Stimulation of energy metabolism by α‐adrenergic agonists in primary cultures of astrocytes

Subbarao, Kala V.; Hertz, Leif

doi:10.1002/jnr.490280312

Cited by 51 publications

(26 citation statements)

References 34 publications

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“…The enhancement of pyruvate dehydrogenation (i.e., entry of pyruvate into the TCA cycle), a-K G dehydro genation (i.e., turnover within the TCA cycle) and gluta mine hydrolysis [78][79][80][81][82] in astrocytes might be evoked by a similar mechanism as in heart muscle, and we have reported that the stimulation of pyruvate dehydrogena tion by NA is abolished during incubation in a medium which has been depicted for calcium [78]. However, this is not always the case and the stimulation is not inhibited by ruthenium red (fig.…”

Section: Oxidative Metabolism and Glutamine Hydrolysismentioning

confidence: 99%

Signalling Effect of Elevated Potassium Concentrations and Monoamines on Brain Energy Metabolism at the Cellular Level (Part 2 of 2)

Peng¹,

Chen²,

Hájek³

et al. 1994

Dev Neurosci

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The effects of elevated K⁺ concentrations and monoamine transmitters on different cell types in the CNS and on different subcellular structures in these cells are reviewed. Pronounced differences exist in the metabolic processes that are stimulated by excess K⁺ and by adrenergic agonists, e.g., noradrenaline. An elevation in the extracellular K⁺ concentration appears to enhance neuronal-astrocytic interaction by stimulating metabolic processes involved in (1) the promotion of supply of precursors for transmitter glutamate, and (2) reestablishment of resting ion distribution following neuronal excitation. The monoamine transmitters stimulate energy production and Na⁺, K⁺-ATPase activity in astrocytes in a complex manner and, in so doing, facilitate their role in ion regulation. However, in contrast to excess K⁺, they do not enhance the production of astrocytic precursors for neuronal glutamate production. Emphasis is placed on possible profound differences in metabolic effects on excitatory and inhibitory neurotransmission and on the importance of stimulation of glycolytic metabolism in astrocytes versus oxidative metabolism in neurons.

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Section: Oxidative Metabolism and Glutamine Hydrolysismentioning

confidence: 99%

Signalling Effect of Elevated Potassium Concentrations and Monoamines on Brain Energy Metabolism at the Cellular Level (Part 2 of 2)

Peng¹,

Chen²,

Hájek³

et al. 1994

Dev Neurosci

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“…23 Its penetration over the intact bloodbrain barrier is poor 24 but increases in animal models after barrier disruption by intracarotid injection of hypertonic urea; simultaneously, CBF and metabolism increase. 4,5 In bacterial meningitis, a certain extent of barrier disruption is likely to occur.…”

Section: Discussionmentioning

confidence: 99%

Cerebral Blood Flow and Metabolism During Infusion of Norepinephrine and Propofol in Patients With Bacterial Meningitis

Møller

Qvist

Tofteng

et al. 2004

Stroke

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Background and Purpose-In patients with severe bacterial meningitis, norepinephrine is often infused to increase mean arterial pressure (MAP). This increases cerebral blood flow (CBF), but it is unknown if this increase is caused by impaired cerebral autoregulation or by a cerebral effect of norepinephrine through increased cerebral metabolism. The latter possibility implies a CBF-metabolism coupling. This has not been studied during meningitis. We studied the effect of norepinephrine and propofol on CBF and oxidative metabolism in patients with severe bacterial meningitis. Methods-In seven patients with pneumococcal meningitis and 7 healthy subjects, norepinephrine was infused intravenously; patients also underwent intravenous propofol infusion. Global CBF was measured by the Kety-Schmidt technique; cerebral oxidative metabolism and net flux of norepinephrine and epinephrine were calculated from measured arterial-to-jugular venous concentration differences (a-vD). [54 to 77] mL/100 g per minute) but remained unchanged in controls. The cerebral metabolic rate of oxygen (CMRO 2 ) decreased in patients and remained unchanged in controls. No cerebral net flux of norepinephrine or epinephrine was found at any time in the 2 groups. During propofol infusion, CMRO 2 , and the a-vDO 2 decreased whereas CBF was unchanged. Conclusions-In patients with severe bacterial meningitis, norepinephrine increases both MAP and CBF but not CMRO 2 , indicating impaired autoregulation. Propofol reduces CBF relatively less than cerebral metabolism, suggesting a resetting of the CBF-CMRO 2 relationship. Results-During

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“…Moreover, there are Ca 2+ -mediated increases of glutaminase activity [253] and a direct enhancement of oxidative phosphorylation [252,254]. A similar response occurs in astrocytes, where noradrenaline and α 2 -adrenergic agonists stimulate pyruvate dehydrogenation [40,118,178], α-ketoglutarate dehydrogenation [221] and hydrolysis of glutamine to glutamate [255] ( Table 2). No corresponding effect on α-ketoglutarate dehydrogenation was observed in cultured neurons [256].…”

Section: Oxidative Metabolismmentioning

confidence: 99%

“…However the effect on glucose uptake is exerted on β 3 -adrenoceptors [159] and that on glycolysis on α 1 -adrenoceptors [221][222].…”

Section: Glucose Uptake and Glycolysismentioning

confidence: 99%

“…Unlike pyruvate dehydrogenase activity and glutamine hydrolysis, α-ketoglutarate dehydrogenase activity is also stimulated by the ·1-adrenergic agonist phenylephrine [221]. Thus, there is no simple correlation beween an increase in astrocytic [Ca 2+ ] i and stimulation of oxidative metabolism, as also indicated by the ability of other transmitters (e.g.…”

Section: Oxidative Metabolismmentioning

confidence: 99%

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Astrocytic Adrenoceptors: A Major Drug Target in Neurological and Psychiatric Disorders?

Hertz¹,

Chen²,

Gibbs³

et al. 2004

CDTCNSND

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Considerable attention has recently been paid to astrocyte functions, which are briefly summarized. A large amount of data is available about adrenoceptor expression and function in astrocytes, some of it dating back to the 1970's and some of it very recent. This material is reviewed in the present paper. The brain is innervated by noradrenergic fibers extending from locus coeruleus in the brain stem, which in turn is connected to a network of adrenergic and noradrenergic nuclei in the medulla and pons, contributing to the control of (nor)adrenergic, serotonergic, dopaminergic and cholinergic function, both in the central nervous system (CNS) and in the periphery. In the CNS astrocytes constitute a major target for noradrenergic innervation, which regulates morphological plasticity, energy metabolism, membrane transport, gap junction permeability and immunological responses in these cells. Noradrenergic effects on astrocytes are essential during consolidation of episodal, long-term memory, which is reinforced by β-adrenergic activation. Glycogenolysis and synthesis of glutamate and glutamine from glucose, both of which are metabolic processes restricted to astrocytes, occurs at several time-specific stages during the consolidation. Astrocytic abnormalities are almost certainly important in the pathogenesis of multiple sclerosis and in all probability contribute essentially to inflammation and malfunction in Alzheimer's disease and to mood disturbances in affective disorders. Noradrenergic function in astrocytes is severely disturbed by chronic exposure to cocaine, which also changes astrocyte morphology. Development of drugs modifying noradrenergic receptor activity and/or down-stream signaling is advocated for treatment of several neurological/psychiatric disorders and for neuroprotection. Astrocytic preparations are suggested for study of mechanism(s) of action of antidepressant drugs and pathophysiology of mood disorders.

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Stimulation of energy metabolism by α‐adrenergic agonists in primary cultures of astrocytes

Cited by 51 publications

References 34 publications

Signalling Effect of Elevated Potassium Concentrations and Monoamines on Brain Energy Metabolism at the Cellular Level (Part 2 of 2)

Signalling Effect of Elevated Potassium Concentrations and Monoamines on Brain Energy Metabolism at the Cellular Level (Part 2 of 2)

Cerebral Blood Flow and Metabolism During Infusion of Norepinephrine and Propofol in Patients With Bacterial Meningitis

Astrocytic Adrenoceptors: A Major Drug Target in Neurological and Psychiatric Disorders?

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