Carbonic Anhydrase, 5′‐Nucleotidase, and 2′,3′‐Cyclic Nucleotide‐3′‐Phosphodiesterase Activities in Oligodendrocytes, Astrocytes, and Neurons Isolated from the Brains of Developing Rats

Snyder, David S.; Zimmerman, Thomas; Farooq, Muhammad; Norton, William T.; Cammer, Wendy

doi:10.1111/j.1471-4159.1983.tb12661.x

Cited by 56 publications

(14 citation statements)

References 47 publications

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“…Regional differences in age-dependent increases in 5'NTs might reflect the changes in glia-neuron distribution and the differential changes of 5'NT activity in glia cells and neurons during development [269]. HGPRT and APRT activity increased with age [242,267], which suggests the importance of salvage purine metabolism in brain development.…”

Section: Age-dependent Changes In Nucleoside Metabolic Enzyme Activitmentioning

confidence: 98%

Area, Age and Gender Dependence of the Nucleoside System in the Brain: a Review of Current Literature

Kovács

Juhász

Palkovits

et al. 2011

CTMC

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Nucleosides, such as uridine, inosine, guanosine and adenosine, may participate in the regulation of sleep, cognition, memory and nociception, the suppression of seizures, and have also been suggested to play a role in the pathophysiology of some neurodegenerative and neuropsychiatric diseases. Under pathological conditions, levels of nucleosides change extremely in the brain, indicating their participation in the pathophysiology of disorders like Alzheimer's disease, Parkinson's disease and schizophrenia. These findings have resulted in an increasing attention to the roles of nucleosides in the central nervous system. The specific effects of nucleosides depend on the expression of their receptors and transporters in neuronal and glial cells, as well as their extracellular concentrations in the brain. A complex interlinked metabolic network and transporters of nucleosides may balance nucleoside levels in the brain tissue under normal conditions and enable the fine modulation of neuronal and glial processes via nucleoside receptor signaling mechanisms. Brain levels of nucleosides were found to vary when measured in a variety of different brain regions. In addition, nucleoside levels also depend on age and gender. Furthermore, distributions of nucleoside transporters and receptors as well as nucleoside metabolic enzyme activities demonstrate the area, age and gender dependence of the nucleoside system, suggesting different roles of nucleosides in functionally different brain areas. The aim of this review article is to summarize our present knowledge of the area-, age- and gender-dependent distribution of nucleoside levels, nucleoside metabolic enzyme activity, nucleoside receptors and nucleoside transporters in the brain.

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Section: Age-dependent Changes In Nucleoside Metabolic Enzyme Activitmentioning

confidence: 98%

Area, Age and Gender Dependence of the Nucleoside System in the Brain: a Review of Current Literature

Kovács

Juhász

Palkovits

et al. 2011

CTMC

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“…These neuroprotective actions depend on a reasonably well developed adenosinergic system in the perinatal brain. That hypoxia and ischemia induce prominent increases in cerebral adenosine levels in several neonatal models (13)(14)(15)(16), and 5'-nucleotidase activity has been measured (10,41), indicate that the synthetic enzymes for adenosine production from AMP are developed early. Of particular relevance to the present study is the ontogeny of adenosine deaminase and adenosine…”

Section: Dcf-treated Animalsmentioning

confidence: 99%

Reduction in Cerebral Ischemic Injury in the Newborn Rat by Potentiation of Endogenous Adenosine

et al. 1995

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Because of ontogenic influences on the pathophysiologic mechanisms of brain injury in the perinatal brain, and in particular, the incomplete development of adenosine receptor systems, we investigated the potential for adenosine to provide cerebroprotection in a well established newborn rat model of hypoxiaischemia. Fifteen litters of postnatal d 7 animals were subjected to unilateral carotid ligation and exposure to hypoxia (8% oxygen) for 3 h. Immediately after hypoxia-ischemia, animals received either the adenosine deaminase inhibitor deoxycoformycin (DCF; 2.5 mg/kg intraperitoneally) or the adenosine uptake inhibitor propentofylline (PPF; 10 mg/kg intraperitoneally); paired littermates received an equivalent volume of normal saline. On postnatal d 14, injury or protection was assessed by differences in hemispheric weights, morphometric determinations of infarct area, and histopathologic analyses. DCF resulted in a 34% (p = 0.02) and 31% ( p = 0.03) reduction in hemispheric weight disparities and infarct area, respectively; for PPF, these reductions were 46% ( p = 0.03) and 32% ( p = 0.04), Although the brain of the newborn exhibits a higher tolerance to ischemia than that of the adult, morbidity and mortality from hypoxic-ischemic encephalopathy in the perinatal period remain high (1). Although the general pathophysiologic mechanisms underlying cerebral ischemic injury are probably similar between age groups, the unique characteristics of energy and glucose metabolism (2), glutamate receptor physiology (3, 4), and vascular regulation (5, 6) in the newborn brain may dictate separate therapeutic regimens for affected neonates relative to adults.In recent years, experimental evidence has accumulated from adult animal models attesting to the neuroprotective properties of the purine nucleoside adenosine in the setting of Received February 3, 1995; accepted April 6, 1995 7 for review), and the mechanistic basis for such an adenosine-mediated reduction in ischemic brain injury has been outlined (8). Ontogenic studies of the brains of fetal and newborn animals indicate that the requisite metabolic enzymes and transporters for adenosine are fully matured at birth or earlier (9-12). There is also consistent evidence that cerebral adenosine production increases in response to perinatal hypoxia-ischemia (13-16). Although cerebral vessels in fetal and newborn animals exhibit the characteristic vasodilatative response to adenosine (17, 18), significant development of neuronal adenosine receptors, particularly in terms of density and coupling to second messengers, may occur postnatally (12,19,20). Thus, adenosinebased treatments may not provide therapeutic efficacy against cerebral hypoxia-ischemia in the perinatal period. To address this possibility, we used two different drugs to determine whether potentiating endogenous adenosine would confer cerebroprotection in a neonatal model of hypoxia-ischemia.

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“…These studies proposed, for the first time, a link between glycolytic metabolism in oligodendrocytes and axonal integrity and function. Analysis of hexokinase levels in the oligodendroglial fractions isolated from rat brain has shown that in comparison with whole brain or with isolated neurons or astrocytes, oligodendroglia express low levels of this enzyme (Snyder and Wilson, 1983). In agreement with this, Rinholm et al (2011) suggest that lactate is transported from neurons to oligodendrocytes.…”

Section: Introductionmentioning

confidence: 99%

Metabolic Aspects of Neuron-Oligodendrocyte-Astrocyte Interactions

Amaral¹,

Meisingset²,

Kotter³

et al. 2013

Front. Endocrinol.

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Whereas astrocytes have been in the limelight of scientific interest in brain energy metabolism for a while, oligodendrocytes are still waiting for a place on the metabolic stage. We propose to term the interaction of oligodendrocytes with astrocytes and neurons: NOA (neuron–oligodendrocyte–astrocyte) interactions. One of the reasons to find out more about metabolic interactions between oligodendrocytes, neurons, and astrocytes is to establish markers of healthy oligodendrocyte metabolism that could be used for the diagnosis and assessment of white matter disease. The vesicular release of glutamate in the white matter has received considerable attention in the past. Oligodendrocyte lineage cells express glutamate receptors and glutamate toxicity has been implicated in diseases affecting oligodendrocytes such as hypoxic-ischaemic encephalopathy, inflammatory diseases and trauma. As oligodendrocyte precursor cells vividly react to injury it is also important to establish whether cells recruited into damaged areas are able to regenerate lost myelin sheaths or whether astrocytic scarring occurs. It is therefore important to consider metabolic aspects of astrocytes and oligodendrocytes separately. The present review summarizes the limited evidence available on metabolic cycles in oligodendrocytes and so hopes to stimulate further research interests in this important field.

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Carbonic Anhydrase, 5′‐Nucleotidase, and 2′,3′‐Cyclic Nucleotide‐3′‐Phosphodiesterase Activities in Oligodendrocytes, Astrocytes, and Neurons Isolated from the Brains of Developing Rats

Cited by 56 publications

References 47 publications

Area, Age and Gender Dependence of the Nucleoside System in the Brain: a Review of Current Literature

Area, Age and Gender Dependence of the Nucleoside System in the Brain: a Review of Current Literature

Reduction in Cerebral Ischemic Injury in the Newborn Rat by Potentiation of Endogenous Adenosine

Metabolic Aspects of Neuron-Oligodendrocyte-Astrocyte Interactions

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