Slow Negative Potential Shift Research Articles

Can ionic diffusion have an effect on extracellular potentials?

Several pathological conditions, such as hypoxia, anoxia, ischemia and spreading depression are associated with ion concentration changes in the extracellular space (ECS) [1]. Also during non-pathological conditions, endured periods of intense neural signaling may cause local ion concentration changes in the millimolar range. Changes in ion concentrations are often accompanied by a slow negative potential shift measured in the ECS [1-3], the origin of which is not properly understood. In computational neuroscience, it is common to use the simplifying assumption that diffusive currents (along concentration gradients) are negligible compared to Ohmic currents (along electrical fields). This is, for example, an underlying assumption in the cable equation used in most multi-compartmental neural models. It is also an underlying assumption in standard current source density (CSD) theory, which predicts neural current sources from recordings of extracellular potentials. However, theoretical studies have identified scenarios where large, but biologically realistic, ion concentration gradients may induce diffusive currents that are comparable in magnitude to Ohmic currents [4,5]. In the current work, we have explored possible effects that diffusive currents may have on the extracellular potential in a cortical column. To do this, we developed a hybrid simulation framework: First, we used the simulator NEURON (and an available multicompartmental neural model with realistic morphology [6]) to simulate the transmembrane ionic output from a small population of cortical neurons driven by realistic synaptic input. Next, we used a separate scheme to predict variations in extracellular potentials and ion concentrations. The scheme was based on the Nernst-Planck equations for electrodiffusion and the constraint of electroneutrality, and represents a novel, efficient and generally applicable method for simulating extracellular dynamics surrounding multicompartmental neural models or networks of such (e.g., the Blue Brain simulator). Our key findings were: (i) Morphology-dependent distributions of transmembrane current sources/sinks induced sustained extracellular potentials. Spatial variations of the ECS potential were of the order of a few mV across the depth of the cortical columns, which is similar to experimentally observed sustained potential profiles [2,3]. (ii) Long periods of neuronal output (simulations were run for 80 s) could change local ECS ion concentrations by several millimolars. (iii) For large, but realistic, concentration gradients in the ECS, diffusive currents were of the same magnitude as Ohmic currents. (iv) Diffusive currents could have a significant impact on the sustained extracellular potentials, and could be a possible explanation to the observed relationship between ionic shifts and voltage drops in the ECS [1-3]. (v) Variation in concentrations and diffusive currents took place at the time scale of several seconds, and had little impact on the frequencies that are of predominant interest in standard CSD-analysis.

Simultaneous measurement of electroencephalography and near-infrared spectroscopy during voluntary motor preparation

We investigated the relationship between electrophysiological activity and haemodynamic response during motor preparation by simultaneous recording of electroencephalography (EEG) and near-infrared spectroscopy (NIRS). It is still unknown how exactly EEG signals correlate with the haemodynamic response, although the activation in the premotor area during motor preparation has been captured by EEG and haemodynamic approaches separately. We conducted EEG-NIRS simultaneous recordings over the sensorimotor area with a self-paced button press task. Participants were instructed to press a button at their own pace after a cue was shown. The result showed that the readiness potential (RP), a negative slow potential shift occurring during motor preparation, on C3 in the extended 10–20 system occurred about 1000 ms before the movement onset. An increase in concentration of oxyhaemoglobin (oxyHb) in the premotor cortex during motor preparation was also confirmed by NIRS, which resulted in a significant correlation between the amplitude of the RP and the change in oxyHb concentration (Pearson’s correlation r2 = 0.235, p = 0.03). We show that EEG-NIRS simultaneous recording can demonstrate the correlation between the RP and haemodynamic response in the premotor cortex contralateral to the performing hand.

Spreading depression features and Iba1 immunoreactivity in the cerebral cortex of developing rats submitted to treadmill exercise after treatment with monosodium glutamate

Physical exercise and excessive consumption of monosodium glutamate (MSG) can affect the morphological and electrophysiological organization of the brain during development. However, the interaction of both factors remains unclear. We analyzed the effect of this interaction on the excitability-related phenomenon known as cortical spreading depression (CSD) and the microglial reaction expressed as Iba1-immunolabeled cells in the rat motor cortex. MSG (2g/kg or 4g/kg) was administered every other day during the first 14 postnatal days. Treadmill exercise started at 21–23 days of life and lasted 3 weeks, 5 days/week, for 30min/day. At 45–60 days, CSD was recorded for 4h at two cortical points and the CSD parameters (velocity, amplitude, and duration of the negative potential change) calculated. Confirming previous observations, exercised rats presented with lower CSD velocities (3.29±0.18mm/min) than the sedentary group (3.80±0.18mm/min; P<0.05). MSG increased CSD velocities in the exercised rats compared to saline-treated and exercised animals in a dose-dependent manner (3.49±0.19, 4.05±0.18, and 3.27±0.26 for 2g/kg MSG, 4g/kg MSG, and saline, respectively; P<0.05). The amplitude (ranging from 14.3±5.9 to 18.7±6.2mV) and duration (46.7±11.1 to 60.5±11.6s) of the negative slow potential shift of the CSD were similar in all groups. Both exercise and MSG treatment increased Iba1 immunolabeling. The results confirm that physical exercise decelerates CSD propagation. However, it does not impede the CSD-accelerating action of MSG. These effects were accompanied by a cortical microglia reaction. Therefore, the data suggest that treadmill exercise early in life can influence the development of cortical electrical activity.

Neonatal treatment with monosodium glutamate lastingly facilitates spreading depression in the rat cortex

AimsMonosodium glutamate (MSG) is a neuroexcitatory amino acid used in human food to enhance flavor. MSG can affect the morphological and electrophysiological organization of the brain. This effect is more severe during brain development. Here, we investigated the electrophysiological and morphological effects of MSG in the developing rat brain by characterizing changes in the excitability-related phenomenon of cortical spreading depression (CSD) and microglial reaction. Main methodsFrom postnatal days 1–14, Wistar rat pups received 2 or 4g/kg MSG (groups MSG-2 and MSG-4, respectively; n=9 in each group), saline (n=10) or no treatment (naïve group; n=5) every other day. At 45–60days, CSD was recorded on two cortical points for 4h. The CSD parameters velocity, and amplitude and duration of the negative potential change were calculated. Fixative-perfused brain sections were immunolabeled with anti-IBA-1 antibodies to identify and quantify cortical microglia. Key findingsMSG-4 rats presented significantly higher velocities (4.59±0.34mm/min) than the controls (saline, 3.84±0.20mm/min; naïve, 3.71±0.8mm/min) and MSG-2 group (3.75±0.10mm/min). The amplitude (8.8±2.2 to 11.2±1.9mV) and duration (58.2±7.1 to 73.6±6.0s) of the negative slow potential shift was similar in all groups. MSG-treatment dose-dependently increased the microglial immunolabeling. SignificanceThe results demonstrate a novel, dose-dependent action of MSG in the developing brain, characterized by acceleration of CSD and significant microglial reaction in the cerebral cortex. The CSD effect indicates that MSG can influence cortical excitability, during brain development, as evaluated by CSD acceleration. Data suggest caution when consuming MSG, especially in developing organisms.

EEG evidence of gender differences in a motor related CNV study

In the present study gender differences related to the contingent negative variation (CNV) were investigated. A series of two acoustic stimuli was presented to participants across a wide age range. The first stimulus was consistent throughout the experiment whereas the second one was either a high frequency or a low frequency tone. One of them had to be answered by a button press (go condition) the other did not require any response (nogo condition). Between the first and the second tone there was a time period of two seconds in which the CNV appeared as a slow negative potential shift. Within this episode data were analysed with respect to gender differences. Statistical analysis revealed topographical differences between men and women in go conditions for both left and right index finger movements. Differences were found over frontal regions where women showed higher brain activity than men and over temporo-parietal regions where men produced higher brain activity than women. In order to explain the fact that only in "go" conditions significant gender differences occurred we introduce the phenomenon of implicit learning. Due to implicit learning assumed predictions related to S2 might have occurred from time to time. This is so, because a 50% chance for one of two different stimuli to occur leads to reasonable assumed predictions after two or more stimuli of a kind occurring in a series. The present data now provide evidence that if such assumed prediction or expectancy is directed towards an upcoming demand to act then brain activity is subject to gender differences. Further studies providing controlled sequences of "go" conditions versus "nogo" conditions have to be done to prove this idea true.

Cortical spreading depression confounds concentration-dependent pial arteriolar dilation during N-methyl-d-aspartate superfusion

Pial arterioles do not express N-methyl-D-aspartate (NMDA) receptors but dilate in response to topical NMDA application. We explored the mechanism underlying NMDA-mediated responses in murine pial arterioles (11-31 microm), using a closed cranial window preparation, and found that arteriolar dilation was not concentration dependent. Pial arteriolar diameter abruptly increased within 3 min of superfusing 50 or 100 microM NMDA. Dilation reached a peak within 1 min (46 +/- 14%) and then declined to a plateau (28 +/- 13%) for the duration of superfusion. Whereas a higher concentration (200 microM) did not produce further dilation, lower concentrations (1-10 microM) did not dilate the arterioles at all. MK-801 (10 microM) abrogated the dilation response, whereas Nomega-nitro-L-arginine (1 mM) attenuated the peak and abolished the sustained dilation during NMDA superfusion. We determined that NMDA-induced pial arteriolar responses were evoked by cortical spreading depression, because abrupt vasodilation during 50 or 100 microM NMDA superfusion was associated with a large negative slow potential shift and electrocorticogram suppression that spread from the superfusion window to distant cortical areas. Our data suggest that the responses of pial arterioles to NMDA are caused in part by neurovascular coupling due to cortical spreading depression.

Neuronal responses are differentially affected by the polarity of tectal DC stimulation in the toad Bufo bufo

Male toads were tested behaviourally for their prey catching responses to worm-like stimuli before being prepared for visual unit and slow potential shift (SPS) recording from the optic tectum. The neuronal responses of toads to a prey-like visual stimulus reflected their motivational tendency prior to operations. One second of DC stimulation to the tectum was followed by an SPS of reversed polarity during which time a visual prey-like stimulus was presented. A negative SPS following positive DC stimulation was associated with enhanced neuronal responses to a visual stimulus. The positive SPS that followed negative stimulation was associated with a decline in neural responses below background when a visual stimulus was additionally given. The SPS was largely a result of DC stimulation that interacted with the motivational tendency to produce enhanced neuronal responses, while the potential was negative and vice versa.

Improving Influence of Insulin on Cognitive Functions in Humans

Insulin receptors have been identified in limbic brain structures, but their functional relevance is still unclear. In order to characterize some of their effects, we evaluated auditory evoked brain potentials (AEP) in a vigilance task, behavioral measures of memory (recall of words) and selective attention (Stroop test) during infusion of insulin. The hormone was infused at two different rates (1.5 mU/kg × min, ‘low insulin’, and 15 mU/kg × min, ‘high insulin’), inducing respectively serum levels of 543 ± 34 and 24,029 ± 1,595 pmol/l. This experimental design allowed to compare cognitive parameters under two conditions presenting markedly different insulin levels, but with minimal incidence on blood glucose concentrations since these were kept constant by glucose infusion. A ‘no insulin treatment’ group was not included in order to avoid leaving patients infused with glucose without insulin treatment. Measures were taken during a baseline phase preceding insulin infusion and every 90 min during the 360 min of insulin infusion. Compared with ‘low insulin’, ‘high insulin’ induced a slow negative potential shift in the AEP over the frontal cortex (average amplitude, high insulin: 0.27 ± 0.48 µV; low insulin: 1.87 ± 0.48 µV, p < 0.005), which was paralleled by enhanced memory performance (words recalled, high insulin: 22.04 ± 0.93; low insulin: 19.29 ± 0.92, p < 0.05). Also, during ‘high insulin’ subjects displayed enhanced performance on the Stroop test (p < 0.05) and expressed less difficulty in thinking than during ‘low insulin’ (p < 0.03). Results indicate an improving effect of insulin on cognitive function, and may provide a frame for further investigations of neurobehavioral effects of insulin in patients with lowered or enhanced brain insulin, i.e., patients with Alzheimer’s disease or diabetes mellitus.

Ischaemia triggered by spreading neuronal activation is inhibited by vasodilators in rats.

It has been previously shown that spreading neuronal activation can generate a cortical spreading ischaemia (CSI) in rats. The purpose of the present study was to investigate whether vasodilators cause CSI to revert to a normal cortical spreading depression (CSD).A KCl-induced CSD travelled from an open cranial window to a closed window where the cortex was superfused with physiological artificial cerebrospinal fluid (ACSF). At the closed window, recordings revealed a short-lasting negative slow potential shift accompanied by a variable, small and short initial hypoperfusion followed by hyperaemia and then oligaemia. In contrast, spreading neuronal activation locally induced CSI at the closed window when ACSF contained a NO. synthase (NOS) inhibitor, N(G)-nitro-L-arginine, and an increased K+ concentration ([K+]ACSF). CSI was characterised by a sharp and prolonged initial cerebral blood flow decrease to 29 +/- 11 % of the baseline and a prolonged negative potential shift. Co-application of a NOá donor, S-nitroso-N-acetylpenicillamine, and NOS inhibitor with high [K+]ACSF re-established a short-lasting negative potential shift and spreading hyperaemia typical of CSD. Similarly, the NO.-independent vasodilator papaverine caused CSI to revert to a pattern characteristic of CSD. In acute rat brain slices, NOS inhibition and high [K+]ACSF did not prolong the negative slow potential shift compared to that induced by high [K+]ACSF alone. The data indicate that the delayed recovery of the slow potential was caused by vasoconstriction during application of high [K+]ACSF and a NOS inhibitor in vivo. This supports the possibility of a vicious circle: spreading neuronal activation induces vasoconstriction, and vasoconstriction prevents repolarisation during CSI. Speculatively, this pathogenetic process could be involved in migraine-induced stroke.

Bilateral subthalamic nucleus stimulation improves frontal cortex function in Parkinson's disease. An electrophysiological study of the contingent negative variation.

Parkinson's disease involves impaired activation of frontal cortical areas, including the supplementary motor area and prefrontal cortex, resulting from impaired thalamocortical output of the basal ganglia. Electrophysiologically, such impaired cortical activation may be seen as a reduced amplitude of the contingent negative variation (CNV), a slow negative potential shift reflecting cognitive processes associated with the preparation and/or anticipation of a response. Surgical interventions aimed at increasing basal ganglia-thalamic outflow to the cortex, such as electrical stimulation of the subthalamic nucleus with chronically implanted electrodes, have been shown to be effective in improving the clinical symptoms of Parkinson's disease. This study examined changes in cortical activity, as reflected in the CNV, associated with bilateral subthalamic nucleus stimulation in Parkinson's disease. The CNV was recorded from 10 patients with Parkinson's disease when on and off bilateral subthalamic nucleus stimulation, and was compared with the CNV of 10 healthy control subjects. Without subthalamic nucleus stimulation, Parkinson's disease patients showed reduced CNV amplitudes over the frontal and frontocentral regions compared with control subjects. With bilateral subthalamic nucleus stimulation, however, CNV amplitudes over the frontal and frontocentral regions were significantly increased. Results therefore suggest that impaired cortical functioning in Parkinson's disease, particularly within the frontal and premotor areas, is improved by subthalamic nucleus stimulation.

Premovement and Cognitive Brain Potentials in Chronic Fatigue Syndrome

SummaryBrain potentials from normals and patients with Chronic Fatigue Syndrome (CFS) were recorded in four different experimental tasks: (1) Auditory target detection, (2) Short-term memory scanning, (3) Fore-warned reaction time (contingent negative variation), and (4) Self-paced movement. In the auditory target detection task, a slow negative potential shift (maximum at Cz), appears prior to stimulus onset in normals, but is markedly reduced in amplitude in patients with CFS. However, all other sensory and cognitive brain potentials do not differ between normals and CFS. Reaction times are slower in CFS compared to normals. In the memory task, a slow negative shift associated with memory scanning is reduced in patients with CFS. For the fore-warned reaction time and self-paced movement tasks, no differences were found between the patients and normals. The finding of premovement related potential abnormalities in CFS supports the concept that central motor preparation and execution are impaired in CFS. In certain tasks, measures of neural processes related to sensory processing and attention are normal for these patients. Results from the memory task suggest that neural processes related to short-term memory are also altered in CFS.

Cortical DC potential shifts accompanying the central processing of visually presented analogue and digital time displays

According to studies in brain-lesioned patients, the cortical substrate subserving the reading of digitally presented time displays seems to differ from that of reading analogue displays. While the right hemisphere has been assumed to be important for reading analogue displays, reading digital displays is attributed to the left hemisphere. This study attempts to localize the cortical substrate of reading analogue versus digital time displays in the intact human brain using scalp-recorded event-related slow negative DC potential shifts. In the arithmetic tasks, subjects had to judge whether or not the time conveyed by the last out of three tachistoscopically presented (analogue or digital) slides was the exact difference between the time conveyed by the first and the second slide. In the control condition, subjects only had to attend to (analogue or digital) time displays. With analogue slides, frontolateral recording sites revealed a right hemispheric preponderance of DC shifts measured in the interval between the second and third slide. Anterior temporal recording sites revealed a right hemispheric preponderance only when calculations were performed. By contrast, there was no hemispheric lateralization with digital slides. The arithmetic versus control manipulation modulated waveforms, but did not influence hemispheric laterality.

Low Mg 2+ induced epileptiform activity in the subiculum before and after disconnection from rat hippocampal and entorhinal cortex slices

The subiculum is an area within the hippocampal complex which participates strongly in ictaform activity generated in the entorhinal cortex (EC). To study the properties of epileptiform activity with intra- and extracellular recording techniques in the subiculum, combined slices containing the EC, subiculum and hippocampus were prepared with and without surgical disconnection of the subiculum from the EC and area CA1. For induction of epileptiform activity extracellular magnesium was lowered. After acute disconnection of the subiculum from the cornu ammonis and the EC, seizure like events similar to those in the more intact preparation did develop. These were characterized by slow negative field potential shifts and, in intracellular recordings by sustained depolarization shifts lasting for 10–43 s. This activity could develop into late recurrent discharges of 1–2 s. These data indicate that the subiculum may be an important zone for epileptogenesis in temporal lobe epilepsy.

Properties of low Mg 2+ induced epileptiform activity in rat hippocampal and entorhinal cortex slices during adolescence

Properties of low Mg 2+ induced epileptiform activity were studied in isolated rat hippocampal slices or in combined slices containing the entorhinal cortex and hippocampus. Slices were prepared from rats which were 1, 2, 3 or more weeks of age. Field potentials and often also changes in [K +] o, [Ca 2+] o and [Mg 2+] o were recorded with appropriate ion selective microelectrodes. In isolated hippocampal and entorhinal cortex/hippocampal combined slices the latency to onset of epileptiform activity upon lowering of extracellular Mg 2+ was shortest in the youngest age group and approached adult levels at about the fourth postnatal week. Washout kinetics of Mg 2+ were fastest in slices from 1-week-old rats. The onset of low Mg 2+ induced epileptiform activity occurred at higher Mg 2+ levels in slices from young compared with those from adult animals. In isolated hippocampal slices the epileptiform discharges varied in appearance during development. Short discharges lasting for 40 to 80 ms were observed in hippocampal slices prepared from 1-week-old and adult animals. Seizure-like events (SLE's) characterized by slow negative potential shifts and characteristic elevations in [K +] o and decreases in [Ca 2+] o lasting for up to 30 s were observed in a proportion of hippocampal slices prepared after the first, second and third postnatal week. In slices from week 2 and 3 seizure- like events often progressed into spreading depressions (SD's). In entorhinal cortex/hippocampal cambined slices seizure-like events were observed in all age groups. The seizure-like events spread readily into dentate gyrus (DG), area CA3 and CA1 after week 1. During development the DG, then area CA3 and finally area CA1 dropped out from active participation in generation of seizure-like events. After prolonged perfusion with low Mg 2+ seizure-like events progressed into recurrent discharges lasting between 800 ms to 10 s. This occurred more rapidly in slices from young compared with those from adult animals. These findings suggest that the seizure susceptibility of entorhinal cortex and hippocampus is greater in juvenile than in adult tissue. Moreover, seizure-like activity seems to spread more readily from the EC to the hippocampus proper.

Tactile mental imagery in sighted persons and in patients suffering from peripheral blindness early in life

Patterns of cortical activity as measured by scalp-recorded event-related slow negative DC potential shifts were recorded in 9 early blind and 23 sighted normals while they imagined the feel of textures with the fingertips of one hand. All sighted subjects reported to have concomitant visual imagery as well. Hence, it was not surprising to observe occipital negative shifts, previously described as a sign of occipital visual cortex involvement in visual mental imagery. Though having never had visual perception, the blind, too, had occipital negativities. Their absolute amplitudes were smaller than in the sighted, not only occipitally but also and more pronounced at other areas, particularly frontally where amplitudes were even positive. On the hypothesis that the smaller overall amplitudes in the blind could obscure topographical differences between groups, the relative distribution of negativity across the scalp was assessed, using normalized data. Such normalized parameters significantly differed between groups, indicating that the occipital potentials of the blind were relatively more negative as related to the other scalp areas, than were the occipital potentials of the sighted as related to the other scalp areas. This occipital finding might indicate a participation of the blind's visually deprived occipital cortex in tactile imagery. Second, parietal DC potentials were maximal over the hemisphere contralateral to the imaging hand, possibly indicating involvement of the contralateral parietal association cortex in tactile imagery. Reasons why this was true only for the sighted, are discussed.

“Probing” the nature of the CNV

A widespread depolarization in the dendritic trees of cortical pyramidal neurons generates surface-negative potentials. In turn, such potentials may indicate facilitatory processes while positive-going waves may result from a lowering in cortical excitability. Accordingly, we may expect the processing of “probe” stimuli presented during surface-positive waves, i.e., during phases of lesser excitability, to be inhibited and probes presented during surface-negative waves to be facilitated. This hypothesis was tested by presenting acoustic probe stimuli at various points in time during a forewarned reaction time task. The warming stimulus (WS) elicited a late positive complex followed by a negative slow potential shift (CNV). In 75% of the total of 120 trials a probe could be presented 1.5 sec prior to the WS interval, 0.5, 1, 1.5 or 2 sec after the onset of the 3 sec visual WS, and 3 sec following the imperative signal (WS offset, requiring a fast button press response), while 25% of the trials were without any probe. Only one probe occurred during a trial. The EEG was recorded along the midsagittal line; responses to the probes were evaluated by reaction time (RT) and probe-evoked potentials. RT to probes presented late in the anticipatory interval were speeded up and probe-evoked potentials were enhanced during this interval, in parallel to the development of the slow potential and the CNV in particular. Results suggest that probe stimuli presented during the development of the CNV were processed more intensely, thereby supporting the hypothesis that slow cortical potentials indicate the timing of excitability in cortical neuronal networks. Such a tuning mechanism may serve as a basis for attentional regulation.

EEG changes related to one-dimensional hand-tracking

Central and occipital EEGs were recorded during one-dimensional eye-hand tracking in humans. A negative slow potential shift followed the commitment of tracking errors at electrode O1 and their correction both at O1 and C3. Error commitments were also followed by a relative decrease in alpha and beta-band power at O1, whereas their corrections followed a decrease in beta-band power at O2 and C3.

Psycho-physiological study by contingent negative variation (CNV) in otolaryngological diseases

Contingent negative variations (CNV) were recorded in patients with tinnitus (N = 20), abnormal sensations of the pharynx and larynx (ASPL) (N = 26) and Meniere's disease (N = 19), and compared with those of healthy adults (N = 20) in order to investigate the characteristics of their information processing mechanisms in the brain. Patients were also subjected to psychological tests: Depression Score and the Cornell Medical Index test. CNV (an event-related potential) is a slow negative cortical potential shift and can be recorded during two stimuli presented at a constant interval under conditions in which the subjects are told to press a key as quickly as possible upon an imperative stimulus (S2) following a warning stimulus (S1). S1 was a 1kHz tone burst of 300 msec duration at a level of 85dB HL. S2 was a light flash. The interstimulus (S1-S2) interval was set at 2 seconds. The CNV can be divided into three components, early, middle, and late, according to latency. Statistical analysis of CNV amplitudes of the three components showed the following differences between groups. In tinnitus patients, the mean amplitudes of both the early and middle component were significantly greater than those in healthy adults (P < 0.05). In ASPL patients, the mean amplitudes of the middle component were significantly greater than those in healthy adults (P < 0.05). In Menière's disease, the mean amplitudes of both the middle and late component were significantly greater than those in healthy adults (P < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

On the functionality of the visually deprived occipital cortex in early blind persons

In early blind mammals, the deprived visual cortex undergoes anatomical and functional alterations. Its functional role was investigated in the early human blind by using patterns of cortical activation as measured by scalp-recorded event-related slow negative DC potential shifts. The blind showed higher occipital negativity than did sighted persons both during a tactile reading task and a non-reading tactile control task. Results point to a possible role for the blind's visual cortex in tactile processes.

Left frontal lobe in verbal associative learning: a slow potential study.

In the present experiment pairs of words had to be memorized. The words were either meaningful or meaningless. The experimental design compares conditions of preestablished learning (L-) with active learning (L+). The effects of these two factors, "semantic content (S)" and "learning (L)", on the slow potential shifts accompanying presentation and processing of the verbal material were tested. In the memorizing tasks, the two words were given in a fixed temporal sequence. A slow negative potential shift having a maximum in parietal leads emerged within the inter-stimulus-interval. Its amplitudes were larger in the learning tasks (L+) than in conditions of pre-established learning (L-). This difference of amplitudes may reflect different levels of attention: In L-, the second word could be anticipated, but not in the L+ tasks. After the presentation of the second item, learning tasks (L+) were characterized by a slow negative potential shift in the recordings of the left dorso-lateral frontal lobe. It is assumed that this potential shift may indicate an importance of the left frontal lobe in the elaborative encoding of verbal material.