injected at 15 mg/kg intraperitoneally for 2, 4, or 6 weeks. Restraint stress  (6 h in a day) was applied alone or in combination with lead acetate for 2, 4, or 6 weeks. The catalepsy, akinesia, and the balance of animals were measured by bar test, elevated beam device, and rotarod to evaluate the movement disorders. 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine, a known neurotoxin causes movement disorders, was used as positive control group. The results showed that exposure to the lead or stress or their combination for 6 weeks caused catalepsy, akinesia, and imbalance in the animals,while exposure for 2 or 4 weeks didn’t affect the movement items indices. The combination of leadand stress did not show any significant difference compared to the exposure to each of them individually.  From the findings, Lead, stress, and their combination caused movement disorders in a time dependent manner. Short time exposure did not change movement behavior. The co-exposure to the lead and stressdid not show additive or synergistic effects.


Keywords


Lead; Mice; Movement disorders; Restraint stress.

Full Text:

PDF

References


Tong S, von Schirnding YE, Prapamontol T. Environmental lead exposure: a public health problem of global dimensions. Bull World Health Organ. 2000;78(9):1068-1077.

Moosavirad SA, Rabbani M, Sharifzadeh M, Hosseini-Sharifabad A. Protective effect of vitamin C, vitamin B12 and omega-3 on lead-induced memory impairment in rat. Res Pharm Sci. 2016;11(5):390-396.

Chin-Chan M, Navarro-Yepes J, Quintanilla-Vega B. Environmental pollutants as risk factors for neurodegenerative disorders: Alzheimer and Parkinson diseases. Front Cell Neurosci. 2015;9:124.

Jones DC, Miller GW. The effects of environmental neurotoxicants on the dopaminergic system: A possible role in drug addiction. Biochem Pharmacol. 2008;76(5):569-581.

Lauretti E, Di Meco A, Merali S, Praticò D. Chronic behavioral stress exaggerates motor deficit and neuroinflammation in the MPTP mouse model of Parkinson’s disease. Transl Psychiatry. 2016;6:e733.

Smith LK, Jadavji NM, Colwell KL, Katrina Perehudoff S, Metz GA. Stress accelerates neural degeneration and exaggerates motor symptoms in a rat model of Parkinson’s disease. Eur J Neurosci. 2008;27(8):2133-2146.

Sugama S, Sekiyama K, Kodama T, Takamatsu Y, Takenouchi T, Hashimoto M, et al. Chronic restraint stress triggers dopaminergic and noradrenergic neurodegeneration: possible role of chronic stress in the onset of Parkinson’s disease. Brain Behav Immun. 2016;51:39-46

Campos AC, Fogaça MV, Aguiar DC, Guimarães FS. Animal models of anxiety disorders and stress. Braz J Psychiatry. 2013;5 Suppl 2:S101-11.

Coors A, De Meester L. Synergistic, antagonistic and additive effects of multiple stressors: predation threat, parasitism and pesticide exposure in Daphnia magna. J Appl Ecol. 2008;45(6):1820-1828.

Xu J, Yan HC, Yang B, Tong LS, Zou YX, Tian Y. Effects of lead exposure on hippocampal metabotropic glutamate receptor subtype 3 and 7 in developmental rats. J Negat Results Biomed. 2009;8(1):5-9.

Gibrat C, Saint-Pierre M, Bousquet M, Lévesque D, Rouillard C, Cicchetti F. Differences between subacute and chronic MPTP mice models: investigation of dopaminergic neuronal degeneration and α‐synuclein inclusions. J Neurochem. 2009;109(5):1469-1482.

Deacon RM. Measuring motor coordination in mice. J Vis Exp. 2013;(75):e2609. DOI: 10.3791/2609.

Khan MM, Kempuraj D, Thangavel R, Zaheer A. Protection of MPTP-induced neuroinflammation and neurodegeneration by Pycnogenol. Neurochem Int. 2013;62(4):379-388.

Sheidaei H. Buspirone improves haloperidol-induced Parkinson disease in mice through 5-HT1A recaptors. Daru. 2010;18(1):41-45.

Sedelis M, Schwarting RK, Huston JP. Behavioral phenotyping of the MPTP mouse model of Parkinson’s disease. Behav Brain Res. 2001; 125(1-2):109-125.

Luong TN, Carlisle HJ, Southwell A, Patterson PH. Assessment of motor balance and coordination in mice using the balance beam. J Vis Exp. 2011;(49). pii:2376. DOI: 10.3791/2376

Tavakoli-Nezhad M, Barron AJ, Pitts DK. Postnatal inorganic lead exposure decreases the number of spontaneously active midbrain dopamine neurons in the rat. Neurotoxicology. 2001;22(2):259-269.

Patra RC, Swarup D. Effect of antioxidant ascorbic acid, l-methionine or α tocopherol alone or along with chelator on cardiac tissue of lead-treated rats. Vet Arh. 2004;74(3):235-244.

Canfield RL, Gendle MH, Cory-Slechta DA. Impaired neuropsychological functioning in lead-exposed children. Dev Neuropsychol. 2004;26(1):513-540.

Adlard PA, Cotman CW. Voluntary exercise protects against stress-induced decreases in brain-derived neurotrophic factor protein expression. Neuroscience. 2004;124(4):985-992.

Ahima RS, Harlan RE. Charting of type II glucocorticoid receptor-like immunoreactivity in the rat central nervous system. Neuroscience. 1990;39(3):579-604.

Ercal N, Gurer-Orhan H, Aykin-Burns N. Toxic metals and oxidative stress part I: mechanisms involved in metal-induced oxidative damage. Curr Top Med Chem. 2001;1(6):529-539

Verma S, Dubey RS. Lead toxicity induces lipid peroxidation and alters the activities of antioxidant enzymes in growing rice plants. Plant Sci. 2003;164(4):645-655.

Lidsky TI, Schneider JS. Lead neurotoxicity in children: basic mechanisms and clinical correlates. Brain. 2003;126(Pt 1):5-19.

Virgolini MB, Chen K, Weston DD, Bauter MR, Cory-Slechta DA. Interactions of chronic lead exposure and intermittent stress: consequences for brain catecholamine systems and associated behaviors and HPA axis function. Toxicol Sci. 2005;87(2):469-482.

Tsigos C, Chrousos GP. Hypothalamic-pituitary-adrenal axis, neuroendocrine factors and stress. J Psychosom Res. 2002;53(4):865-871.

Stewart WF, Schwartz BS. Effects of lead on the adult brain: a 15‐year exploration. Am J Ind Med. 2007;50(10):729-739.

Gump BB, Stewart P, Reihman J, Lonky E, Darvill T, Parsons PJ, et al. Low-level prenatal and postnatal blood lead exposure and adrenocortical responses to acute stress in children. Environ Health Perspect. 2007;116(2):249-255.

Cory-Slechta DA, Virgolini MB, Thiruchelvam M, Weston DD, Bauter MR. Maternal stress modulates the effects of developmental lead exposure. Environ Health Perspect. 2004;112(6):717-730.

Virgolini MB, Rossi-George A, Weston D, Cory-Slechta DA. Influence of low level maternal Pb exposure and prenatal stress on offspring stress challenge responsivity. Neurotoxicology. 2008;29(6):928-939.

da Silva Torres IL, Cucco SN, Bassani M, Duarte MS, Silveira PP, Vasconcellos AP, et al. Long-lasting delayed hyperalgesia after chronic restraint stress in rats-effect of morphine administration. Neurosci Res. 2003;45(3):277-283.

McEwen BS. Plasticity of the hippocampus: adaptation to chronic stress and allostatic load. Ann N Y Acad Sci. 2001;933:265-277.

Van de Kar LD, Blair ML. Forebrain pathways mediating stress-induced hormone secretion. Front Neuroendocrinol. 1999;20(1):1-48.

Rougé-Pont F, Deroche V, Le Moal M, Piazza PV. Individual differences in stress‐induced dopamine release in the nucleus accumbens are influenced by corticosterone. Eur J Neurosci. 1998;10(12):3903-3907.


Refbacks

  • There are currently no refbacks.


Creative Commons LicenseThis work is licensed under a Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International License which allows users to read, copy, distribute and make derivative works for non-commercial purposes from the material, as long as the author of the original work is cited properly.