Autoimmune encephalomyelitis is accompanied by the injury of hippocampal neurons

• Autorzy: Kurkowska-Jastrzebska L. , Zaremba M. , Cudna A. , Piechal A. , Swiatkiewicz M. , Zaremba M. , Czlonkowska A. , Oderfeld-Nowak B.
• Języki publikacji: EN

Abstrakty

EN

Multiple sclerosis (MS) is associated with cognitive defi cits, developing independently from motor disorders. These defi cits may be associated with brain neuronal damage. In this study, using the experimental model for MS – autoimmune encephalomyelitis (EAE), we investigated whether EAE will result in the damage of hippocampal neurons and selective defi cits in learning and memory, and whether there may be a correlation between the two phenomena. Lewis rats 3 months old were injected with 4 millions of anti-MBP CD4+ T cells to evoke EAE. Animals suffered from tail and hind limb paresis and recovered after 10 dpi. T cells infi ltrated spinal cord and many brain regions including hippocampus. We demonstrated the decrease of pyramidal neurons in CA4 region by about 20%, as evaluated by stereological measurements, at 21 dpi. This was preceded by prolonged glial activation as well as by a rise of the pro-infl ammatory cytokine mRNA expression (IL-1β, IL-6 and TNF α). However, no differences in the water maze test were detected between the EAE and control groups, on 21 dpi and on 90 dpi. In conclusion, anti-MBP CD4+ T cells are capable of injuring hippocampal pyramidal neurons during EAE, probably, through the secretion of pro-infl ammatory cytokines. However, in the studied conditions, hippocampal neurodegeneration caused by T cells did not result in memory disturbances. Supported by the grant no N401- 1293-33 of the Ministry of Scientifi c Research and Information Technology in Poland.

• Wydawca: -
• Czasopismo: Acta Neurobiologiae Experimentalis
• Rocznik: 2009
• Tom: 69
• Numer: 3
• Opis fizyczny: p.321

Twórcy

autor

Kurkowska-Jastrzebska L.

• 2nd Department of Neurology, Institute of Psychatry and Neurology, Warsaw, Poland

autor

Zaremba M.

• Department of Experimental and Clinical Pharmacology, Medical University of Warsaw, Warsaw, Poland

autor

Cudna A.

• 2nd Department of Neurology, Institute of Psychiatry and Neurology, Warsaw, Poland

autor

Piechal A.

• Department of Experimental and Clinical Pharmacology, Medical University of Warsaw, Warsaw, Poland

autor

Swiatkiewicz M.

• Department of Experimental and Clinical Pharmacology, Medical University of Warsaw, Warsaw, Poland

autor

Zaremba M.

• Department of Molecular and Cellular Neurobiology, Nencki Institute of Experimental Biology Polish Academy of Sciences, Warsaw, Poland

autor

Czlonkowska A.

• 2nd Department of Neurology, Institute of Psychiatry and Neurology, Warsaw, Poland; Department of Experimental and Clinical Pharmacology, Medical University of Warsaw, Warsaw, Poland

autor

Oderfeld-Nowak B.

• Department of Molecular and Cellular Neurobiology, Nencki Institute of Experimental Biology Polish Academy of Sciences, Warsaw, Poland