Glycogen in the Central Nervous System

Koizumi, Junzo

doi:10.1016/s0079-6336(74)80003-3

Cited by 67 publications

(55 citation statements)

References 87 publications

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“…Besides, EGCs characteristically possess a large membrane surface relative to their small size, which is consistent with their potential role in regulating metabolite exchanges between enteric neurons and the blood supply (Gershon and Bursztajn, 1978;Hanani and Reichenbach, 1994). Secondly, as EGCs are rich in glycogen granules, they may constitute a major source of glucose for enteric neurons, similar to that provided by astrocytes to CNS neurons (Koizumi, 1974;Cataldo and Broadwell, 1986). Thirdly, EGCs have recently been shown to be the only cells within the ENS that are immunoreactive for L-arginine (Nagahama et al, 2001), a substrate required for the nitric oxide (NO) synthesis.…”

Section: Neuroprotective and Neuromodulatory Functions Of Egcmentioning

confidence: 61%

Role of enteric glial cells in inflammatory bowel disease

Cabarrocas

Savidge

Liblau

2002

Glia

160

154

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Enteric glial cells (EGCs) represent an extensive but relatively poorly described cell population within the gastrointestinal tract. Accumulating data suggest that EGCs represent the morphological and functional equivalent of CNS astrocytes within the enteric nervous system (ENS). The EGC network has trophic and protective functions toward enteric neurons and is fully implicated in the integration and the modulation of neuronal activities. Moreover, EGCs seem to be active elements of the ENS during intestinal inflammatory and immune responses, sharing with astrocytes the ability to act as antigen-presenting cells and interacting with the mucosal immune system via the expression of cytokines and cytokine receptors. Transgenic mouse systems have demonstrated that specific ablation of EGC by chemical ablation or autoimmune T-cell targeting induces an intestinal pathology that shows similarities to the early intestinal immunopathology of Crohn's disease. EGCs may also share with astrocytes the ability to regulate tissue integrity, thereby postulating that similar interactions to those observed for the blood-brain barrier may also be partly responsible for regulating mucosal and vascular permeability in the gastrointestinal tract. Disruption of the EGC network in Crohn's disease patients may represent one possible cause for the enhanced mucosal permeability state and vascular dysfunction that are thought to favor mucosal inflammation. GLIA 41:81-93, 2003.

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Section: Neuroprotective and Neuromodulatory Functions Of Egcmentioning

confidence: 61%

Role of enteric glial cells in inflammatory bowel disease

Cabarrocas

Savidge

Liblau

2002

Glia

160

154

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“…First, cortical astrocytes in vivo and in culture are known to contain substantial amounts of glycogen (Cataldo and Broadwell, 1986;Rosenberg and Dichter, 1987) whereas neurons both in adult brain (Koizumi, 1974;Phelps, 1975;Cataldo and Broadwell, 1986) and fetal brain (Bruckner and Biesold,198 1) have negligible glycogen stores. Second, we observed much higher glycogen levels in glial-confluent cul tures containing both NSE-positive neurons and GF AP-positive astrocytes than in glial-poor cul tures containing predominantly NSE-positive neu rons.…”

Section: Discussionmentioning

confidence: 99%

“…The major energy reserve in brain is glycogen (Lowry et aI., 1964), accounting for about 65% of ATP that can be generated under ischemic conditions. Almost all of this glycogen is localized to astrocytes, with other glial elements and neurons having minimal stores (Koizumi, 1974;Phelps, 1975;Cataldo and Broadwell, 1986).…”

mentioning

confidence: 99%

Glial Glycogen Stores Affect Neuronal Survival during Glucose Deprivation in vitro

Swanson

Choi

1993

J Cereb Blood Flow Metab

225

155

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Summary: Glia perform several energy-dependent func tions that may aid neuronal survival under pathological conditions. Glycogen is the major energy reserve in brain, and it is localized almost exclusively to astrocytes. Using murine cortical cell cultures containing both glia and neu rons, we examined the effect of altered glial glycogen stores on neuronal survival following glucose depriva tion. As previously reported, cultures exposed for several hours to media lacking glucose developed widespread neuronal degeneration without glial degeneration. If glial astrocyte glycogen content was increased to 2-3 times Astrocytes perform multiple functions essential for the normal activity of neurons in the brain. In addition to providing mechanical support and trophic factors (Bunge and Waksman, 1985), astro cytes maintain homeostasis of the brain extracellu lar fluid (ECF). Astrocytes are largely responsible for the uptake and catabolism of excitatory amino acids and other neurotransmitters (Ericinska et aI., 1986;Hertz, 1979;Varon and Somjen, 1979), and for the uptake and redistribution of K + (Hertz, 198 1; Jendelova and Sykova, 199 1). Astrocytic am monia fixation provides the only mechanism other than diffusion for clearing brain ammonia (Cooper and Lai, 1987). Astrocytes may also play an impor-

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“…Glycogen is confined mainly to the astrocytes (Cataldo and Broadwell, 1986;Koizumi, 1974;Phelps, 1975), where its breakdown feeds glycolysis and lactate production (Brown et al, 2003;Dringen et al, 1993) (Figure 10). Secondarily, glycogen can maintain the glucose concentration in the extracellular fluid (Dringen and Hamprecht, 1992).…”

Section: Glycogen Metabolismmentioning

confidence: 99%

“…after attenuation of neuronal activity as in hibernation (Koizumi, 1974) and anaesthesia (Phelps, 1972), presumably because the rate of synthesis stays high (Watanabe and Passonneau, 1973). Hence, when the brain is deprived of periods with low activity and metabolism as during sleep (Madsen and Vorstrup, 1991), glycogen remains low (Kong et al, 2002).…”

Section: Glycogen Metabolismmentioning

confidence: 99%

Fuelling Cerebral Activity in Exercising Man

Dalsgaard

2005

J Cereb Blood Flow Metab

137

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The metabolic response to brain activation in exercise might be expressed as the cerebral metabolic ratio (MR; uptake O 2 /glucose + 1/2 lactate). At rest, brain energy is provided by a balanced oxidation of glucose as MR is close to 6, but activation provokes a 'surplus' uptake of glucose relative to that of O 2 . Whereas MR remains stable during light exercise, it is reduced by 30% to 40% when exercise becomes demanding. The MR integrates metabolism in brain areas stimulated by sensory input from skeletal muscle, the mental effort to exercise and control of exercising limbs. The MR decreases during prolonged exhaustive exercise where blood lactate remains low, but when vigorous exercise raises blood lactate, the brain takes up lactate in an amount similar to that of glucose. This lactate taken up by the brain is oxidised as it does not accumulate within the brain and such pronounced brain uptake of substrate occurs independently of plasma hormones. The 'surplus' of glucose equivalents taken up by the activated brain may reach B10 mmol, that is, an amount compatible with the global glycogen level. It is suggested that a low MR predicts shortage of energy that ultimately limits motor activation and reflects a biologic background for 'central fatigue'.

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Glycogen in the Central Nervous System

Cited by 67 publications

References 87 publications

Role of enteric glial cells in inflammatory bowel disease

Role of enteric glial cells in inflammatory bowel disease

Glial Glycogen Stores Affect Neuronal Survival during Glucose Deprivation in vitro

Fuelling Cerebral Activity in Exercising Man

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