Neuroinflammatory and behavioural changes in Atp7b knockout mice, an animal model for Morbus Wilson

AbstractBackground and aimTail docking has been suggested as an animal model of neuropathy and pain based on findings of relations between the degree of neuroma formation and the docking length. We examined effects of docking length on behaviour of piglets during and 6 h after tail docking.MethodsPiglets were tail docked 2–4 d post-partum. We used 53 piglets and four treatments: intact (I), removal of either 25 (Q), 50 (H) or 75% (T) of the tail. The piglets were kept with sow and littermates under production conditions, and docked using a gas-heated instrument. Behaviour was observed during docking and for the following 6 h.ResultsTail docking led to behavioural changes, the magnitude of which to some extend depended on docking length. Increased docking length led to increased intra-procedural vocalization score (0, 0.6 ± 0.2, 1.4 ± 0.2 and 1.4 ± 0.2 for I, Q, H and T, respectively, P<0.001). In the initial 6h, increased docking length led to increased time spent in the heated creep area (2 ± 1%, 15 ± 6%, 18±8% and 30±6% for I, Q, H and T, respectively; P<0.05). Piglet posture was affected as well, showing that increased docking length led to decreased lying (71 ± 2%, 68 ± 2%, 61 ± 2% and 61 ± 2% for I, Q, H and T, respectively, P<0.01) and increased time spent active (24 ± 2%, 23 ± 2%, 32 ± 2% and 30 ± 3% for I, Q, H and T, respectively, P< 0.05). Pain specific behaviours such as trembling or tail flicking were registered and occurred in 5 ± 1% and 9 ± 1% of observations. However, no effects of docking length could be shown.ConclusionsPiglets responded behaviourally to tail docking. Increasing docking length led to increased pain responses such as intra-procedural vocalizations, hiding behaviour and reduced rest, indicative of increased pain. These results confirm earlier reports suggesting that tail docking might be suitable as an animal model for neuropathy and pain.

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Alterations of Amino Acids and Monoamine Metabolism in Male Fmr1 Knockout Mice: A Putative Animal Model of the Human Fragile X Mental Retardation Syndrome

Neural Plasticity ◽

10.1155/np.2001.285 ◽

2001 ◽

Vol 8 (4) ◽

pp. 285-298 ◽

Cited By ~ 17

Author(s):

Michael Gruss ◽

Katharina Braun

Keyword(s):

Amino Acids ◽

Animal Model ◽

Mental Retardation ◽

Fragile X Syndrome ◽

Knockout Mice ◽

Fragile X ◽

Fragile X Mental Retardation ◽

Behavioral Abnormalities ◽

Cortical Regions ◽

Knockout Animals

The Fragile X syndrome, a common form of mental retardation in humans, is caused by silencing the fragile X mental retardation (FMR1) geneleading to the absence of the encoded fragile X mental retardation protein 1 (FMRP). We describe morphological and behavioral abnormalities for both affected humans and Fmr1 knockout mice, a putative animal model for the human Fragile X syndrome. The aim of the present study was to identify possible neurochemical abnormalities in Fmr1 knockout mice, with particular focus on neurotransmission. Significant region-specific differences: of basal neurotransmitter and metabolite levels were found between wildtype and Fmr1 knockout animals, predominantly in juveniles (post-natal days 28 to 31). Adults (postnatal days 209 to 221) showed only few abnormalities as compared with the wildtype. In juvenile knockout mice, aspartate and taurine were especially increased in cortical regions, striatum, hippocampus, cerebellum, and brainstem. In addition, juveniles showed an altered balance between excitatory and inhibitory amino acids in the caudal cortex, hippocampus, and brainstem. We detected very few differences in monoamine turnover in both age stages. The results presented here provide the first evidence that lack of FMRP expression in FMRP knockout mice is accompanied by age-dependent, region-specific alterations in neurotransmission.

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