TABLE 3

Latency to veratridine-mediated (100.0 μM) depolarization in EAE and naive mice Spinal cords were removed from SJL/PLP-inoculated EAE and sham (age-matched) mice at between 2 and 5 weeks PI and placed in a grease-gap bath. The d.c. potential between the two compartments was assessed in response to local application of veratridine (10.0, 30.0, and 100.0 μM). The data are represented as the mean ± S.E.M. of the group for the latency to reach the maximum level of depolarization from the point of application of the 100.0 μM concentration of veratridine. Induction of EAE did not affect the latency to maximal depolarization.


Drug Application

Weeks PI

Avg. Sec. (±S.E.M.)

n

EAE Deficit Score Avg. Score (±S.E.M.)
Region
Group
A. Veratridine (100.0 μM) latency to peak in EAE and sham mice
Lumbar Sham 2 weeks PI 501 (±31) 20 0
3 weeks PI 519 (±23) 19 0
4 weeks PI 464 (±35) 18 0
5 weeks PI 436 (±25) 19 0
Lumbar EAE 2 weeks PI 411 (±30) 21 2.6 (±0.2)
3 weeks PI 570 (±53) 8 2.2 (±0.4)
4 weeks PI 532 (±52) 16 2.4 (±0.3)
5 weeks PI 526 (±42) 11 1.1 (±0.3)
B. Veratridine (100.0 μM) latency to peak in EAE and sham mice
Sacral Sham 2 weeks PI 449 (±29) 20 0
3 weeks PI 453 (±18) 19 0
4 weeks PI 478 (±28) 20 0
5 weeks PI 451 (±16) 19 0
Sacral EAE 2 weeks PI 458 (±32) 16 2.5 (±0.2)
3 weeks PI 507 (±26) 7 2.3 (±0.5)
4 weeks PI 428 (±17) 17 2.4 (±0.2)



532 (±41)
13
1.2 (±0.3)