Fos activation patterns related to acute ethanol and conditioned taste aversion in adolescent and adult rats

Saalfield, Jessica; Spear, Linda P.

doi:10.1016/j.alcohol.2019.02.004

Cited by 18 publications

(16 citation statements)

References 94 publications

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“…The BNST is known to play a role in modulating neurobiological responses to both appetitive and aversive stimuli [ 42 ]. The acute ethanol-induced increase in BNST c-Fos expression observed in the HS and iHDID2 lines is consistent with previous works in Long–Evans and Sprague–Dawley rats and C57BL6/J mice [ 21 , 43 , 44 , 45 , 46 ]. The precise impact of impaired ethanol-induced c-Fos expression in the BNST in the iHDID1 line on the drive to consume ethanol is presently unknown.…”

Section: Discussionsupporting

confidence: 91%

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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Section: Discussionsupporting

confidence: 91%

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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“…91 The reaction of the BNST in adolescents tends to be stronger than in adults. 92 This may partially explain the high susceptibility of adolescents to anxiety disorders. After all, during adolescence, hyperactivation of the BNST and the basolateral amygdala accompanies increment of anxiety-like behaviours in individuals.…”

Section: Insufficient Cognitive Control In Adolescencementioning

confidence: 99%

Adolescent anxiety disorders and the developing brain: comparing neuroimaging findings in adolescents and adults

et al. 2021

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Adolescence is the peak period for the incidence of anxiety disorders. Recent findings have revealed the immaturity of neural networks underlying emotional regulation in this population. Brain vulnerability to anxiety in adolescence is related to the unsynchronised development of anxiety-relevant brain functional systems. However, our current knowledge on brain deficits in adolescent anxiety is mainly borrowed from studies on adults. Understanding adolescent-specific brain deficits is essential for developing biomarkers and brain-based therapies targeting adolescent anxiety. This article reviews and compares recent neuroimaging literature on anxiety-related brain structural and functional deficits between adolescent and adult populations, and proposes a model highlighting the differences between adolescence and adulthood in anxiety-related brain networks. This model emphasises that in adolescence the emotional control system tends to be hypoactivated, the fear conditioning system is immature, and the reward and stress response systems are hypersensitive. Furthermore, the striatum’s functional links to the amygdala and the prefrontal cortex are strengthened, while the link between the prefrontal cortex and the amygdala is weakened in adolescence. This model helps to explain why adolescents are vulnerable to anxiety disorders and provides insights into potential brain-based approaches to intervene in adolescent anxiety disorders.

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“…However, EtOH still elicits CTA at doses that would typically be cognitively impairing in both general anesthetic-na€ ıve adolescents and adults, lending greater support to the ability of exposed animals to form CS/US pairings at amnestic doses. Such pairings likely involve engrams less related to traditional learning and memory as evident elsewhere (Saalfield and Spear, 2019;Uematsu et al, 2015). Related, it was surprising to observe that adult control rats also exhibited memory impairment 24 hours following 1.0 g/kg EtOH as prior findings tend to indicated reduced sensitivity in na€ ıve adults (see: Spear & Swartzwelder 2014, for review).…”

Section: Discussionmentioning

confidence: 99%

General Anesthetic Exposure During Early Adolescence Persistently Alters Ethanol Responses

Landin

Gore-Langton

Spear

et al. 2020

Alcoholism Clin & Exp Res

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Background Adolescent alcohol abuse can lead to behavioral dysfunction and chronic, relapsing alcohol use disorder (AUD) in adulthood. However, not all adolescents that consume alcohol will develop an AUD; therefore, it is critical to identify neural and environmental risk factors that contribute to increases in susceptibility to AUDs following adolescent alcohol (ethanol [EtOH]) exposure. We previously found that adolescent anesthetic exposure led to strikingly similar behavioral and neural effects as adolescent alcohol exposure. Therefore, we tested the hypothesis that general anesthetic exposure during early adolescence would alter EtOH responses consistent with an exacerbation of the adolescent alcohol phenotype. Methods To test this hypothesis, early‐adolescent male Sprague‐Dawley rats were exposed for a short duration to the general anesthetic isoflurane and tested on multiple EtOH‐induced behaviors in mid‐late adolescence or adulthood. Results Adolescent rats exposed to isoflurane exhibited decreases in sensitivity to negative properties of EtOH such as its aversive, hypnotic, and socially suppressive effects, as well as increases in voluntary EtOH intake and cognitive impairment. Select behaviors were noted to persist into adulthood following adolescent isoflurane exposure. Similar exposure in adults had no effects on EtOH sensitivity. Conclusions This study demonstrates for the first time that early‐adolescent isoflurane exposure alters EtOH sensitivity in a manner consistent with an exacerbation of adolescent‐typical alcohol responding. These findings suggest that general anesthetic exposure during adolescence may be an environmental risk factor contributing to an enhanced susceptibility to developing AUDs in an already vulnerable population.

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Fos activation patterns related to acute ethanol and conditioned taste aversion in adolescent and adult rats

Cited by 18 publications

References 94 publications

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

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

Adolescent anxiety disorders and the developing brain: comparing neuroimaging findings in adolescents and adults

General Anesthetic Exposure During Early Adolescence Persistently Alters Ethanol Responses

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