Beta-adrenergic receptor activation increases GABA uptake in adolescent mice frontal cortex: Modulation by cannabinoid receptor agonist WIN55,212-2

Martins, Robertta Silva; Freitas, Isis Grigorio de; Sathler, Matheus F.; Borges-Martins, Vladimir Pedro Peralva; Schitine, Clarissa De Sampaio; Sampaio, Luzia da Silva; Freitas, Hércules Rezende; Manhães, Alex C.; Pereira, Maurício dos Santos; Reis, Ricardo Augusto de Melo; Kubrusly, Regina Célia Cussa

doi:10.1016/j.neuint.2018.08.011

Cited by 7 publications

(2 citation statements)

References 68 publications

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“…Data from AD patients show diminished GABAergic signaling in both the temporal cortex and the cerebrospinal fluid (CSF), associated with dysfunctional synaptic transmission (60, 61). Furthermore, adrenergic receptors have been shown to regulate GABAergic signaling whereby pharmacological activation of badrenergic receptors coupled to Gs increases cAMP levels through adenosine triphosphate (ATP) conversion via adenylyl cyclase, thus activating PKA and triggering GABA transporter 1 (GAT-1) phosphorylation, which, in turn, increases the uptake and release of GABA (62). This interaction perhaps describes how an increase of both the adrenergic and GABAergic pathways results in the significant improvement in cognition in the mouse model of AD following treatment with the modified C5aR agonist EP67.…”

Section: B Amentioning

confidence: 99%

Pharmacological activation of the C5a receptor leads to stimulation of the β-adrenergic receptor and alleviates cognitive impairment in a murine model of familial Alzheimer’s disease

et al. 2022

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Alzheimer’s disease (AD) is a progressive neurodegenerative disease of the brain causing either familial or sporadic dementia. We have previously administered the modified C5a receptor agonist (EP67) for a short period to a transgenic mouse model of AD (5XFAD) and have observed not only reduction in β-amyloid deposition and gliosis but also improvement in cognitive impairment. Inquiring, however, on the effects of EP67 in an already heavily burdened animal, thus representing a more realistic scenario, we treated 6-month-old 5XFAD mice for a period of 14 weeks. We recorded a significant decrease in both fibrillar and pre-fibrillar β-amyloid as well as remarkable amelioration of cognitive impairment. Following proteomic analysis and pathway association, we postulate that these events are triggered through the upregulation of β-adrenergic and GABAergic signaling. In summary, our results reveal how inflammatory responses can be employed in inducing tangible phenotype improvements even in advanced stages of AD.

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Section: B Amentioning

confidence: 99%

Pharmacological activation of the C5a receptor leads to stimulation of the β-adrenergic receptor and alleviates cognitive impairment in a murine model of familial Alzheimer’s disease

et al. 2022

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“…Conversely, an endogenous agonist of endocannabinoid receptors, 2-arachidonoylglycerol (2-AG), increases GABA uptake (Romero et al, 1998;Venderova et al, 2005). CB1 receptors have been suggested to interact or colocalize with β 2 adrenergic receptors (Hudson et al, 2010), the activation of which also increases GAT1 expression and GABA uptake (Martins et al, 2018). The ability of β 2 adrenergic receptors to promote GABA uptake (and that of β 1 adrenergic receptors to inhibit it) are mediated by a PKA pathway controlled by cannabinoid receptors, because the modulation of GABA update by adrenergic receptors is inhibited by the cannabinoid receptor agonist WIN55,212-2 (Martins et al, 2018).…”

Section: Regulation Of Gaba Uptakementioning

confidence: 99%

Regulation of Glutamate, GABA and Dopamine Transporter Uptake, Surface Mobility and Expression

Ryan

Ingram

Scimemi

2021

Front. Cell. Neurosci.

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Neurotransmitter transporters limit spillover between synapses and maintain the extracellular neurotransmitter concentration at low yet physiologically meaningful levels. They also exert a key role in providing precursors for neurotransmitter biosynthesis. In many cases, neurons and astrocytes contain a large intracellular pool of transporters that can be redistributed and stabilized in the plasma membrane following activation of different signaling pathways. This means that the uptake capacity of the brain neuropil for different neurotransmitters can be dynamically regulated over the course of minutes, as an indirect consequence of changes in neuronal activity, blood flow, cell-to-cell interactions, etc. Here we discuss recent advances in the mechanisms that control the cell membrane trafficking and biophysical properties of transporters for the excitatory, inhibitory and modulatory neurotransmitters glutamate, GABA, and dopamine.

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NMDA Receptor Activation and Ca2+/PKC Signaling in Nicotine-Induced GABA Transport Shift in Embryonic Chick Retina

et al. 2023

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Beta-adrenergic receptor activation increases GABA uptake in adolescent mice frontal cortex: Modulation by cannabinoid receptor agonist WIN55,212-2

Cited by 7 publications

References 68 publications

Pharmacological activation of the C5a receptor leads to stimulation of the β-adrenergic receptor and alleviates cognitive impairment in a murine model of familial Alzheimer’s disease

Pharmacological activation of the C5a receptor leads to stimulation of the β-adrenergic receptor and alleviates cognitive impairment in a murine model of familial Alzheimer’s disease

Regulation of Glutamate, GABA and Dopamine Transporter Uptake, Surface Mobility and Expression

NMDA Receptor Activation and Ca2+/PKC Signaling in Nicotine-Induced GABA Transport Shift in Embryonic Chick Retina

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