Effect of noradrenergic system on the anxiolytic-like effect of DOI (5-HT2A/2C agonists) in the four-plate test

Massé, Fabienne; Hascoët, Martine; Dailly, Éric; Bourin, Michel

doi:10.1007/s00213-005-0220-3

Cited by 32 publications

(15 citation statements)

References 59 publications

(63 reference statements)

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“…The same anxiolytic-like effect following the use of various antidepressants has been proposed [39] . The evidence suggests a strong connection between 5-HT 2A receptors and noradrenaline neurotransmission [39] – [40] . It has been demonstrated that another serotonin receptor (5-HT 1A ) not only is involved in the establishment of normal anxiety-like behavior but also that this effect is acting during prenatal and postnatal development [41] – [42] .…”

Section: Discussionmentioning

confidence: 95%

Clonidine Treatment Delays Postnatal Motor Development and Blocks Short-Term Memory in Young Mice

Calvino-Núñez

Domínguez-del-Toro

2014

PLoS ONE

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During the development of the nervous system, the perinatal period is particularly sensitive as neuronal connections are still forming in the brain of the neonate. Alpha2-adrenergic receptors are overexpressed temporarily in proliferative zones in the developing brain, reaching a peak during the first postnatal week of life. Both stimulation and blocking of these receptors during this period alter the development of neural circuits, affecting synaptic connectivity and neuronal responses. They even affect motor and cognitive skills later on in the adult. It's especially important to look for the early neurological consequences resulting from such modifications, because they may go unnoticed. The main objective of the present study has been to reaffirm the importance of the maturation of alpha-adrenergic system in mice, by carrying out a comprehensive examination of motor, behavioral and cognitive effects in neonates, during early postnatal development, following chronic administration of the drug Clonidine, an alpha2 adrenergic system agonist. Our study shows that mice treated postnatally with clonidine present a temporal delay in the appearance of developmental markers, a slow execution of vestibular reflexes during first postnatal week of life and a blockade of the short term memory in the novel object recognition task. Shortly after the treatment the startle response is hyperreactive.

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Section: Discussionmentioning

confidence: 95%

Clonidine Treatment Delays Postnatal Motor Development and Blocks Short-Term Memory in Young Mice

Calvino-Núñez

Domínguez-del-Toro

2014

PLoS ONE

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“…The α 2A AR plays an important role in controlling norepinephrine release and response. This discovery that APP can affect α 2A AR internalization may have an impact on modulation of noradrenergic activity and sympathetic tone, but also affecting pain perception and decreasing epileptogenesis and anxiety ( Hein, 2006 ; Masse et al, 2006 ; Gyires et al, 2009 ; Zhang et al, 2017 ). The noradrenergic system regulates arousal, learning and memory, which has also been implicated in regulating neuroinflammation ( Ardestani et al, 2017 ).…”

Section: β-Arrestin In Agingmentioning

confidence: 99%

β-Arrestin Based Receptor Signaling Paradigms: Potential Therapeutic Targets for Complex Age-Related Disorders

et al. 2018

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G protein coupled receptors (GPCRs) were first characterized as signal transducers that elicit downstream effects through modulation of guanine (G) nucleotide-binding proteins. The pharmacotherapeutic exploitation of this signaling paradigm has created a drug-based field covering nearly 50% of the current pharmacopeia. Since the groundbreaking discoveries of the late 1990s to the present day, it is now clear however that GPCRs can also generate productive signaling cascades through the modulation of β-arrestin functionality. β-Arrestins were first thought to only regulate receptor desensitization and internalization – exemplified by the action of visual arrestin with respect to rhodopsin desensitization. Nearly 20 years ago, it was found that rather than controlling GPCR signal termination, productive β-arrestin dependent GPCR signaling paradigms were highly dependent on multi-protein complex formation and generated long-lasting cellular effects, in contrast to G protein signaling which is transient and functions through soluble second messenger systems. β-Arrestin signaling was then first shown to activate mitogen activated protein kinase signaling in a G protein-independent manner and eventually initiate protein transcription – thus controlling expression patterns of downstream proteins. While the possibility of developing β-arrestin biased or functionally selective ligands is now being investigated, no additional research has been performed on its possible contextual specificity in treating age-related disorders. The ability of β-arrestin-dependent signaling to control complex and multidimensional protein expression patterns makes this therapeutic strategy feasible, as treating complex age-related disorders will likely require therapeutics that can exert network-level efficacy profiles. It is our understanding that therapeutically targeting G protein-independent effectors such as β-arrestin will aid in the development of precision medicines with tailored efficacy profiles for disease/age-specific contextualities.

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“…The a 2A -adrenergic receptor (a 2A AR) is a prototypical GPCR, and mediates a variety of critical physiologic/ pharmacological responses, which include lowering blood pressure, evoking sedation, reducing pain perception, and decreasing epileptogenesis and anxiety (10)(11)(12).…”

mentioning

confidence: 99%

The amyloid precursor protein modulates α _2A ‐adrenergic receptor endocytosis and signaling through disrupting arrestin 3 recruitment

et al. 2017

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The amyloid precursor protein (APP) has long been appreciated for its role in Alzheimer's disease (AD) pathology. However, less is known about the physiologic function of APP outside of AD. Particularly, whether and how APP may regulate functions of cell surface receptors, including GPCRs, remains largely unclear. In this study, we identified a novel direct interaction between APP and the α-adrenergic receptor (αAR) that occurs at the intracellular domains of both proteins. The APP interaction with αAR is promoted by agonist stimulation and competes with arrestin 3 binding to the receptor. Consequently, the presence of APP attenuates αAR internalization and desensitization, which are arrestin-dependent processes. Furthermore, in neuroblastoma neuro-2A cells and primary superior cervical ganglion neurons, where APP is highly expressed, the lack of APP leads to a dramatic increase in plasma membrane recruitment of endogenous arrestin 3 following αAR activation. Concomitantly, agonist-induced internalization of αAR is significantly enhanced in these neuronal cells. Our study provided the first evidence that APP fine tunes GPCR signaling and trafficking. Given the important role of αAR in controlling norepinephrine release and response, this novel regulation of αAR by APP may have an impact on modulation of noradrenergic activity and sympathetic tone.-Zhang, F., Gannon, M., Chen, Y., Zhou, L., Jiao, K., Wang, Q. The amyloid precursor protein modulates α-adrenergic receptor endocytosis and signaling through disrupting arrestin 3 recruitment.

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Effect of noradrenergic system on the anxiolytic-like effect of DOI (5-HT2A/2C agonists) in the four-plate test

Abstract: These results indicate that the DOI seems to act on the 5-HT2 receptors post-synaptically located. The effect of DOI is regulated by the alpha2-adrenoceptors.

Cited by 32 publications

References 59 publications

Clonidine Treatment Delays Postnatal Motor Development and Blocks Short-Term Memory in Young Mice

Clonidine Treatment Delays Postnatal Motor Development and Blocks Short-Term Memory in Young Mice

β-Arrestin Based Receptor Signaling Paradigms: Potential Therapeutic Targets for Complex Age-Related Disorders

The amyloid precursor protein modulates α _2A ‐adrenergic receptor endocytosis and signaling through disrupting arrestin 3 recruitment

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Effect of noradrenergic system on the anxiolytic-like effect of DOI (5-HT2A/2C agonists) in the four-plate test

Abstract: These results indicate that the DOI seems to act on the 5-HT2 receptors post-synaptically located. The effect of DOI is regulated by the alpha2-adrenoceptors.

Cited by 32 publications

References 59 publications

Clonidine Treatment Delays Postnatal Motor Development and Blocks Short-Term Memory in Young Mice

Clonidine Treatment Delays Postnatal Motor Development and Blocks Short-Term Memory in Young Mice

β-Arrestin Based Receptor Signaling Paradigms: Potential Therapeutic Targets for Complex Age-Related Disorders

The amyloid precursor protein modulates α 2A ‐adrenergic receptor endocytosis and signaling through disrupting arrestin 3 recruitment

Contact Info

Product

Resources

About

The amyloid precursor protein modulates α _2A ‐adrenergic receptor endocytosis and signaling through disrupting arrestin 3 recruitment