Hippocampal and cortical neuroinflammation in experimental autoimmune encephalomyelitis is not accompanied by deficits of spatial memory in a late phase of the disease

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

Abstrakty

EN

Cognitive dysfunctions are common features of multiple sclerosis. The exact mechanism of their appearance is unknown. The disconnection of some parts of the cortex reflecting an axonal loss, neuronal damage and alterations in synaptic transmission, have been postulated. In the present study, an autoimmune encephalomyelitis (EAE), a common model of multiple sclerosis, was induced passively by lymphocytes transfer, to evoke a one-phase disease in Lewis rats. The inflammatory reactions and neural injury in the hippocampus and frontal cortex were investigated. We found a decrease of the number of CA1 and CA4 pyramidal neurons by about 25% on 30 dpi and by about 50% in CA1 region on 90 dpi. This was accompanied by prolonged astroglial activation and by a rise of the pro-inflammatory cytokine mRNA expression (IL-1β, IL-6 and TNFα). A significant rise of NGF and BDNF was also found. In the frontal cortex, neural degeneration was not so evident. A slight astrocyte activation and a strong increase of expression of IL 6 on 30 dpi and IL1β and TNFα on 90 dpi was seen. Learning and memory abilities (Morris water-maze tests) were also evaluated 30 and 90 dpi. The mean latency of reaching the platform, the swimming distance, the time spent in the goal quadrant and crossing parameters were estimated. The reaction of animals suffering from EAE was not different from that of the control group, in any of the tasks except 20% higher chance for reaching the platform on 30 dpi. We demonstrated therefore the lack of correlation between strong neuroinflammation in the hippocampus and cortex and the deficits in memory and learning ability at a late phase of the disease. However, the severity of motor impairment during earlier stages of the disease made difficult identification of any early cognitive deficits. The possibility exists that early deficits could be later compensated due to simultaneously occurring compensatory processes involving activity of neurotrophic factors.

• Wydawca: -
• Czasopismo: Acta Neurobiologiae Experimentalis
• Rocznik: 2011
• Tom: 71
• Numer: S
• Opis fizyczny: p.74-75

Twórcy

autor

Kurkowska-Jastrzebska I.

• Second Department of Neurology, Institute of Psychiatry and Neurology, Warsaw, Poland

autor

Swiatkiewicz M.

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

autor

Zaremba M.

• Department of Experimental and Clinical Pharmacology, Medical University of Warsaw, Warsaw, Poland
• Department of Molecular and Cellular Neurobiology, Nencki Institute of Experimental Biology PAS, Warsaw, Poland

autor

Piechal A.

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

autor

Cudna A.

• Second Department of Neurology, Institute of Psychiatry and Neurology, Warsaw, Poland

autor

Oderfeld-Nowak B.

• Department of Molecular and Cellular Neurobiology, Nencki Institute of Experimental Biology PAS, Warsaw, Poland

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