Faculty Bibliography

Magnetic trigeminal somatosensory responses from human subjects were recorded using a 14-channel magnetoencephalographic system. Sensory stimuli comprising a 15-ms vibration at frequencies of 50 Hz, 150 Hz and 250 Hz were given at randomized interstimulus intervals. Using a single dipole model, the neuronal sources of the evoked responses were determined, and mapped onto magnetic resonance images of each subject. Source localization analysis was based on the main peak of the averaged signal (M55). All of the sources were located deep in the anterior bank of the postcentral gyrus, corresponding to area 3b of somatosensory cortex SI. In all cases, the source for the upper lip was significantly higher in the vertical axis (0.6-1.1 cm) than for the lower lip, while the lower lip stimulation produced a larger response than the upper lip. Furthermore, statistically significant differences were found between the locations of the dipoles evoked by different frequency stimulation. The location of the response shifted with change in stimulation frequency, showing a trend among all subjects with medial shift between 150 and 250 Hz for both upper and lower lip. The accuracy of source localization calculated from magnetic fields ranged between +/- 0.9 and +/- 3.0 mm (SEM). These results demonstrate (1) that a large area of the somatosensory cortex is utilized for lip representation and (2) that the spatial displacement of the trigeminal somatosensory response may be related to the discrimination of frequency

The effect of the IgG from amyotrophic lateral sclerosis (ALS) patients was tested on the voltage-dependent barium currents (IBa) in mammalian dissociated Purkinje cells and in isolated P-type calcium channels in lipid bilayers. Whole cell clamp of Purkinje cells demonstrates that ALS IgG increases the amplitude of IBa without modifying their voltage kinetics. This increased IBa could be blocked by a purified nonpeptide toxin from Agelenopsis aperta venom (purified funnel-web spider toxin) or by a synthetic polyamine analog (synthetic funnel-web spider toxin) and by a peptide toxin from the same spider venom, omega-Aga-IVA. Similar results were obtained on single-channel recordings from purified P channel protein. The addition of ALS IgG increased single-channel IBa open time without affecting slope conductance. The results described above were not seen with normal human IgG nor with boiled ALS IgG. It is concluded that ALS IgG enhances inward current through P-type calcium channels. Since P-type Ca2+ channels are present in motoneuron axon terminals, we propose that the enhanced calcium current triggered by ALS IgG may contribute to neuronal damage in ALS