Early dysfunction of central serotonin system in a murine model of bovine spongiform encephalopathy Export

@article{citeulike:4196748, abstract = {The hypothesis of an early vulnerability of the serotonergic system to prion infection was investigated in a murine model of bovine spongiform encephalopathy (BSE). Behavioral tests targeted to serotonin functions were performed in the course of infection to evaluate circadian activity, anxiety-like behavior, pain sensitivity and the serotonin syndrome. The first behavioral change was a decrease in nocturnal activity detected at 30\% of incubation time. Further behavioral alterations including nocturnal hyperactivity, reduced anxiety, hyperalgesia and exaggerated serotonin syndrome were observed at 60-70\% of incubation time, before the onset of clinical signs. The same tests performed in serotonin-depleted mice and in prion protein-deficient mice revealed behavioral abnormalities similar in many aspects to those of BSE-infected mice. Histological and biochemical analysis showed alterations of the serotonergic system in BSE-infected and prion protein-deficient mice. These results indicate that BSE infection affects the homeostasis of serotonergic neurons and suggest that the disruption of prion protein normal function contributes to the early pathological changes in our mouse model of BSE. A similar process may occur in the human variant Creutzfeldt-Jacob disease, as suggested by the early symptoms of alterations in mood, sleep and pain sensitivity.}, author = {Vidal, C. and Herzog, C. and Haeberle, A. M. and Bombarde, G. and Miquel, M. C. and Carimalo, J. and Launay, J. M. and Mouillet-Richard, S. and Lasm\'{e}zas, C. and Dormont, D.}, citeulike-article-id = {4196748}, citeulike-linkout-0 = {http://dx.doi.org/10.1016/j.neuroscience.2009.02.072}, citeulike-linkout-1 = {http://linkinghub.elsevier.com/retrieve/pii/S0306452209002516}, day = {10}, doi = {10.1016/j.neuroscience.2009.02.072}, issn = {03064522}, journal = {Neuroscience}, keywords = {5ht, bse, neurotransmitter, prion}, month = {March}, posted-at = {2009-03-20 02:08:08}, priority = {0}, title = {Early dysfunction of central serotonin system in a murine model of bovine spongiform encephalopathy}, url = {http://dx.doi.org/10.1016/j.neuroscience.2009.02.072}, year = {2009} }

TY - JOUR ID - citeulike:4196748 L3 - citeulike-article-id:4196748 N2 - The hypothesis of an early vulnerability of the serotonergic system to prion infection was investigated in a murine model of bovine spongiform encephalopathy (BSE). Behavioral tests targeted to serotonin functions were performed in the course of infection to evaluate circadian activity, anxiety-like behavior, pain sensitivity and the serotonin syndrome. The first behavioral change was a decrease in nocturnal activity detected at 30% of incubation time. Further behavioral alterations including nocturnal hyperactivity, reduced anxiety, hyperalgesia and exaggerated serotonin syndrome were observed at 60-70% of incubation time, before the onset of clinical signs. The same tests performed in serotonin-depleted mice and in prion protein-deficient mice revealed behavioral abnormalities similar in many aspects to those of BSE-infected mice. Histological and biochemical analysis showed alterations of the serotonergic system in BSE-infected and prion protein-deficient mice. These results indicate that BSE infection affects the homeostasis of serotonergic neurons and suggest that the disruption of prion protein normal function contributes to the early pathological changes in our mouse model of BSE. A similar process may occur in the human variant Creutzfeldt-Jacob disease, as suggested by the early symptoms of alterations in mood, sleep and pain sensitivity. JF - Neuroscience SN - 03064522 TI - Early dysfunction of central serotonin system in a murine model of bovine spongiform encephalopathy KW - 5ht KW - bse KW - neurotransmitter KW - prion AU - Vidal, C AU - Herzog, C AU - Haeberle, AM AU - Bombarde, G AU - Miquel, MC AU - Carimalo, J AU - Launay, JM AU - Mouillet-Richard, S AU - Lasmézas, C AU - Dormont, D PY - 2009/03/10/ UR - http://dx.doi.org/10.1016/j.neuroscience.2009.02.072 ER -