Acute ethanol modulation of neurocircuit function in the nucleus of the tractus solitarius

Aimino, Michael A; Coker, Caitlin R.; Silberman, Yuval

doi:10.1016/j.brainresbull.2017.07.019

Cited by 26 publications

(13 citation statements)

References 27 publications

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“…Notably, c‐Fos activity was essentially quiescent (less than 5% of controls) in LOFC, dHPC1, and dSub. In contrast to these findings, previous studies have reported increased c‐Fos in several of these brain areas following acute ethanol injections or ethanol drinking, although a history of ethanol vapor exposure resulted in decreased injection‐induced c‐Fos 1,19,26,27 (reviewed by 20 ). These opposing observations can likely be attributed to differences in ethanol dose, route of administration, and duration of exposure.…”

Section: Discussionmentioning

confidence: 76%

Dynamic c‐Fos changes in mouse brain during acute and protracted withdrawal from chronic intermittent ethanol exposure and relapse drinking

et al. 2019

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Alcohol dependence promotes neuroadaptations in numerous brain areas, leading to escalated drinking and enhanced relapse vulnerability. We previously developed a mouse model of ethanol dependence and relapse drinking in which repeated cycles of chronic intermittent ethanol (CIE) vapor exposure drive a significant escalation of voluntary ethanol drinking. In the current study, we used this model to evaluate changes in neuronal activity (as indexed by c-Fos expression) throughout acute and protracted withdrawal from CIE (combined with or without a history of ethanol drinking). We analyzed c-Fos protein expression in 29 brain regions in mice sacrificed 2, 10, 26, and 74 hours or 7 days after withdrawal from 5 cycles of CIE. Results revealed dynamic time- and brain region-dependent changes in c-Fos activity over the time course of withdrawal from CIE exposure, as compared with nondependent air-exposed control mice, beginning with markedly low expression levels upon removal from the ethanol vapor chambers (2 hours), reflecting intoxication. c-Fos expression was enhanced during acute CIE withdrawal (10 and 26 hours), followed by widespread reductions at the beginning of protracted withdrawal (74 hours) in several brain areas. Persistent reductions in c-Fos expression were observed during prolonged withdrawal (7 days) in prelimbic cortex, nucleus accumbens shell, dorsomedial striatum, paraventricular nucleus of thalamus, and ventral subiculum. A history of ethanol drinking altered acute CIE withdrawal effects and caused widespread reductions in c-Fos that persisted during extended abstinence even without CIE exposure. These data indicate that ethanol dependence and relapse drinking drive long-lasting neuroadaptations in several brain regions.

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Section: Discussionmentioning

confidence: 76%

Dynamic c‐Fos changes in mouse brain during acute and protracted withdrawal from chronic intermittent ethanol exposure and relapse drinking

et al. 2019

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“…Thus, since NE innervation in the BNST originates mostly in the NTS, we can hypothesize that ethanol increases NE release by acting on the complex network that includes GABA and glutamate inputs to NTS, including the GABA interneurons 48–49 . Concurring with this view, Aimino et al 50 reported that ethanol stimulated NE neurons within the NTS by inhibiting NMDA transmission in mice. In addition, Lee et al reported that the acute administration of ethanol in rats activated the NE neurons originating in the A1‐A2, and C1‐C3 areas as well those originating in the LC 51 …”

Section: Discussionmentioning

confidence: 93%

“…47 Thus, since NE innervation in the BNST originates mostly in the NTS, we can hypothesize that ethanol increases NE release by acting on the complex network that includes GABA and glutamate inputs to NTS, including the GABA interneurons. 48,49 Concurring with this view, Aimino et al 50 reported that ethanol stimulated NE neurons within the NTS by inhibiting NMDA transmission in mice.…”

Section: Ethanolmentioning

confidence: 90%

Nicotine, cocaine, amphetamine, morphine, and ethanol increase norepinephrine output in the bed nucleus of stria terminalis of freely moving rats

et al. 2019

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The bed nucleus of stria terminalis (BNST) is a complex limbic area involved in neuroendocrine and behavioural responses and, in particular, in the modulation of the stress response. BNST is innervated by dopamine and norepinephrine, which are known to be involved in drug addiction. It is also known that several drugs of abuse increase dopamine transmission in the BNST, but there has been less research regarding the effect on norepinephrine transmission. Here, we have used the microdialysis technique to investigate the effect of several drugs of abuse on norepinephrine transmission in the BNST of freely moving rats. We observed that nicotine (0.2-0.4 mg/kg), cocaine (2.5-5 mg/kg), amphetamine (0.25-0.5 mg/kg), and ethanol (0.5-1.0 g/kg), dose-dependently increased norepinephrine output while the effect of morphine at 3.0 was lower than that of 1.0 mg/kg. These results suggest that many drugs of abuse, though possessing diverse mechanisms of action, share the property of increasing norepinephrine transmission in the BNST. Furthermore, we suggest that the recurring activation of NE transmission in the BNST, due to drug administration, contributes to the alteration of the function that BNST assumes in how the behavioural response to stress manifests, favouring the establishment of the stress-induced drug seeking.

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“…activated norepinephrine neurons in the NTS. 39 Experiment 1 yielded subtle, yet encouraging, signs of ethanol-induced conditioned neuroimmune responses. Experiment 2 aimed at better addressing the potential of IL-6 and IjBa conditioning and pursued possible agedifferences in these responses.…”

Section: Discussionmentioning

confidence: 96%

Conditioning the neuroimmune response to ethanol using taste and environmental cues in adolescent and adult rats

Gano

Pautassi

Doremus-Fitzwater

et al. 2019

Exp Biol Med (Maywood)

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Our work in adult Sprague-Dawley rats has shown elevation of the cytokine Interleukin (IL)-6 in the hippocampus and amygdala following acute and repeated binge-like doses of ethanol during intoxication. Previously, we have shown that in adults, the central IL-6 response to a sub-threshold dose of ethanol was sensitized by repeated pairings of ethanol as an unconditioned stimulus (US) with an odor conditioned stimulus (CS).In the present studies, acute ethanol exposure (4 g/kg intraperitoneal) was paired with a combined odor and taste cue using a single trial learning procedure, after which rats were tested for conditioned effects of the CS on neuroimmune gene expression. We found that IL-6 was significantly elevated in the amygdala based on exposure to the CS after just one CS–US pairing in young adolescent rats (age P32–40), an effect that was more modest in young adults (P72–80). These data indicate that, despite a normal disposition toward a blunted neuroimmune response to ethanol, adolescents were more sensitive than adults to forming learned associations between ethanol’s neuroimmune effects and conditioned stimuli. Given the emergent role of the immune system in alcoholism, such as regulating ethanol intake, these ethanol-induced conditioned effects on cytokine levels may contribute to our understanding of the unique attributes that make adolescence a time period of vulnerability in the development of later alcohol abuse behaviors. Impact statement A combined odor and taste cue was paired with a binge-like ethanol exposure (4 g/kg intraperitoneal) using a single-trial learning paradigm. Re-exposure to the CS alone was sufficient to evoke a conditioned Interleukin (IL)-6 elevation in the amygdala in adolescents, an effect that was not observed in young adults. This demonstrates a particular sensitivity of adolescents to alcohol-associated cues and neuroimmune learning, whereas prior work indicated that adults require multiple pairings of ethanol to the CS in order to achieve a conditioned amygdala IL-6 response. While the role of immune conditioning has been studied in other drugs of abuse, these findings highlight a previously unknown aspect of alcohol-related learning. Given the emergent importance of the neuroimmune system in alcohol abuse, these findings may be important for understanding cue-induced reinstatement of alcohol intake among problem drinkers.

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Acute ethanol modulation of neurocircuit function in the nucleus of the tractus solitarius

Cited by 26 publications

References 27 publications

Dynamic c‐Fos changes in mouse brain during acute and protracted withdrawal from chronic intermittent ethanol exposure and relapse drinking

Dynamic c‐Fos changes in mouse brain during acute and protracted withdrawal from chronic intermittent ethanol exposure and relapse drinking

Nicotine, cocaine, amphetamine, morphine, and ethanol increase norepinephrine output in the bed nucleus of stria terminalis of freely moving rats

Conditioning the neuroimmune response to ethanol using taste and environmental cues in adolescent and adult rats

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