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. 2011 May 20;217(1):63–79. doi: 10.1007/s00429-011-0327-8

Table 1.

List of monkeys subjected to permanent primary motor cortex lesion and included in the present study with identification code

Mk-CE Mk-JU Mk-GE Mk-RO Mk-BI Mk-VA Mk-SL Mk-MO Mk-AV Mk-JO Mk-JA
Treatment None None None None None Anti-Nogo-A antibody Anti-Nogo-A antibody Anti-Nogo-A antibody Sham-cell therapy Cell therapy Cell therapy
Age at time of lesion (rounded 0.5 year) 4.5 5 5 4 5 5.5 5.5 5.5 3.5 3.5 4
Weight at time of lesion 3.8 3.6 2.8 3.2 5 4.9 4.6 5.6 4.3 3.4 4.3
Volume of ibotenic acid injected (μl) 40 40 13 18 29.7 15.5 18 20 15 15 38a
No. of ICMS sites injected with ibotenic acid 21 21 13 12 29 11 12 20 10 10 38
Total volume of lesion (mm³), gray matter (motor cortex + post-central gyrus) 112.8 63.01 48.7 14 20.13 20 78.2 41.8 33.2 33.6 22.2
Volume of lesion in post-central gyrus (mm³) 10.1 0 7.6 0 0 5.8 1.8 0 0 3.8 2.5
Lesion spread subcortically to the white matter (mm³) 86.5 28.9 0 0 0 0 130.6 0 69.8 23.6 38.4

Mk-LA (involved only in the transient inactivation of M1 with infusion of muscimol) was 5 years old and weighted 2.6 kg. A total volume of 15 μl of muscimol was infused in M1, at 10 sites, previously identified based on ICMS (see text)

aIn Mk-JA, nearly the same amount of ibotenic acid was injected as in the first two monkeys (Mk-CE and Mk-JU). However, in contrast to the other two monkeys, Mk-JA suffered several epileptic attacks immediately after the lesion. The monkey Mk-JA was treated with an anti-epileptic drug (Luminal), preventing other episodes. The anti-epileptic drug is known to counteract the excitotoxic effect of ibotenic acid, yielding a smaller volume of lesion as compared to the other two monkeys which received a comparable volume of ibotenic acid