Negative Direct Current Potential Shift Research Articles

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.

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.

A modified rat model of middle cerebral artery thread occlusion under electrophysiological control for magnetic resonance investigations.

Previous magnetic resonance (MR) investigations of middle cerebral artery (MCA) occlusion in rats were limited by the lack of early post-occlusion MR measurements and/or electrophysiological monitoring. Therefore, we have developed a technique which allows to perform MCA occlusion inside the magnet under simultaneous recording of EEG and direct current (DC) potentials for monitoring the ischemic insult. Rats underwent intraluminal thread occlusion of the right MCA inside the MR tomograph via a catheter extension device, while EEG and DC potentials were recorded by non-magnetic graphite electrodes. The thread was slowly advanced until electrophysiological changes appeared. Diffusion-weighted MR images (DWI) were obtained before and repeatedly after MCA occlusion for up to 7 h. Thereafter, rat brains were frozen in situ or fixed by transcardiac perfusion and investigated by biochemical and histological techniques. In 15 of 18 animals (83%), MCA thread insertion caused immediate EEG changes and a negative DC potential shift at 4.4 +/- 1.8 min (mean +/- SD) after occlusion. In all animals with electrophysiological changes, signal intensity of DWI began to increase within the MCA territory at 12-14 min post-occlusion (the end of the first measurement), and continued to rise throughout the observation period. Ischemia was confirmed by demonstrating focal areas of energy depletion on ATP images. In the animals without electrophysiological changes, DWI or biochemical alterations were absent or confined to the central part of caudate-putamen. The histological lesion area of successfully occluded animals amounted to 70.1 +/- 5.8% of the ipsilateral hemisphere at the level of caudate-putamen.(ABSTRACT TRUNCATED AT 250 WORDS)

Study of local cerebral glucose utilization in experimental head injury. Natural course and presence of hypermetabolic state after cerebral contusion.

Local cerebral glucose utilization (LCGU) was studied in 23 awake rats following fluid percussion injury (cerebral contusion). In this system, percussion energy was created by a hammer hitting a vinyl chloride membrane with thickness of 0.5 mm and diameter of 100 mm. This system produced a biphasic impact, which would do no unfavorable damage to the brain stem, but cause a reproducible localized cerebral contusion. The LCGU was quantitatively measured by the [14C]deoxyglucose autoradiographic method (Sokoloff). Six rats were controls. LCGU was studied at 1, 2, 4, and 24 hours following injury. [14C]deoxyglucose uptake was remarkably decreased at the center of the contusion and LCGU was mildly decreased at 1 and 4 hours, and definitely at 24 hours over the ipsilateral hemisphere. Interestingly there were two different types of behavior in LCGU changes at 2 hours after injury; no change or slight decrease in 4 of 6 rats (Group A) and remarkable increase (more than 150%) all over the cortex and the hippocampus of the ipsilateral side in 2 of 6 rats (Group B). This unique phenomenon in Group B—“hypermetabolic state”—resembles the autoradiographic findings in cortical spreading depression, which reportedly show remarkable increase of extracellular K+ and negative shift of direct current (DC) potential, associated with increased glucose uptake of the brain. Persistent oligemia was also reported following cortical spreading depression. The authors observed negative shift of DC potential between 1 and 4 hours, most frequently around 2 hours, after fluid percussion injury (unpublished data). If this hypermetabolic state following experimental head injury is associated with persistent oligemia, as reported in cortical spreading depression, cerebral metabolism would be trapped in a vicious cycle. Secondary brain damage is quite possible due to the above reason, and 2 hours after injury would be the critical period for any trial of treatment.