In vivo voltammetric evidence that locus coeruleus activation predominantly releases norepinephrine in the infralimbic cortex: Effect of acute ethanol

Deal, Aaron; Mikhailova, Maria A.; Grinevich, Valentina P.; Weiner, Jeff L.; Gainetdinov, Raul R.; Budygin, Evgeny A.

doi:10.1002/syn.22080

Cited by 8 publications

(8 citation statements)

References 26 publications

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“…Ethanol inhibition of BG activation was dose-dependent, reaching almost complete inhibition at 1.5 g/kg (i.p.). This ethanol dosage is within the range used for acute ethanol exposure studies of rodents 23,28,37 , and caused temporary ataxic motor coordination as discussed below, but did not impair their ability to walk on the treadmill while head restrained (Fig. 1d).…”

Section: Resultsmentioning

confidence: 88%

“…Fastscan cyclic voltammetry is an electrochemical approach to monitor neurotransmitter dynamics at subsecond time resolution 65 ; however, despite considerable recent progress it can be challenging to distinguish between the detection of dopamine and NE 66 . Both, microdialysis and fast-scan cyclic voltammetry experiments revealed that depending on the brain region and experimental paradigm acute ethanol can lower, raise or leave extracellular NE concentration unchanged [26][27][28]37 .…”

Section: Discussionmentioning

confidence: 99%

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Ethanol abolishes vigilance-dependent astroglia network activation in mice by inhibiting norepinephrine release

et al. 2020

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Norepinephrine adjusts sensory processing in cortical networks and gates plasticity enabling adaptive behavior. The actions of norepinephrine are profoundly altered by recreational drugs like ethanol, but the consequences of these changes on distinct targets such as astrocytes, which exhibit norepinephrine-dependent Ca2+ elevations during vigilance, are not well understood. Using in vivo two-photon imaging, we show that locomotion-induced Ca2+ elevations in mouse astroglia are profoundly inhibited by ethanol, an effect that can be reversed by enhancing norepinephrine release. Vigilance-dependent astroglial activation is abolished by deletion of α1A-adrenergic receptor from astroglia, indicating that norepinephrine acts directly on these ubiquitous glial cells. Ethanol reduces vigilance-dependent Ca2+ transients in noradrenergic terminals, but has little effect on astroglial responsiveness to norepinephrine, suggesting that ethanol suppresses their activation by inhibiting norepinephrine release. Since abolition of astroglia Ca2+ activation does not affect motor coordination, global suppression of astroglial networks may contribute to the cognitive effects of alcohol intoxication.

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Section: Resultsmentioning

confidence: 88%

Section: Discussionmentioning

confidence: 99%

Ethanol abolishes vigilance-dependent astroglia network activation in mice by inhibiting norepinephrine release

et al. 2020

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“…Fox et al, 2016;Deal et al, 2019), our results for the first time demonstrate the possibility to measure real-time NE efflux in the BLA. Based on pharmacological characterizations, we ruled out the involvement of DA efflux in the signal measured in naïve rats as previously reported for the prefrontal cortex and bed nucleus of the stria terminals (Park et al, 2011;Fox et al, 2016;Deal et al, 2019). As expected, the electrically-evoked NE release was frequency-dependent, while the average maximum concentrations were ∼2-3 fold lower than concentrations in the prefrontal cortex (Deal et al, 2019).…”

Section: Discussionmentioning

confidence: 58%

“…The locus coeruleus (LC) is a key brainstem nucleus involved in stress and arousal (Szabadi, 2013;Naegeli et al, 2018;Daviu et al, 2019). This pontine structure is the primary source of noradrenergic projections in the central nervous system which target many regions throughout the brain, such as the amygdala, thalamus, hypothalamus, and prefrontal cortex, associating the LC with myriad behavioral, motor, and sensory processes (Samuels and Szabadi, 2008;Deal et al, 2019). In particular, the projection from the LC to the basolateral amygdala (BLA) has been proposed as an important pathway in anxiety-related processes and behaviors.…”

Section: Introductionmentioning

confidence: 99%

Stress Alters the Effect of Alcohol on Catecholamine Dynamics in the Basolateral Amygdala

Deal

Park

Weiner

et al. 2021

Front. Behav. Neurosci.

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The current rodent study applied in vivo fast-scan cyclic voltammetry (FSCV), paired with a pharmacological approach, to measure the release of the catecholamines (CA) dopamine (DA) and norepinephrine (NE) in the basolateral amygdala (BLA) following locus coeruleus (LC) stimulation. The primary goal was to determine if exposure to either social (social defeat) or non-social (forced swim) stress altered LC-evoked catecholamine release dynamics in the BLA. We used idazoxan (α2 adrenergic receptor antagonist) and raclopride (D2 dopamine receptor antagonist) to confirm the presence of NE and DA, respectively, in the measured CA signal. In non-stressed rats, injection of idazoxan, but not raclopride, resulted in a significant increase in the detected CA signal, indicating the presence of NE but not DA. Following exposure to either stress paradigm, the measured CA release was significantly greater after injection of either drug, suggesting the presence of both NE and DA in the LC-induced CA signal after social or non-social stress. Furthermore, acute administration of alcohol significantly decreased the CA signal in stressed rats, while it did not have an effect in naïve animals. Together, these data reveal that, while LC stimulation primarily elicits NE release in the BLA of control animals, both social and non-social stress unmask a novel dopaminergic component of LC catecholamine signaling. Future studies will be needed to identify the specific neural mechanism(s) responsible for these plastic changes in LC-BLA catecholamine signaling and to assess the possible contribution of these changes to the maladaptive behavioral phenotypes that develop following exposure to these stressors.

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“…The LC is a catecholamine nucleus and NE is its primary neurotransmitter [23]. With extensive projections throughout the central nervous system [24], this brainstem region has a major role in stress-related behaviors [25], and is involved in the shaping of alcohol-drinking behaviors [21,26]. It is known that aversive states induce LC activation, including ethanol in doses that support CTA [27][28][29][30].…”

Section: Hindbrain Regionsmentioning

confidence: 99%

Distinct and Overlapping Patterns of Acute Ethanol-Induced C-Fos Activation in Two Inbred Replicate Lines of Mice Selected for Drinking to High Blood Ethanol Concentrations

et al. 2020

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The inbred high drinking in the dark (iHDID1 and iHDID2) strains are two replicate lines bred from the parent HS/Npt (HS) line for achieving binge levels of blood ethanol concentration (≥80 mg/dL BEC) in a four-hour period. In this work, we sought to evaluate differences in baseline and ethanol-induced c-Fos activation between the HS, iHDID1, and iHDID2 genetic lines in brain regions known to process the aversive properties of ethanol. Methods: Male and female HS, iHDID1, and iHDID2 mice underwent an IP saline 2 3 g/kg ethanol injection. Brain sections were then stained for c-Fos expression in the basolateral/central amygdala (BLA/CeA), bed nucleus of the stria terminals (BNST), A2, locus coeruleus (LC), parabrachial nucleus (PBN), lateral/medial habenula (LHb/MHb), paraventricular nucleus of the thalamus (PVT), periaqueductal gray (PAG), Edinger–Westphal nuclei (EW), and rostromedial tegmental nucleus (RMTg). Results: The iHDID1 and iHDID2 lines showed similar and distinct patterns of regional c-Fos; however, in no region did the two both significantly differ from the HS line together. Conclusions: Our findings lend further support to the hypothesis the iHDID1 and the iHDID2 lines arrive at a similar behavior phenotype through divergent genetic mechanisms.

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In vivo voltammetric evidence that locus coeruleus activation predominantly releases norepinephrine in the infralimbic cortex: Effect of acute ethanol

Cited by 8 publications

References 26 publications

Ethanol abolishes vigilance-dependent astroglia network activation in mice by inhibiting norepinephrine release

Ethanol abolishes vigilance-dependent astroglia network activation in mice by inhibiting norepinephrine release

Stress Alters the Effect of Alcohol on Catecholamine Dynamics in the Basolateral Amygdala

Distinct and Overlapping Patterns of Acute Ethanol-Induced C-Fos Activation in Two Inbred Replicate Lines of Mice Selected for Drinking to High Blood Ethanol Concentrations

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