Animals |
Female SJL/J mice |
Female C57BL/6 mice |
Female C57BL/6 mice |
Female C57BL/6 mice |
Female C57BL/6 mice |
EAE protocol |
150 μg of PLP139–151 15–20 × 106 activated lymph node cells i.p. |
50 μg of MOG35–55 100 ng of PTX i.p. |
100 μg of MOG35–55 300 ng of PTX i.p. |
200 μg of MOG35–55 500 ng of PTX i.p. |
100 μg of MOG35–55 800 ng of PTX i.p. |
Onset of motor deficits (days) |
Not specified |
Signs of tail weakness at 60 dpi |
Clinical signs of disease at 11 dpi |
Expected at 10–11 dpi [according to Ref. (29)] |
Limp tails at 9–13 dpi |
Behavioral parameters/paradigms |
Food and sucrose intake; social exploration |
Open field; rotarod; light/dark box; startle response and pre-pulse inhibition; learned helplessness paradigm |
Elevated plus maze; inhibitory avoidance task; object recognition task |
Open field; elevated plus maze |
Open field; elevated plus maze; forced swim test; tail suspension; sociability test; fear conditioning |
Cytokine levels |
IL-1β expression/level (RT-PCR/ELISA) and TNF-α expression (RT-PCR); PGE2 production (RIA assay); brain (cerebellum, hypothalamus, hippocampus, brain stem) |
IL-6 and TNF-α expression (RT-PCR); brain (hippocampus); 15, 29, 41, 59 dpi |
– |
TNF-α levels (ELISA); Brain (striatum); 10 dpi |
IL-1β and TNF-α expression (RT-PCR); brain (hippocampus, hypothalamus, amygdala) 7 dpi |
Main results |
Transient sickness behavior episodes associated with EAE attacks; Increased pro-inflammatory cytokine levels before the onset of motor impairment; decrease in pro-inflammatory cytokines at the peak of the neurological symptoms |
Anxiety- and depression-like behavior before the occurrence of motor deficits; Increased TNF-α and neuronal loss in the hippocampus |
No differences in anxiety-like behavior and memory in animals induced with EAE |
Anxiety-like behavior before the occurrence of motor deficits; Increased TNF-α levels and activated microglia in the striatum |
Anxiety- and depression-like behavior, memory loss and conditioned learning deficits in early stage of EAE; elevated levels of IL-1β and TNF-α in the hypothalamus and increased basal plasma corticosterone levels |