Brain-machine interfaces (BMIs) use signals recorded directly from the brain to control an external device, such as a computer cursor or prosthetic limb. These control signals have been recorded from different levels of the brain, from field potentials at the scalp or cortical surface to single neuron action potentials. At present, the more invasive recordings have better signal quality, but also lower stability over time. Recently, subdural field potentials have been proposed as a stable, good quality source of control signals, with the potential for higher spatial and temporal bandwidth than EEG. Here we used finite element modeling in rats and humans and spatial spectral analysis in rats to compare the spatial resolution of signals recorded epidurally (outside the dura), with those recorded from subdural and scalp locations. Resolution of epidural and subdural signals was very similar in rats, and somewhat less so in human models. Both were substantially better than signals recorded at the scalp. Resolution of epidural and subdural signals in humans was much more similar when the cerebrospinal fluid layer thickness was reduced. This suggests that the less invasive epidural recordings may yield signals of similar quality to subdural recordings, and hence may be more attractive as a source of control signals for BMIs.

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SUMMARY1. Current through Ca2" channels was studied in acutely isolated guinea-pig pyramidal neurones from the CA3 region of the hippocampus. Both the whole-cell and single-channel patch-clamp configuration were used.2. Both whole-cell and single-channel currents displayed holding potential sensitivity indicative of two high-threshold currents similar to L-and N-type Ca2" currents.3. A low-threshold whole-cell current, similar to T-type current seen in dorsal root ganglion (DRG) neurones, activated at -60 to -50 mV and was blocked by nickel (100 /M) and amiloride (500 #M). Exposure to 50 /M-cadmium left a fraction of the T-type current intact but blocked N-and L-type current. This T-like component needed extremely negative holding potentials to be completely reprimed.4. Whole-cell N-type Ca2" channel current was blocked by wo-conotoxin (1 ,tM). From a holding potential of -90 mV, wo-conotoxin decreased the peak whole-cell current by 33 %.5. A slowly inactivating high-threshold Ca2+ current (L-type) that was present at depolarized holding potentials, displayed dihydropyridine sensitivity. From a holding potential of -50 mV, addition of the dihydropyridine Ca2+ channel antagonist nimodipine (2 /UM) to the bath decreased whole-cell peak current by 45 %. Interestingly, at negative holding potentials nimodipine worked as an agonist. From a holding potential of -90 mV, nimodipine (2 ,UM) increased peak current at test potentials from -50 to -20 mV and shifted the peak of the current-voltage relationship in the hyperpolarizing direction similar to the effect of Ca2+ channel agonist Bay K 8644. Exposure to Bay K 8644 (2,M) increased peak current and single channel open probability independent of holding potential while shifting the peak of the whole-cell current-voltage relationship 11 mV in the hyperpolarizing direction. Our experiments suggest that there are approximately the same number of L-type as wt)-conotoxin sensitive N-type Ca2+ channels in CA3 neurones.6. A high-voltage-activated whole-cell current was still present in cells exposed to both nimodipine and w)-conotoxin (2 and 1 AM, respectively) suggesting the existence of a fourth type of Ca2`channel in these neurones or that a population of either L-type or N-type Ca2+ channels did not respond to dihydropyridine antagonists or wi-conotoxin, respectively. From a holding potential of -50 mV, the combination of MS 8476 9-2 D. J. MOGUL AND A. P. FOX nimodipine and wo-conotoxin substantially blocked the Ca2" channel currents of some cells while others showed little effect. These results indicate that the multiple types of Ca2" channels were differentially distributed rather than incompletely blocked by one of the drugs.7. Single-channel current in cell-attached patches from CA3 neuronal somas showed three different unitary conductance levels of 7, 12 and 23 pS with 90 mmBa2+ as the external charge carrier. Ensemble average currents resembled currents recorded in the whole-cell configuration. No evidence for a fourth channel type was seen at the unitary level, sugg...

Background Currently, it is difficult to predict precise regions of cortical activation in response to transcranial magnetic stimulation (TMS). Most analytical approaches focus on applied magnetic field strength in the target region as the primary factor, placing activation on the gyral crowns. However, imaging studies support M1 targets being typically located in the sulcal banks. Objective/hypothesis To more thoroughly investigate this inconsistency, we sought to determine whether neocortical surface orientation was a critical determinant of regional activation. Methods MR images were used to construct cortical and scalp surfaces for 18 subjects. The angle (θ) between the cortical surface normal and its nearest scalp normal for ~50,000 cortical points per subject was used to quantify cortical location (i.e., gyral vs. sulcal). TMS-induced activations of primary motor cortex (M1) were compared to brain activations recorded during a finger-tapping task using concurrent positron emission tomographic (PET) imaging. Results Brain activations were primarily sulcal for both the TMS and task activations (P < 0.001 for both) compared to the overall cortical surface orientation. Also, the location of maximal blood flow in response to either TMS or finger-tapping correlated well using the cortical surface orientation angle or distance to scalp (P < 0.001 for both) as criteria for comparison between different neocortical activation modalities. Conclusion This study provides further evidence that a major factor in cortical activation using TMS is the orientation of the cortical surface with respect to the induced electric field. The results show that, despite the gyral crown of the cortex being subjected to a larger magnetic field magnitude, the sulcal bank of M1 had larger cerebral blood flow (CBF) responses during TMS.