Physiologic coupling of glial glycogen metabolism to neuronal activity in brain

1992 ◽  
Vol 70 (S1) ◽  
pp. S138-S144 ◽  
Author(s):  
Raymond A. Swanson
Keyword(s):  
Neuronal Activity ◽  
Tactile Stimulation ◽  
Glycogen Content ◽  
Brain Activity ◽  
Glycogen Metabolism ◽  
Normal Brain ◽  
Brain Glycogen ◽  
Glycogen Utilization ◽  
Glucose Supply ◽  
Stimulation Of

Brain glycogen is localized almost exclusively to glia, where it undergoes continuous utilization and resynthesis. We have shown that glycogen utilization increases during tactile stimulation of the rat face and vibrissae. Conversely, decreased neuronal activity during hibernation and anesthesia is accompanied by a marked increase in brain glycogen content. These observations support a link between neuronal activity and glial glycogen metabolism. The energetics of glycogen metabolism suggest that glial glycogen is mobilized to meet increased metabolic demands of glia rather than to serve as a substrate for neuronal activity. An advantage to the use of glycogen may be the potentially faster generation of ATP from glycogen than from glucose. Alternatively, glycogen could be utilized if glucose supply is transiently insufficient during the onset of increased metabolic activity. Brain glycogen may have a dynamic role as a buffer between the abrupt increases in focal metabolic demands that occur during normal brain activity and the compensatory changes in focal cerebral blood flow or oxidative metabolism.Key words: brain, glia, glycogen, glycolysis, hibernation.

Effect of estradiol on tissue glycogen metabolism and lipid availability in exercised male rats

1991 ◽  
Vol 71 (5) ◽  
pp. 1694-1699 ◽  
Author(s):  
Z. V. Kendrick ◽  
G. S. Ellis
Keyword(s):  
Fatty Acids ◽  
Body Weight ◽  
Exercise Performance ◽  
Glycogen Content ◽  
Day Treatment ◽  
Glycogen Metabolism ◽  
Liver Glycogen ◽  
Male Rats ◽  
Plasma Lactate ◽  
Glycogen Utilization

The effect of 17 beta-estradiol 3-benzoate (10 micrograms.0.1 ml sunflower oil-1.100 g body wt-1) on exercise performance, tissue glycogen utilization, and lipid availability was determined in male rats. In experiment 1, estradiol or oil was administered 1 h or 1–6 days before a treadmill run to exhaustion. No differences in body weight between oil- and estradiol-administered animals were observed during the 6-day treatment. Animals receiving estradiol for 3–6 days ran significantly longer and completed more work than oil-administered animals. Significant degradation of red and white vastus muscle, myocardial, and liver glycogen was observed in all animals run to exhaustion. In experiment 2, animals were administered estradiol for 5 days and then run for 2 h. The submaximal run for 2 h significantly reduced tissue glycogen content in red and white vastus muscle, heart, and liver of oil-administered animals. The latter effect was attenuated in both vastus muscles, liver, and myocardial tissues in the estradiol-administered animals. Estradiol administration significantly increased plasma fatty acids and lowered plasma lactate during the submaximal run. These data indicate that when body weight remained constant between groups of male rats, estradiol administration for 3–6 days increased exercise performance. Furthermore, estradiol administration for 5 days resulted in greater lipid availability and less tissue glycogen utilization during submaximal running for 2 h.

scholarly journals Human brain glycogen content and metabolism: implications on its role in brain energy metabolism

2007 ◽  
Vol 292 (3) ◽  
pp. E946-E951 ◽  
Author(s):  
Gülin Öz ◽  
Elizabeth R. Seaquist ◽  
Anjali Kumar ◽  
Amy B. Criego ◽  
Luke E. Benedict ◽  
...  
Keyword(s):  
Human Brain ◽  
Glycogen Content ◽  
Visual Stimulation ◽  
Occipital Lobe ◽  
Glycogen Metabolism ◽  
Adult Brain ◽  
Brain Glycogen ◽  
Free Glucose ◽  
Time Courses

The adult brain relies on glucose for its energy needs and stores it in the form of glycogen, primarily in astrocytes. Animal and culture studies indicate that brain glycogen may support neuronal function when the glucose supply from the blood is inadequate and/or during neuronal activation. However, the concentration of glycogen and rates of its metabolism in the human brain are unknown. We used in vivo localized 13C-NMR spectroscopy to measure glycogen content and turnover in the human brain. Nine healthy volunteers received intravenous infusions of [1-13C]glucose for durations ranging from 6 to 50 h, and brain glycogen labeling and washout were measured in the occipital lobe for up to 84 h. The labeling kinetics suggest that turnover is the main mechanism of label incorporation into brain glycogen. Upon fitting a model of glycogen metabolism to the time courses of newly synthesized glycogen, human brain glycogen content was estimated at ∼3.5 μmol/g, i.e., three- to fourfold higher than free glucose at euglycemia. Turnover of bulk brain glycogen occurred at a rate of 0.16 μmol·g−1·h−1, implying that complete turnover requires 3–5 days. Twenty minutes of visual stimulation ( n = 5) did not result in detectable glycogen utilization in the visual cortex, as judged from similar [13C]glycogen levels before and after stimulation. We conclude that the brain stores a substantial amount of glycogen relative to free glucose and metabolizes this store very slowly under normal physiology.

Effect of estradiol on tissue glycogen metabolism in exercised oophorectomized rats

1987 ◽  
Vol 63 (2) ◽  
pp. 492-496 ◽  
Author(s):  
Z. V. Kendrick ◽  
C. A. Steffen ◽  
W. L. Rumsey ◽  
D. I. Goldberg
Keyword(s):  
Skeletal Muscle ◽  
Exercise Performance ◽  
Sunflower Oil ◽  
Glycogen Content ◽  
Vastus Lateralis ◽  
Glycogen Metabolism ◽  
Submaximal Exercise ◽  
Total Work ◽  
Glycogen Utilization ◽  
Glycogen Sparing

The effect of both physiological and pharmacological doses of estradiol on exercise performance and tissue glycogen utilization was determined in oophorectomized estradiol-replaced (ER) rats. Doses of beta-estradiol 3-benzoate (0.02, 0.04, 0.1, 0.2, 1, 2, 4, or 10 micrograms.0.1 ml of sunflower oil-1.100 g body wt-1) were injected 5 days/wk for 4 wk. Controls were sham injected (SI). After treatment, the animals were run to exhaustion on a motorized treadmill. ER animals receiving the 0.02-microgram dose ran significantly longer and completed more total work than the SI group. ER animals receiving doses of greater than or equal to 0.04 microgram ran longer and performed more work than the 0.02-microgram group. At exhaustion, myocardial glycogen content was significantly decreased in animals that were ER with less than or equal to 0.1 microgram, whereas those replaced with doses greater than 0.1 microgram utilized significantly less glycogen. With the 10-micrograms dose no significant decrease in heart glycogen content was observed at exhaustion. A submaximal 2-h run significantly reduced glycogen content in heart, red and white portions of the vastus lateralis, and the livers of SI animals. The latter effect was attenuated in skeletal muscle and liver, and there was no effect in the hearts of the ER animals receiving 2 micrograms. These data indicate that estradiol replacement in oophorectomized rats influenced myocardial glycogen utilization during exhaustive exercise and spared tissue glycogen during submaximal exercise. These glycogen sparing effects may have contributed to the significant improvements in exercise performance observed in this study.

K+ changes in the extracellular space of the spinal cord and their physiological role

1981 ◽  
Vol 95 (1) ◽  
pp. 93-109
Author(s):  
E. Sykova
Keyword(s):  
Spinal Cord ◽  
Neuronal Activity ◽  
Tactile Stimulation ◽  
Current Flow ◽  
Physiological Role ◽  
Primary Afferent Depolarization ◽  
Flow Through ◽  
K Concentration ◽  
Dorsal Root Potentials ◽  
Stimulation Of

K+ accumulates in the intercellular space as a result of neuronal activity. The changes in extracellular K+ concentration, delta[K]e (estimated by K+-selective microelectrodes), depends on neuronal activity, on the density of discharging neurones and the removal of the accumulated K+ by diffusion, active transport and current flow through cells. In the mammalian as well as the amphibian spinal cord a single volley in a peripheral nerve increases [K]e by 0.2-0.5 mmol. 1-1, while tetanic stimulation (100 Hz) by 7-8 m-mol. 1-1, with a maximum in the lower dorsal horn. Increased [K]e was also found in lumbar segments when the somatosensory cortex of the cat and medulla of the frog were stimulated. In the frog spinal cord, the tactile stimulation of the hindlimb evoked delta[K]e by about 0.1 mumol. 1-1, nociceptive stimulation by 0.2-1.0 mmol. 1-1. Spontaneous delta[K]e and dorsal root potentials (DRPs) were observed at various intervals after stimulation, associated with the decay phase of delta[K]e. It was shown that primary afferent depolarization (PAD) consists of two components: the ‘early’ component (mediated by GABA and depressed by picrotoxin or bicuculline) and the ‘late’ K+ component (potentiated by picrotoxin and bicuculline). Even when increased [K]e produces PAD, this does not mean that it also results in presynaptic inhibition. It was found that the delta[K]e produced depolarization of motoneurones and neuroglia and there is every reason to believe that this also applies to the interneurones. Evidence is available that an increase of [K]e up to 6 mmol. 1-1 facilitates impulse transmission in the spinal cord while higher levels result in its inhibition.

Primary Somatosensory Cortical Neuronal Activity During Monkey's Detection of Perceived Change in Tooth-Pulp Stimulus Intensity

1998 ◽  
Vol 79 (4) ◽  
pp. 1717-1725 ◽  
Author(s):  
Koichi Iwata ◽  
Yoshiyuki Tsuboi ◽  
Rhyuji Sumino
Keyword(s):  
Neuronal Activity ◽  
Stimulus Intensity ◽  
Tactile Stimulation ◽  
Firing Frequency ◽  
Projection Area ◽  
Tooth Pulp ◽  
Detection Latency ◽  
Perceived Change ◽  
3.0 T ◽  
Stimulation Of

Iwata, Koichi, Yoshiyuki Tsuboi, and Rhyuji Sumino. Primary somatosensory cortical neuronal activity during monkey's detection of perceived change in tooth-pulp stimulus intensity. J. Neurophysiol. 79: 1717–1725, 1998. To elucidate the functional properties of primary somatosensory cortical neurons for the perception of tooth-pulp sensation, neuronal activity was recorded from the primary somatosensory cortex (SI) in awake behaving monkeys. Monkeys were trained to detect changes in tooth-pulp stimulus intensity applied to the upper canine or incisor tooth pulp. Stimulus intensities applied to the tooth pulp were multiples of the threshold intensity for the jaw opening reflex (1.0 T) elicited by tooth-pulp stimulation. When monkeys pressed a button, baseline electrical pulses (V1: 0.5 T, 1.0 T, 2.0 T, or 3.0 T) were applied to the tooth pulp. After 4–8 s, a V2 stimulus (0.3 T, 0.5 T, 1.0 T, or 2.0 T) was added to V1. Percent escapes at V1 stimulus intensity of 0.5 T and 1.0 T were ∼10%, 22% at 2.0 T, and 40% at 3.0 T (total of 1,997 trials). A total of 862 single units were recorded from the SI. Thirty-seven SI neurons responded to electrical stimulation of the tooth pulp (tooth-pulp–driven neurons; TPNs), 139 SI neurons responded to tactile stimulation of the lateral face area, 90 to upper lip and 99 to lower lip, 44 to tongue and 102 to periodontal membrane, whereas 351 SI neurons were not responsive to tactile stimulation of the orofacial regions. Thirty of 37 TPNs were recorded long enough to test with V1 stimuli ranging from 0.5 T to 3.0 T. Eleven of 30 TPNs linearly increased their firing frequency following increases in stimulus intensity (encoding TPNs), whereas 19 did not (nonencoding TPNs). Mean first spike latency of encoding TPNs was 24.8 ± 1.7 ms ( n = 11), that of nonencoding TPNs was 23.6 ± 1.5 ms ( n = 19), and that of unclassified TPNs was 24.7 ± 3.7 ms ( n = 7). TPNs were distributed in the areas 1–2, 3a, and 3b within the oral projection area and the transition zone between the face and oral projection areas of the SI. All of them received inputs from the intraoral structures, facial skin, or both. The firing frequency of eight encoding and nonencoding TPNs was correlated with detection latency at stimulus intensities of 0.5 and 1.0 T. On the other hand, when the baseline stimulus was increased to 2.0 T and 3.0 T, the discharge of most TPNs did not increase in firing frequency with the reduction in detection latency. These results indicate that the discharge rates of some SI TPNs are correlated with detection latency at near-noxious threshold and noxious stimulus intensities. These findings suggest that some TPNs are involved in the sensory-discriminative aspect of tooth-pulp sensation in the near-pain threshold and pain ranges.

Central Nervous Function and Changes in Brain Metabolite Concentration

1953 ◽  
Vol 30 (4) ◽  
pp. 468-475
Author(s):  
M. R. A. CHANCE
Keyword(s):  
Glycogen Content ◽  
Brain Activity ◽  
Defensive Behaviour ◽  
Normal Behaviour ◽  
External Stimulation ◽  
Brain Glycogen ◽  
Brain Metabolite ◽  
Nervous Function ◽  
The Brain ◽  
Different Parts

1. The changes in the glycogen content of different parts of the brain have been studied in mice in relation to the behaviour of these animals. 2. Increases in glycogen content have been demonstrated after a jump, a fall, after the righting reaction accompanying a fall, and after aggressive behaviour has been shown in a fight. 3. No increase has been demonstrated during sleep, after running or walking, or after defensive behaviour in a fight. 4. It was shown earlier that external stimulation must reach convulsive intensity to produce an increase in brain glycogen, and it is suggested that the particular forms of normal behaviour associated with increase in brain glycogen involve a ‘convulsive’ type of brain activity. ‘Convulsive’ in this context may mean either a disturbance of the metabolism in some or all of the brain cells, or alternatively the mobilization of cell populations for simultaneous, and probably rapid, discharge. At present there is no evidence to suggest whether either or both of these possibilities are involved.

scholarly journals Postprandial Glycogen Content Is Increased in the Hepatocytes of Human and Rat Cirrhotic Liver

Cells ◽  
2021 ◽  
Vol 10 (5) ◽  
pp. 976
Author(s):  
Natalia N. Bezborodkina ◽  
Sergey V. Okovityi ◽  
Boris N. Kudryavtsev
Keyword(s):  
Rat Liver ◽  
Liver Tissue ◽  
Glycogen Content ◽  
Glycogen Synthase ◽  
Fibrous Tissue ◽  
Glycogen Metabolism ◽  
Liver Parenchyma ◽  
Dry Mass ◽  
Cirrhotic Liver ◽  
Liver Biopsies

Chronic hepatitises of various etiologies are widespread liver diseases in humans. Their final stage, liver cirrhosis (LC), is considered to be one of the main causes of hepatocellular carcinoma (HCC). About 80–90% of all HCC cases develop in LC patients, which suggests that cirrhotic conditions play a crucial role in the process of hepatocarcinogenesis. Carbohydrate metabolism in LC undergoes profound disturbances characterized by altered glycogen metabolism. Unfortunately, data on the glycogen content in LC are few and contradictory. In this study, the material was obtained from liver biopsies of patients with LC of viral and alcohol etiology and from the liver tissue of rats with CCl4-induced LC. The activity of glycogen phosphorylase (GP), glycogen synthase (GS), and glucose-6-phosphatase (G6Pase) was investigated in human and rat liver tissue by biochemical methods. Total glycogen and its labile and stable fractions were measured in isolated individual hepatocytes, using the cytofluorometry technique of PAS reaction in situ. The development of LC in human and rat liver was accompanied by an increase in fibrous tissue (20- and 8.8-fold), an increase in the dry mass of hepatocytes (by 25.6% and 23.7%), and a decrease in the number of hepatocytes (by 50% and 28%), respectively. The rearrangement of the liver parenchyma was combined with changes in glycogen metabolism. The present study showed a significant increase in the glycogen content in the hepatocytes of the human and the rat cirrhotic liver, by 255% and 210%, respectively. An increased glycogen content in cells of the cirrhotic liver can be explained by a decrease in glycogenolysis due to a decreased activity of G6Pase and GP.

scholarly journals Enhanced Expectation of External Sensations of the Chest Regulates the Emotional Perception of Fearful Faces

2021 ◽  
Vol 11 (7) ◽  
pp. 946
Author(s):  
Won-Mo Jung ◽  
In-Seon Lee ◽  
Ye-Seul Lee ◽  
Yeonhee Ryu ◽  
Hi-Joon Park ◽  
...  
Keyword(s):  
Visual Cues ◽  
Brain Activity ◽  
Body Parts ◽  
Emotional Perception ◽  
Fearful Faces ◽  
Bodily Sensations ◽  
Facial Expression Classification ◽  
Bodily States ◽  
Expression Classification ◽  
Stimulation Of

Emotional perception can be shaped by inferences about bodily states. Here, we investigated whether exteroceptive inferences about bodily sensations in the chest area influence the perception of fearful faces. Twenty-two participants received pseudo-electrical acupuncture stimulation at three different acupoints: CV17 (chest), CV23 (chin), and PC6 (left forearm). All stimuli were delivered with corresponding visual cues, and the control condition included visual cues that did not match the stimulated body sites. After the stimulation, the participants were shown images with one of five morphed facial expressions, ranging from 100% fear to 100% disgust, and asked to classify them as fearful or disgusted. Brain activity was measured using functional magnetic resonance imaging during the facial expression classification task. When the participants expected that they would receive stimulation of the chest (CV17), the ratio of fearful to non-fearful classifications decreased compared to the control condition, and brain activities within the periaqueductal gray and the default mode network decreased when they viewed fearful faces. Our findings suggest that bodily sensations around the chest, but not the other tested body parts, were selectively associated with fear perception and that altering external inferences inhibited the perception of fearful faces.

Control of feeding motor output by paracerebral neurons in brain of Pleurobranchaea californica

1982 ◽  
Vol 47 (5) ◽  
pp. 885-908 ◽  
Author(s):  
R. Gillette ◽  
M. P. Kovac ◽  
W. J. Davis
Keyword(s):  
Feeding Behavior ◽  
Action Potentials ◽  
Tactile Stimulation ◽  
Natural Food ◽  
Buccal Ganglion ◽  
Pleurobranchaea Californica ◽  
Feeding Rhythm ◽  
Intracellular Stimulation ◽  
Motor Rhythm ◽  
Stimulation Of

1. A population of interneurons that control feeding behavior in the mollusk Pleurobranchaea has been analyzed by dye injection and intracellular stimulation/recording in whole animals and reduced preparations. The population consists of 12-16 somata distributed in two bilaterally symmetrical groups on the anterior edge of the cerebropleural ganglion (brain). On the basis of their position adjacent to the cerebral lobes, these cells have been named paracerebral neurons (PCNs). This study concerns pme subset pf [MCs. the large, phasic ones, which have the strongest effect on the feeding rhythm (21). 2. Each PCN sends a descending axon via the ipsilateral cerebrobuccal connective to the buccal ganglion. Axon branches have not been detected in other brain or buccal nerves and hence the PCNs appear to be interneurons. 3. In whole-animal preparations, tonic intracellular depolarization of the PNCs causes them to discharge cyclic bursts of action potentials interrupted by a characteristic hyperpolarization. In all specimens that exhibit feeding behavior, the interburst hyperpolarization is invariably accompanied by radula closure and the beginning of proboscis retraction (the "bite"). No other behavorial effect of PCN stimulation has been observed. 4. In whole-animal preparations, the PCNs are excited by food and tactile stimulation of the oral veil, rhinophores, and tentacles. When such stimuli induce feeding the PCNs discharge in the same bursting pattern seen during tonic PCN depolarization, with the cyclic interburst hyperpolarization phase locked to the bit. When specimens egest an unpalatable object by cyclic buccal movements, however, the PCNs are silent. The PCNs therefore exhibit properties expected of behaviorally specific "command" neurons for feeding. 5. Silencing one or two PCNs by hyperpolarization may weaken but does not prevent feeding induced by natural food stimuli. Single PCNs therefore can be sufficient but are not necessary to induction of feeding behavior. Instead the PCNs presumably operate as a population to control feeding. 6. In isolated nervous system preparations tonic extracellular stimulation of the stomatogastric nerve of the buccal ganglion elicits a cyclic motor rhythm that is similar in general features to the PNC-induced motor rhythm. Bursts of PCN action potentials intercalated at the normal phase position in this cycle intensify the buccal rhythm. Bursts of PCN impulses intercalated at abnormal phase positions reset the buccal rhythm. The PCNs, therefore, also exhibit properties expected of pattern-generator elements and/or coordinating neurons for the buccal rhythm. 7. The PCNs are recruited into activity when the buccal motor rhythm is elicited by stomatogastric nerve stimulation or stimulation of the reidentifiable ventral white cell. The functional synergy between the PCNs and the buccal rhythm is therefore reciprocal. 8...

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