Presumably, second-language (L2) learning is mediated by changes in the brain. Little is known about what changes in the brain, how the brain changes, or when these changes occur during learning. Here, we illustrate by way of example how modern brain-based methods can be used to discern some of the changes that occur during L2 learning. Preliminary results from three studies indicate that classroom-based L2 instruction can result in changes in the brain's electrical activity, in the location of this activity within the brain, and in the structure of the learners' brains. These changes can occur during the earliest stages of L2 acquisition.

This cortical stimulation mapping study investigates the neural representation of action and object naming. Data from 13 neurosurgical subjects undergoing awake cortical mapping is presented. Our findings indicate clear evidence of differential disruption of noun and verb naming in the context of this naming task. At the individual level, evidence was found for punctuate regions of perisylvian cortex subserving noun and verb function. Across subjects, however, the location of these sites varied. This finding may help explain discrepancies between lesion and functional imaging studies of noun and verb naming. In addition, an alternative coding of these data served to highlight the grammatical class vulnerability of the target response. The use of this coding scheme implicates a role for the supramarginal gyrus in verb-naming behavior. These data are discussed with respect to a functional-anatomical pathway underlying verb naming.

After large lesions of the primary motor cortex (M1), voluntary movements of affected body parts are weak and slow. In addition, the relative independence of moving one body part without others is lost; attempts at individuated movements of a given body part are accompanied by excessive, unintended motion of contiguous body parts. The effects of partial inactivation of the M1 hand area are comparatively unknown, however. If the M1 hand area contains the somatotopically ordered finger representations implied by the classic homunculus or simiusculus, then partial inactivation might produce weakness, slowness, and loss of independence of one or two adjacent digits without affecting other digits. But if control of each finger movement is distributed in the M1 hand area as many studies suggest, then partial inactivation might produce dissociation of weakness, slowness, and relative independence of movement, and which fingers movements are impaired might be unrelated to the location of the inactivation along the central sulcus.To investigate the motoric deficits resulting from partial inactivation of the M1 hand area, we therefore made single intracortical injections of muscimol as trained monkeys performed visually cued, individuated flexion-extension movements of the fingers and wrist. We found little if any evidence that which finger movements were impaired after each injection was related to the injection location along the central sulcus. Unimpaired fingers could be flanked on both sides by impaired fingers, and the flexion movements of a given finger could be unaffected even though the extension movements were impaired, or vice versa. Partial inactivation also could produce dissociated weakness and slowness versus loss of independence in a given finger movement. These findings suggest that control of each individuated finger movement is distributed widely in the M1 hand area.Key words: cortex; dexterity; finger; individuation; macaque; motor; muscimol; response time, somatotopy; weaknessThe classic homunculus and simiusculus implied that a separate region of the primary motor cortex (M1) moves each digit of the hand (Penfield and Rasmussen, 1950;Woolsey et al., 1951). Evidence now suggests, however, that control of any finger movement is distributed throughout the M1 hand area (see Discussion), calling into question the degree to which a somatotopic map of the fingers mediates the crucial contribution of M1 to performance of individuated finger movements. Clearly, lesions of lateral M1 impair voluntary movement of the face much more than the leg and vice versa for medial M1 lesions. If such somatotopic organization extends to the level of different fingers, then lateral lesions within the hand area should impair thumb movements more than little finger movements and vice versa for medial lesions. We therefore sought to reversibly inactivate only part of the M1 hand area, because such within-hand somatotopic effects would not have been evident in previous studies of lesions in M1 or the corticospinal tract. These ...

1. We studied the responses of rat hypoglossal and cat lumbar motoneurones to a variety of excitatory and inhibitory injected current transients during repetitive discharge. The amplitudes and time courses of the transients were comparable to those of the synaptic currents underlying unitary and small compound postsynaptic potentials (PSPs) recorded in these cells. Poisson trains of ten of these excitatory and ten inhibitory current transients were combined with an additional independent, high-frequency random waveform to approximate band limited white noise. The white noise waveform was then superimposed on long duration (39 s) suprathreshold current steps. 2. We measured the effects of each of the current transients on motoneurone discharge by compiling peristimulus time histograms (PSTHs) between the times of occurrence of individual current transients and motoneurone discharges. We estimated the changes in membrane potential associated with each current transient by approximating the passive response of the motoneurone with a simple resistance-capacitance circuit. The relations between the features of these simulated PSPs and those of the PSTHs were similar to those reported previously for real PSPs: the short-latency PSTH peak (or trough) was generally longer than the initial phase of the PSP derivative, but shorter than the time course of the PSP itself. Linear models of the PSP to PSTH transform based on the PSP time course, the time derivative of the PSP, or a linear combination of the two parameters could not reproduce the full range of PSTH profiles observed. 3. We also used the responses of the motoneurones to the white noise stimulus to derive zero-, first-and second-order Wiener kernels, which provide a quantitative description of the relation between injected current and discharge probability. The convolution integral computed for an injected current waveform and the first-order Wiener kernel should provide the best linear prediction of the associated PSTH. This linear model provided good matches to the PSTHs associated with a wide range of current transients. However, for the largest amplitude current transients, a significant improvement in the PSTH match was often achieved by expanding the model to include the convolution of the second-order Wiener kernel with the input. 4. The overall transformation of current inputs into firing rate could be approximated by a second-order Wiener model, i.e. a cascade of a dynamic, linear filter followed by a static nonlinearity. At a given mean firing rate, the non-linear component of the response of the motoneurone could be described by the square of the linear component multiplied by a constant coefficient. The amplitude of the response of the linear component increased with the average firing rate, whereas the value of the multiplicative coefficient in the non-linear component decreased. As a result, the overall transform could be predicted from the mean firing rate and the linear impulse response, yielding a relatively simple, general description of the mo...

1. We studied the responses of rat hypoglossal motoneurones to excitatory current transients (ECTs) using a brainstem slice preparation. Steady, repetitive discharge at rates of 12-25 impulses s-' was elicited from the motoneurones by injecting long (40 s) steps of constant current. Poisson trains of the ECTs were superimposed on these steps. The effects of additional synaptic noise was simulated by adding a zero-mean random process to the stimuli. 2. We measured the effects of the ECTs on motoneurone discharge probability by compiling peristimulus time histograms (PSTHs) between the times of occurrence of the ECTs and the motoneurone spikes. The ECTs produced modulation of motoneurone discharge similar to that produced by excitatory postsynaptic currents. 3. The addition of noise altered the pattern of the motoneurone response to the current transients: both the amplitude and the area of the PSTH peaks decreased as the power of the superimposed noise was increased. Noise tended to reduce the efficacy of the ECTs, particularly when the motoneurones were firing at lower frequencies. Although noise also increased the firing frequency of the motoneurones slightly, the effects of noise on ECT efficacy did not simply result from noise-induced changes in mean firing rate. 4. A modified version of the experimental protocol was performed in lumbar motoneurones of intact, pentobarbitone-anaesthetized cats. These recordings yielded results similar to those obtained in rat hypoglossal motoneurones in vitro. 5. Our results suggest that the presence of concurrent synaptic inputs reduces the efficacy of any one input. The implications of this change in efficacy and the possible underlying mechanisms are discussed.