Effect of adrenergic agonists on glycogenolysis in primary cultures of astrocytes

doi:10.1016/0006-8993(90)90028-A

Brain Research

Volume 536, Issues 1–2, 17 December 1990, Pages 220-226

https://doi.org/10.1016/0006-8993(90)90028-A Get rights and content

Abstract

A stimulation of glycogenolysis in astrocytes by adrenergic agonists has repeatedly been demonstrated in the literature. However, some confusion exists regarding which type of adrenergic receptor subtype is involved, and little information is available about rates of glycogenolysis and potencies of adrenergic agonists. In the present study, we have investigated these parameters using primary cultures of mouse astrocytes which constitute a reliable model for their in vivo counterparts. Antagonist as well as agonist studies revealed that noradrenaline acts both on a β- and on anα₂-receptor. Isoproterenol and clonidine, agonists acting relatively specifically on only one of these receptor subtypes could, on their own, stimulate glycogenolysis and the effect by noradrenaline could be inhibited by alprenolol (β-adrenergic antagonist) and/or yohimbine (α₂-adrenergic antagonist) but not by prazosin (α₁-adrenergic antagonist). Excess potassium also stimulated glycogenolysis but this effect was not antagonized by adrenergic antagonists, alone or in combination. The involvement of anα₂-adrenergic receptor in a homogeneous culture of astrocytes provides proof that not alla₂-adrenergic receptors in brain are presynaptic. The maximum rate of stimulated glycogenolysis was calculated to be 3–7 nmol/min per mg protein. Computer analysis showed that the EC₅₀ values for noradrenaline, isoproterenol and clonidine were 4.6 × 10⁻⁸ M, 3.0 × 10⁻⁷ M, and 6.5 × 10⁻⁷ M, respectively.

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In the brain and periphery, glycogen metabolism is controlled by opposing actions of glycogen synthase (GS) and glycogen phosphorylase (GP), which respectively catalyze glycogen synthesis or breakdown. NE has well-documented stimulatory effects on astrocyte glycogenolysis in vitro (Magistretti, 1988; Quach et al., 1988; Subbarao and Hertz, 1990). Recent in vivo studies indicate that the ovarian steroid hormone estradiol regulates basal and hypoglycemic patterns of GP expression in key hypothalamic glucoregulatory structures, e.g. ventromedial hypothalamic nucleus (VMN) and lateral hypothalamic area (LHA) (Tamrakar et al., 2015).
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Effect of adrenergic agonists on glycogenolysis in primary cultures of astrocytes

Abstract

Pharmacol. Biochem. Behav.

Brain Research

Brain Research

Brain Research

Prog. Neuropsychopharmacol. Biol. Psychiat.

J. Biol. Chem.

Regul. Pept.

Neuropharmacology

Ion channels in vertebrate glia

Annu. Rev. Neurosci.

Fine structure of monoamine axon terminals in cerebral cortex

Alpha-adrenergic receptors on glial cells

Norepinephrine sensitive properties of c-6 astrocytoma cells

Mol. Pharmacol.

Characterization of alpha-1 and alpha-2 adrenergic receptors

Int. Rev. Neurobiol.

Effects of neurotransmitters on astrocyte glycogen stores in vitro

J. Neurochem.

Regulation of glycogen metabolism in primary and transformed astrocytes in vitro

J. Neurochem.

Regulation of glycogenolysis in transformed astrocytes in vitro

J. Neurochem.

New look at the aminergic neuron systems

Nature (Lond.)

Capacity for substrate utilization in oxidative metabolism by neurons, astrocytes and oligodendrocytes from developing brain in primary culture

J. Neurosci. Res.

Identification of the beta adrenergic receptor subtype on astroglia purified from rat brain

J. Pharmacol. Exp. Ther.

Acute and chronic effects of antidepressant drugs on beta-adrenergic function in astrocytes in primary cultures — an indication of glial involvement in effective disorders?

J. Neurosci. Res.

Cell cultures

Energy metabolism in glutamatergic neurons, GABAergic neurons and astrocytes in primary cultures

Neurochem. Res.