Direct Current Potential Shift Research Articles

Preictal neuronal and vascular activity precedes the onset of childhood absence seizure: direct current potential shifts and their correlation with hemodynamic activity.

The neurovascular mechanisms underlying the initiation of absence seizures and their dynamics are still not well understood. The objective of this study was to better noninvasively characterize the dynamics of the neuronal and vascular network at the transition from the interictal state to the ictal state of absence seizures and back to the interictal state using a combined electroencephalography (EEG), functional near-infrared spectroscopy (fNIRS), and diffuse correlation spectroscopy (DCS) approach. The second objective was to develop hypotheses about the neuronal and vascular mechanisms that propel the networks to the 3-Hz spikes and wave discharges (SWDs) observed during absence seizures. We evaluated the simultaneous changes in electrical (neuronal) and optical dynamics [hemodynamic, with changes in (Hb) and cerebral blood flow] of 8 pediatric patients experiencing 25 typical childhood absence seizures during the transition from the interictal state to the absence seizure by simultaneously performing EEG, fNIRS, and DCS. Starting from before the onset of the SWD, we observed a transient direct current potential shift that correlated with alterations in functional fNIRS and DCS measurements of the cerebral hemodynamics detecting the preictal changes. Our noninvasive multimodal approach highlights the dynamic interactions between the neuronal and vascular compartments that take place in the neuronal network near the time of the onset of absence seizures in a very specific cerebral hemodynamic environment. These noninvasive approaches contribute to a better understanding of the electrical hemodynamic environment prior to seizure onset. Whether this may ultimately be relevant for diagnostic and therapeutic approaches requires further evaluation.

Combined Effect of Alternating Current Interference and Cathodic Protection on Pitting Corrosion and Stress Corrosion Cracking Behavior of X70 Pipeline Steel in Near-Neutral pH Environment.

Influence of alternating current (AC) on pitting corrosion and stress corrosion cracking (SCC) behavior of X70 pipeline steel in the near-neutral pH environment under cathodic protection (CP) was investigated. Both corrosion and SCC are inhibited by −0.775 VSCE CP without AC interference. With the superimposition of AC current (1–10 mA/cm2), the direct current (DC) potential shifts negatively under the CP of −0.775 VSCE and the cathodic DC current decreases and shifts to the anodic direction. Under the CP potential of −0.95 VSCE and −1.2 VSCE, the applied AC current promotes the cathodic reaction and leads to the positive shift of DC potential and increase of cathodic current. Local anodic dissolution occurs attributing to the generated anodic current transients in the positive half-cycle of the AC current, resulting in the initiation of corrosion pits (0.6–2 μm in diameter). AC enhances the SCC susceptibility of X70 steel under −0.775 VSCE CP, attributing to the promotion of anodic dissolution and hydrogen evolution. Even an AC current as low as 1 mA/cm2 can enhance the SCC susceptibility.

Age or ischemia uncouples the blood flow response, tissue acidosis, and direct current potential signature of spreading depolarization in the rat brain.

Spreading depolarization (SD) events contribute to lesion maturation in the acutely injured human brain. Neurodegeneration related to SD is thought to be caused by the insufficiency of the cerebral blood flow (CBF) response; yet the mediators of the CBF response, or their deficiency in the aged or ischemic cerebral cortex, remain the target of intensive research. Here, we postulated that tissue pH effectively modulates the magnitude of hyperemia in response to SD, the coupling of which is prone to be dysfunctional in the aged or ischemic cerebral cortex. To test this hypothesis, we conducted systematic correlation analysis between the direct current (DC) potential signature of SD, SD-associated tissue acidosis, and hyperemic element of the CBF response in the isoflurane-anesthetized, young or old, and intact or ischemic rat cerebral cortex. The data demonstrate that the amplitude of the SD-related DC potential shift, tissue acidosis, and hyperemia are tightly coupled in the young intact cortex; ischemia and old age uncouples the amplitude of hyperemia from the amplitude of the DC potential shift and acidosis; the duration of the DC potential shift, hyperemia and acidosis positively correlate under ischemia alone; and old age disproportionally elongates the duration of acidosis with respect to the DC potential shift and hyperemia under ischemia. The coincidence of the variables supports the view that local CBF regulation with SD must have an effective metabolic component, which becomes dysfunctional with age or under ischemia. Finally, the known age-related acceleration of ischemic neurodegeneration may be promoted by exaggerated tissue acidosis.NEW & NOTEWORTHY The hyperemic element of the cerebral blood flow response to spreading depolarization is effectively modulated by tissue pH in the young intact rat cerebral cortex. This coupling becomes dysfunctional with age or under ischemia, and tissue acidosis lasts disproportionally longer in the aged cortex, making the tissue increasingly more vulnerable.

Ischemia-induced spreading depolarization in the retina

Cortical spreading depolarization is a metabolically costly phenomenon that affects the brain in both health and disease. Following severe stroke, subarachnoid hemorrhage, or traumatic brain injury, cortical spreading depolarization exacerbates tissue damage and enlarges infarct volumes. It is not known, however, whether spreading depolarization also occurs in the retina in vivo. We report now that spreading depolarization episodes are generated in the in vivo rat retina following retinal vessel occlusion produced by photothrombosis. The properties of retinal spreading depolarization are similar to those of cortical spreading depolarization. Retinal spreading depolarization waves propagate at a velocity of 3.0 ± 0.1 mm/min and are associated with a negative shift in direct current potential, a transient cessation of neuronal spiking, arteriole constriction, and a decrease in tissue O2 tension. The frequency of retinal spreading depolarization generation in vivo is reduced by administration of the NMDA antagonist MK-801 and the 5-HT(1D) agonist sumatriptan. Branch retinal vein occlusion is a leading cause of vision loss from vascular disease. Our results suggest that retinal spreading depolarization could contribute to retinal damage in acute retinal ischemia and demonstrate that pharmacological agents can reduce retinal spreading depolarization frequency after retinal vessel occlusion. Blocking retinal spreading depolarization generation may represent a therapeutic strategy for preserving vision in branch retinal vein occlusion patients.

PSD-95 uncoupling from NMDA receptors by Tat-N-dimer ameliorates neuronal depolarization in cortical spreading depression

Cortical spreading depression is associated with activation of NMDA receptors, which interact with the postsynaptic density protein 95 (PSD-95) that binds to nitric oxide synthase (nNOS). Here, we tested whether inhibition of the nNOS/PSD-95/NMDA receptor complex formation by anti-ischemic compound, UCCB01-144 (Tat-N-dimer) ameliorates the persistent effects of cortical spreading depression on cortical function. Using in vivo two-photon microscopy in somatosensory cortex in mice, we show that fluorescently labelled Tat-N-dimer readily crosses blood-brain barrier and accumulates in nerve cells during the first hour after i.v. injection. The Tat-N-dimer suppressed stimulation-evoked synaptic activity by 2–20%, while cortical blood flow and cerebral oxygen metabolic (CMRO2) responses were preserved. During cortical spreading depression, the Tat-N-dimer reduced the average amplitude of the negative shift in direct current potential by 33% (4.1 mV). Furthermore, the compound diminished the average depression of spontaneous electrocorticographic activity by 11% during first 40 min of post-cortical spreading depression recovery, but did not mitigate the suppressing effect of cortical spreading depression on cortical blood flow and CMRO2. We suggest that uncoupling of PSD-95 from NMDA receptors reduces overall neuronal excitability and the amplitude of the spreading depolarization wave. These findings may be of interest for understanding the neuroprotective effects of the nNOS/PSD-95 uncoupling in stroke.

Variation of repetitive cortical spreading depression waves is related with relative refractory period: a computational study

Cortical spreading depression (CSD) is an important experimental model for diseases such as stroke, epilepsy and migraine. Previous observations indicated that the amplitude and velocity of the typical direct current potential shift during repetitive CSD waves were varying. The recovery state of the tissue was found related with the variation of successive CSD waves. A computational model in this paper aimed to investigate the role of relative refractory period of CSD. This model simulated that continuous injection of KCl solution induced repetitive CSD waves. The first CSD wave often had a larger amplitude and faster velocity than those of the succeeding secondary waves. The relative refractory period lasted much longer than the recovery of ions turbulence. If the induction interval was long enough for recovery, a series of CSD waves would have the same profile as the first one. In the relative refractory period, an early stimulation might lead to a late initiation of CSD, i.e., “haste makes waste”. The amplitude and velocity of CSD waves were found increasing with the initiation interval and asymptotic to those of the first CSD wave. This study verified that the propagation dynamics of CSD waves is modulated by the relative refractory period. It suggested that the refractory period is critical for preventing undesirable CSD waves.

Acoustic noise alters selective attention processes as indicated by direct current (DC) brain potential changes.

Acoustic environmental noise, even of low to moderate intensity, is known to adversely affect information processing in animals and humans via attention mechanisms. In particular, facilitation and inhibition of information processing are basic functions of selective attention. Such mechanisms can be investigated by analyzing brain potentials under conditions of externally directed attention (intake of environmental information) versus internally directed attention (rejection of environmental stimuli and focusing on memory/planning processes). This study investigated brain direct current (DC) potential shifts—which are discussed to represent different states of cortical activation—of tasks that require intake and rejection of environmental information under noise. It was hypothesized that without background noise rejection tasks would show more positive DC potential changes compared to intake tasks and that under noise both kinds of tasks would show positive DC shifts as an expression of cortical inhibition caused by noise. DC potential shifts during intake and rejection tasks were analyzed at 16 standard locations in 45 persons during irrelevant speech or white noise vs. control condition. Without noise, rejection tasks were associated with more positive DC potential changes compared to intake tasks. During background noise, however, this difference disappeared and both kinds of tasks led to positive DC shifts. Results suggest—besides some limitations—that noise modulates selective attention mechanisms by switching to an environmental information processing and noise rejection mode, which could represent a suggested “attention shift”. Implications for fMRI studies as well as for public health in learning and performance environments including susceptible persons are discussed.

Restraint Stress Intensifies Interstitial K+ Accumulation during Severe Hypoxia

Chronic stress affects neuronal networks by inducing dendritic retraction, modifying neuronal excitability and plasticity, and modulating glial cells. To elucidate the functional consequences of chronic stress for the hippocampal network, we submitted adult rats to daily restraint stress for 3 weeks (6 h/day). In acute hippocampal tissue slices of stressed rats, basal synaptic function and short-term plasticity at Schaffer collateral/CA1 neuron synapses were unchanged while long-term potentiation was markedly impaired. The spatiotemporal propagation pattern of hypoxia-induced spreading depression episodes was indistinguishable among control and stress slices. However, the duration of the extracellular direct current potential shift was shortened after stress. Moreover, K+ fluxes early during hypoxia were more intense, and the postsynaptic recoveries of interstitial K+ levels and synaptic function were slower. Morphometric analysis of immunohistochemically stained sections suggested hippocampal shrinkage in stressed rats, and the number of cells that are immunoreactive for glial fibrillary acidic protein was increased in the CA1 subfield indicating activation of astrocytes. Western blots showed a marked downregulation of the inwardly rectifying K+ channel Kir4.1 in stressed rats. Yet, resting membrane potentials, input resistance, and K+-induced inward currents in CA1 astrocytes were indistinguishable from controls. These data indicate an intensified interstitial K+ accumulation during hypoxia in the hippocampus of chronically stressed rats which seems to arise from a reduced interstitial volume fraction rather than impaired glial K+ buffering. One may speculate that chronic stress aggravates hypoxia-induced pathophysiological processes in the hippocampal network and that this has implications for the ischemic brain.

Direction of selective attention modulates direct current (DC) brain potentials

Event Abstract Back to Event Direction of selective attention modulates direct current (DC) brain potentials Michael Trimmel1*, Julia Hintermayr1 and Karin Trimmel1 1 Medical University Vienna, Austria Facilitation of relevant information and inhibition of non-relevant stimuli are basic mechanisms of selective attention. They were investigated by the manipulation of the direction of attention by means of externally (intake of information) versus internally (rejection of environmental stimuli) directed attention. This study investigated effects of intake and of rejection tasks on brain direct current (DC) potential shifts, which are discussed as a sign of cortical activation/inhibition. It was hypothesized that rejection tasks are associated with more positive DC potential changes compared to intake tasks as an expression of cortical inhibition. Attention tasks consisted of a figural and a verbal task to take into account modality effects. Based on a 2 (Direction of Attention; intake vs. rejection)  2 (Modality; figural vs. verbal)  9 (Recording Location)  3 (Time on Task; 30-s blocks) repeated measures ANOVA design, DC potential shifts were analyzed at frontal (F3, Fz, F4), central (C3, Cz, C4), and parietal (P3, Pz, P4) locations. Forty-eight test persons performed 4 attention tasks: Intake figural (viewing and memorizing pictures), Intake verbal (Listening to and memorizing a text), Reject figural (completing figures in mind), and Reject verbal (creating words), all of a duration of 90 sec with a balanced order across test persons. Additionally, vertical EOG and skin potential were recorded to control for confounding factors. Rejection tasks were associated with more positive DC potential changes compared to intake tasks, this effect was independent of modality and recording location. Positive DC potential shifts during the rejection tasks, which are discussed as a sign of cortical inhibition, are suggested to be related to filtering out non task-relevant information. Keywords: Cognition, DC brain potentials Conference: XI International Conference on Cognitive Neuroscience (ICON XI), Palma, Mallorca, Spain, 25 Sep - 29 Sep, 2011. Presentation Type: Poster Presentation Topic: Poster Sessions: Neurophysiology of Cognition and Attention Citation: Trimmel M, Hintermayr J and Trimmel K (2011). Direction of selective attention modulates direct current (DC) brain potentials. Conference Abstract: XI International Conference on Cognitive Neuroscience (ICON XI). doi: 10.3389/conf.fnhum.2011.207.00436 Copyright: The abstracts in this collection have not been subject to any Frontiers peer review or checks, and are not endorsed by Frontiers. They are made available through the Frontiers publishing platform as a service to conference organizers and presenters. The copyright in the individual abstracts is owned by the author of each abstract or his/her employer unless otherwise stated. Each abstract, as well as the collection of abstracts, are published under a Creative Commons CC-BY 4.0 (attribution) licence (https://creativecommons.org/licenses/by/4.0/) and may thus be reproduced, translated, adapted and be the subject of derivative works provided the authors and Frontiers are attributed. For Frontiers’ terms and conditions please see https://www.frontiersin.org/legal/terms-and-conditions. Received: 24 Nov 2011; Published Online: 28 Nov 2011. * Correspondence: Dr. Michael Trimmel, Medical University Vienna, Vienna, Austria, michael.trimmel@univie.ac.at Login Required This action requires you to be registered with Frontiers and logged in. To register or login click here. Abstract Info Abstract The Authors in Frontiers Michael Trimmel Julia Hintermayr Karin Trimmel Google Michael Trimmel Julia Hintermayr Karin Trimmel Google Scholar Michael Trimmel Julia Hintermayr Karin Trimmel PubMed Michael Trimmel Julia Hintermayr Karin Trimmel Related Article in Frontiers Google Scholar PubMed Abstract Close Back to top Javascript is disabled. Please enable Javascript in your browser settings in order to see all the content on this page.

Periodic fasting alters neuronal excitability in rat neocortical and hippocampal tissues

Dietary restriction has been shown to be associated with marked changes in brain function. Periodic fasting was suggested to be beneficial in reducing both the incidence and severity of some neurological disorders. The aim of this investigation was to study the effect of periodic fasting on the neuronal network excitability in the neocortex and hippocampus and its possible influence on the brain under pathological conditions. Direct current (DC) recordings in the somatosensory neocortex of fasting rats (15 h water and food deprivation per day) during drinking revealed a negative potential shift. Using voltage sensitive dye imaging and tetanus-induced long-term potentiation (LTP) in ex vivo/ in vitro experiments, neuronal network activities as well as synaptic efficacy were investigated in rat neocortical and hippocampal slices after 4 weeks of periodic fasting. Stimulus-induced patterns of bioelectric activity showed enhanced neuronal network excitability in the neocortex and decreased bioelectric activity in the hippocampus. LTP was significantly increased in neocortical slices and inhibited in hippocampal tissues. Both hippocampal and neocortical tissues exhibited a higher tolerance to hypoxic stress but not to 0-Mg 2+-eliciting epileptiform field potentials. Neocortical slices also exhibited a higher threshold for the initiation of spreading depression. These experiments indicate that repetitive DC potential shifts occurring in fasting rats change the pattern of bioelectrical activities in cortical and subcortical regions. Through these alterations, the neocortex and hippocampus may become tuned for the efficient regulation of consummatory behaviour.

Time course of changes in extracellular lactate evoked by transient K(+)-induced depolarisation in the rat striatum.

The purpose of this study was to establish whether excessive lactate production associated with local application of K+ is reflected at the extracellular level during or after the K+ challenge. Changes in extracellular lactate were continuously monitored by microdialysis coupled to on-line fluorimetric analysis. K(+)-induced changes in dialysate lactate were closely related to those of the direct current potential. High K+ evoked a large and sustained negative shift of direct current potential onto which were superimposed a variable number of transient peaks of further depolarisation. The initial negative shift in direct current potential was associated with a decrease in dialysate lactate, but after each transient depolarisation, the positive shift in direct current potential indicating cell repolarisation was associated with a marked increase in extracellular lactate. When repetitive transient depolarisations occurred during a stimulus, only a small increase after each depolarisation was observed. However, recordings consistently revealed a marked and rapid increase in extracellular lactate after the K+ stimulus. These data indicate that extracellular lactate mostly increased during periods of repolarisation. This suggests strongly that lactic acid transport out of brain cells may be impaired when their transmembrane ionic gradients are disrupted.

Effects of anesthesia on the responses to cortical spreading depression in the rat brain in vivo

Objectives: The aim of this study was to evaluate the effect of cortical spreading depression (CSD) on the metabolic, hemodynamic, electrical and ionic properties during anesthesia as compared with the awake state.Methods: The mitochondrial NADH redox state, reflected light, direct current (DC) potential, electrocorticography (ECoG), cerebral blood flow (CBF) and volume (CBV), and extracellular K+ concentrations ([K+]e), were measured continuously and simultaneously in real time using two unique monitoring systems that evaluate brain function. Three consecutive CSD waves were initiated using a KCl solution in both awake and anesthetized rats.Results and discussion: CSD caused typical amplitude changes: biphasic waves in reflectance, oxidation cycles in NADH, an increase in CBF, CBV and in [K+]e, a negative shift in DC potential and depression in ECoG. Anesthesia by equithesin decreased significantly the baseline levels of CBF and [K+]e, showing a reduction in oxygen supply and demand. After anesthesia, CSD significantly decreased [K+]e and NADH oxidation cycles, indicating a reduction in oxygen demand and in oxygen balance, respectively. Furthermore, anesthesia reduced CSD wave frequencies by slowing the recovery period, showing a decline in energy production during brain activation, or by changing electrophysiological properties of the tissue. No changes were found in the propagation rate and in the initiation period of CSD, which may indicate that equithesin does not block CSD initiation. In addition, we found that the whole cerebral cortex reacts homogenously to CSD and that equithesin may reduce oxygen demand and energy production, which may have a protective effect on the brain exposed to pathophysiological conditions.

Suppression of Energy Requirement by Lidocaine in the Ischemic Mouse Brain

Effects of lidocaine on parameters of membrane functional integrity were investigated in the mouse brain. Changes in the direct-current potential shift in the cerebral cortex provoked by decapitation ischemia were compared in animals given lidocaine (0.05, 0.25, or 1.0 micromol, intracerebroventricular) or saline 15 minutes before ischemia. The brain content of adenosine 5'-triphosphate (ATP) was measured in animals subjected to 0, 0.5, 1, and 2 minutes of decapitation ischemia, and the effect of preischemic administration of lidocaine (0.25 micromol, intracerebroventricular) was evaluated. Na+, K+-ATPase, and Ca2+-ATPase activity was evaluated in brains pretreated with lidocaine (0.25 micromol, intracerebroventricular) or saline 15 minutes before decapitation. Changes in the intracellular Ca concentration ([Ca2+]i) were evaluated in hippocampal slices and the effects of lidocaine (50, 100, or 400 microM) were assessed in the hippocampal CA1 field and dentate gyrus at pH 7.4 and pH 6.8 every 60s for a duration of 50 min. The preischemic administration of lidocaine (1.0 and 0.25 micromol) delayed the onset of anoxic depolarization to 49 seconds and 44 seconds, respectively, as compared with that in the saline group at 27 seconds. Lidocaine maintained ATP levels higher than those in corresponding saline groups, values being 165% after 1 minute of ischemia and 212% after 2 minutes, respectively. Lidocaine did not affect Na+, K+-ATPase, and Ca2+-ATPase activity. Lidocaine did not affect changes in the [Ca2+]i in either area at either pH. The findings may suggest that lidocaine maintains the energy level by delaying depolarization in neurons, which may contribute to removal of cytosolic Ca2+ in ischemic states.

Spindle and slow wave rhythms at slow wave sleep transitions are linked to strong shifts in the cortical direct current potential

Electroencephalographic activity at the transition from wakefulness to sleep is characterized by the appearance of spindles (12–15 Hz) and slow wave rhythms including delta activity (1–4 Hz) and slow oscillations (0.2–1 Hz). While these rhythms originate within neocortico-thalamic circuitry, their emergence during the passage into slow wave sleep (SWS) critically depends on the activity of neuromodulatory systems. Here, we examined the temporal relationships between these electroencephalogram rhythms and the direct current (DC) potential recorded from the scalp in healthy men ( n=10) using cross-correlation analyses. Analyses focused on transitions from wakefulness to SWS in the beginning of the sleep period, and from SWS to lighter sleep and rapid eye movement (REM) sleep at the end of the first sleep cycle. For spindle, delta and slow oscillatory activity strong negative correlations with the DC potential were found at the transition into SWS with peak correlation coefficients (at zero time lag) averaging r=−0.81, −0.88 and −0.88, respectively ( P<0.001). Though slightly lower, distinct negative correlations between these measures were also found at the transition from SWS to REM sleep (−0.78, −0.77 and −0.77, respectively, P<0.001). Fast oscillatory activity in the beta frequency band (15-25 Hz) was correlated positively with the DC potential (r=+0.75, P<0.05, at the passage to SWS). Data indicate close links between increasing spindle, delta and slow oscillatory activity and the occurrence of a steep surface negative cortical DC potential shift during the transition from wake to SWS. Likewise, a DC potential shift toward surface positivity accompanies the disappearance of these oscillatory phenomena at the end of the non-REM sleep period. The DC potential shifts may reflect gradual changes in extracellular ionic (Ca 2+) concentration resulting from the generation of spindle and slow wave rhythms, or influences of neuromodulating systems on cortical excitability thereby controlling the emergence of cortical spindle and slow wave rhythms at SWS transitions.

Light scattering in rat neocortical slices differs during spreading depression and ischemia

Spreading depression (SD) and ischemia are different pathophysiological events but have similar characteristics. This study investigated whether similarity exists in the light scattering (LS) properties during SD and ischemia in rat neocortical slices. SD was induced by injection of K + while ischemia was simulated by removing oxygen and glucose. LS was simultaneously recorded with changes in extracellular direct current (DC) potential and extracellular space (ECS) volume. LS was measured using a photon counting fiber optic system and the ECS volume change was determined by measuring the ECS concentration of tetramethylammonium (TMA +). Slices maintained in normal artificial cerebrospinal fluid (ACSF) showed a consistent LS increase during SD, but exhibited two different LS behaviors during 6 min of ischemia. In eight slices, LS decreased and remained so until the end of the ischemic challenge. In another 10 slices, LS diminished initially but, after 2 min, suddenly reversed sign, accompanied by a rapid negative shift in extracellular DC potential. When 50 or 91% of Cl − in the ACSF was replaced by membrane-permeable propionate, LS retained its increase during SD, but always showed the sudden LS reversal during ischemia. In contrast, when Cl − was substituted with membrane-impermeant methylsulfate, the SD-induced LS increase was replaced by an LS decrease, and the sudden LS reversal during ischemia was absent. While the LS signal showed different characteristics during SD and ischemia, the DC potential always presented negative shifts and the ECS volume always exhibited similar decreases. These results suggest that the polarity of the LS signal is determined by the competition of at least two factors: cell swelling and anion influx.

APPROACH TO THE STUDY OF NEUROPHYSIOLOGICAL MECHANISM OF FOOD MOTIVATION

The present article estimates depolarization-polarization processes in the nerve tissue of afferent systems, including visceral ones, according to the changes of the direct current (DC) potential level. Food motivation is formed and satisfied concurrently with changes in the neocortex direct current potential level and a number of cerebral brain limbic structures in rats. Lateral hypothalamic nucleus, basolateral amygdala area, and auditory cortex in hungry rats have a more negative DC potential shift than in satisfied animals, while a reverse relation is observed in the ventromedial hypothalamic nucleus. The results obtained are considered an indication of polarization shifts in the mechanism of motivated and emotional behavior. An idea of the determining role of polarization processes in the mechanism of motivated and emotional behavior is developed.

Scalp recorded direct current (DC) potential shifts associated with food intake in hungry humans

In humans, eating is assumed to be regulated within a neuronal circuitry integrating hypothalamic ‘feeding centers’ with neocortical regions. Here, DC potentials were recorded in food deprived men to demonstrate a graded tuning of neocortical excitability in conjunction with meal ingestion. In the beginning of food ingestion a pronounced negative DC potential shift developed ( P<0.01) which was replaced by a gradual positive potential shift reaching a maximum within 5 min after cessation of food intake ( P<0.05). Both negative and positive shifts showed a widespread cortical distribution. The initial negative DC potential presumably reflecting increased depolarisation of apical cortical dendrites, may serve to facilitate eating behavior. The succeeding positivity points to a growing inhibitory influence on cortical processing with increasing satiety that may support termination of meal intake.

Changes in direct current (DC) potentials and infra-slow EEG oscillations at the onset of the luteinizing hormone (LH) pulse.

An essential function of the neuroendocrine system lies in the coordination of hypothalamo-pituitary secretory activity with neocortical neuronal activity. Cortical direct current (DC) potential shifts and EEG were monitored in conjunction with the circulating concentration of luteinizing hormone (LH) in humans while asleep to assess a hypothalamic-neocortical interaction. The onset of an LH pulse was accompanied (i) at frontocortical locations by a transient positive DC potential shift of approximately 3 min duration and peak amplitude 50 microV; (ii) at frontal and central locations by an increase in power of infra-slow EEG oscillations for periodicities between 64 and 320 s. Results uniquely demonstrate a coupling of hypothalamo-pituitary activity with regulation of neocortical excitability.

Scalp recorded direct current potential shifts associated with quenching thirst in humans

As an indicator of cortical excitability, direct current (DC) potentials were recorded from thirsted subjects before, during and after drinking 400 ml of water. Self-rated thirst was distinctly reduced after drinking. Compared with control conditions in which the subjects remained thirsty, during drinking a widespread negative potential shift occurred averaging over -70 microV at Cz. At the transition from the consumatory phase to the postconsumption phase, a slow positive potential shift commenced that was most pronounced over the anterior cortex (averaging over +40 microV at Fz) and persisted for more than 3 min after drinking. Control conditions excluded muscle activity, ocular movements, and changes in body fluid and serum osmolality as possible non-neuronal sources of the DC-potential changes. The sequence of negative and positive potential shifts associated with drinking indicates a coordinate regulation of cortical excitability that may facilitate consumatory behavior and its context-dependent encoding into memory.

Scalp recorded direct current potential shifts associated with quenching thirst in humans

As an indicator of cortical excitability, direct current (DC) potentials were recorded from thirsted subjects before, during and after drinking 400 ml of water. Self-rated thirst was distinctly reduced after drinking. Compared with control conditions in which the subjects remained thirsty, during drinking a widespread negative potential shift occurred averaging over −70 μV at Cz. At the transition from the consumatory phase to the postconsumption phase, a slow positive potential shift commenced that was most pronounced over the anterior cortex (averaging over +40 μV at Fz) and persisted for more than 3 min after drinking. Control conditions excluded muscle activity, ocular movements, and changes in body fluid and serum osmolality as possible non-neuronal sources of the DC-potential changes. The sequence of negative and positive potential shifts associated with drinking indicates a coordinate regulation of cortical excitability that may facilitate consumatory behavior and its context-dependent encoding into memory.