Dopamine and norepinephrine uptake and metabolism by astroglial cells in culture

Pelton, Elaine; Kimelberg, Harold K.; Shipherd, Susan V.; Bourke, Robert S.

doi:10.1016/0024-3205(81)90322-2

Cited by 125 publications

(71 citation statements)

References 26 publications

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“…At rest, the LC is spontaneously active, while acute stress shifts the firing patterns to increased tonic activity (5-8 Hz) or initiates phasic bursting to cause temporally distinct release of NE (Abercrombie and Jacobs, 1987a, b;Galvez et al, 1996;Mana and Grace, 1997;Quirarte et al, 1998). The kinetics of NE release, degradation, and uptake have been loosely examined (Iversen, 1971;Pelton et al, 1981), and as such it is unclear whether our stimulation paradigm truly mimics endogenous NE release. Thus it is possible that utilizing a different stimulation paradigm could result in different behavioral outputs and could represent different elements of noradrenergic tone into the BLA.…”

Section: Discussionmentioning

confidence: 99%

Chemogenetic and Optogenetic Activation of Gαs Signaling in the Basolateral Amygdala Induces Acute and Social Anxiety-Like States

Siuda

Al‐Hasani

McCall

et al. 2016

Neuropsychopharmacol

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Anxiety disorders are debilitating psychiatric illnesses with detrimental effects on human health. These heightened states of arousal are often in the absence of obvious threatening cues and are difficult to treat owing to a lack of understanding of the neural circuitry and cellular machinery mediating these conditions. Activation of noradrenergic circuitry in the basolateral amygdala is thought to have a role in stress, fear, and anxiety, and the specific cell and receptor types responsible is an active area of investigation. Here we take advantage of two novel cellular approaches to dissect the contributions of G-protein signaling in acute and social anxiety-like states. We used a chemogenetic approach utilizing the Gαs DREADD (rM3Ds) receptor and show that selective activation of generic Gαs signaling is sufficient to induce acute and social anxiety-like behavioral states in mice. Second, we use a recently characterized chimeric receptor composed of rhodopsin and the β 2 -adrenergic receptor (Opto-β 2 AR) with in vivo optogenetic techniques to selectively activate Gαs β-adrenergic signaling exclusively within excitatory neurons of the basolateral amygdala. We found that optogenetic induction of β-adrenergic signaling in the basolateral amygdala is sufficient to induce acute and social anxiety-like behavior. These findings support the conclusion that activation of Gαs signaling in the basolateral amygdala has a role in anxiety. These data also suggest that acute and social anxiety-like states may be mediated through signaling pathways identical to β-adrenergic receptors, thus providing support that inhibition of this system may be an effective anxiolytic therapy.

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Section: Discussionmentioning

confidence: 99%

Chemogenetic and Optogenetic Activation of Gαs Signaling in the Basolateral Amygdala Induces Acute and Social Anxiety-Like States

Siuda

Al‐Hasani

McCall

et al. 2016

Neuropsychopharmacol

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“…In the brain slice, the rate at which dopamine, released by electrical stimulation, is removed from the extracellular medium is governed primarily by the neuronal uptake system into nerve terminals and the extraneuronal uptake systems into glial cells (Pelton et al, 1981). The relative importance of these two uptake systems is not established.…”

Section: Discussionmentioning

confidence: 99%

Differential action of (+)‐amphetamine on electrically evoked dopamine overflow in rat brain slices containing corpus striatum and nucleus accumbens

Wieczorek

Kruk

1994

British J Pharmacology

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1 The effects of (+)-amphetamine on electrically evoked dopamine overflow were examined in the rat brain slice containing either anterior caudate putamen (aCPu) 6 t,12, the rate of removal of [dopamine],x following electrical stimulation was not significantly different in the aCPu and NAc for any of the stimulation conditions. After a 40 min superfusion with (+)-amphetamine (1 AM), t1/2 for ip, 4p/10 Hz and 20p/20 Hz was significantly increased in both the aCPu and NAc, the increase in t1/2 being significantly greater in the aCPu than in the NAc. 7 In conclusion, this study indicates that the dopamine displacement and uptake inhibitory actions of (+ )-amphetamine result in complex and differential effects on electrically evoked dopamine overflow in the aCPu and NAc.

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“…There are many reports that rat or mouse astrocytes in primary cultures or explant culture take up [ 3 H]noradrenaline [120][121][122][123][124]. However, the uptake mechanism is disputed.…”

Section: Cellular Uptakementioning

confidence: 99%

“…However, the uptake mechanism is disputed. The Kimelberg group [121,123] has repeatedly observed a high-affinity, sodiumdependent, concentrative uptake of noradrenaline, which is blocked by tricyclic antidepressants. The other investigators have found only modest accumulation of noradrenaline by facilitated diffusion and little evidence that the uptake should be saturable.…”

Section: Cellular Uptakementioning

confidence: 99%

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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Dopamine and norepinephrine uptake and metabolism by astroglial cells in culture

Cited by 125 publications

References 26 publications

Chemogenetic and Optogenetic Activation of Gαs Signaling in the Basolateral Amygdala Induces Acute and Social Anxiety-Like States

Chemogenetic and Optogenetic Activation of Gαs Signaling in the Basolateral Amygdala Induces Acute and Social Anxiety-Like States

Differential action of (+)‐amphetamine on electrically evoked dopamine overflow in rat brain slices containing corpus striatum and nucleus accumbens

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

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