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Escalation of alcohol intake is associated with regionally decreased insular cortex activity but not changes in taste quality

Escalation of alcohol intake is associated with regionally decreased insular cortex activity but... INTRODUCTIONA key feature of alcohol use disorders (AUDs) is the transition from recreational to escalated use that persists despite the negative consequences associated with drinking. A similar phenomenon exists in rodent models, as repeated, intermittent access to ethanol (EtOH) drives escalation of voluntary intake of EtOH, particularly at higher concentrations that are often treated as aversive in naïve rats (Carnicella et al., 2014; Lundqvist et al., 1994; Rosenwasser et al., 2013; Simms et al., 2008). Intermittent‐EtOH access and/or presentation of EtOH‐predictive cues can sufficiently escalate intake above that observed in continuous‐access paradigms, mimicking moderate‐to‐excessive EtOH drinking behaviors in humans (Carnicella et al., 2014), and this occurs whether EtOH is presented intermittently across days (Simms et al., 2008), or within session (Loney & Meyer, 2018; Tomie et al., 2006). We previously demonstrated that 30‐min sessions consisting of intermittent brief‐access (≤10s) to multiple EtOH concentrations (brief‐access EtOH exposure; BAEE) in mildly water‐restricted rats is sufficient to induce rapid escalation of intake in rats to levels typically observed following intermittent access 24‐h two‐bottle choice tests (IA2BC; Loney & Meyer, 2018). Importantly, within that study, there was no observation of escalation of intake of the bitter taste stimulus quinine dihydrochloride (QHCl) following identical http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Alcoholism Wiley

Escalation of alcohol intake is associated with regionally decreased insular cortex activity but not changes in taste quality

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Publisher
Wiley
Copyright
© 2023 by the Research Society on Alcoholism
ISSN
0145-6008
eISSN
1530-0277
DOI
10.1111/acer.15060
Publisher site
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Abstract

INTRODUCTIONA key feature of alcohol use disorders (AUDs) is the transition from recreational to escalated use that persists despite the negative consequences associated with drinking. A similar phenomenon exists in rodent models, as repeated, intermittent access to ethanol (EtOH) drives escalation of voluntary intake of EtOH, particularly at higher concentrations that are often treated as aversive in naïve rats (Carnicella et al., 2014; Lundqvist et al., 1994; Rosenwasser et al., 2013; Simms et al., 2008). Intermittent‐EtOH access and/or presentation of EtOH‐predictive cues can sufficiently escalate intake above that observed in continuous‐access paradigms, mimicking moderate‐to‐excessive EtOH drinking behaviors in humans (Carnicella et al., 2014), and this occurs whether EtOH is presented intermittently across days (Simms et al., 2008), or within session (Loney & Meyer, 2018; Tomie et al., 2006). We previously demonstrated that 30‐min sessions consisting of intermittent brief‐access (≤10s) to multiple EtOH concentrations (brief‐access EtOH exposure; BAEE) in mildly water‐restricted rats is sufficient to induce rapid escalation of intake in rats to levels typically observed following intermittent access 24‐h two‐bottle choice tests (IA2BC; Loney & Meyer, 2018). Importantly, within that study, there was no observation of escalation of intake of the bitter taste stimulus quinine dihydrochloride (QHCl) following identical

Journal

Alcoholism – Wiley

Published: Mar 20, 2023

Keywords: alcohol; c‐ Fos; intermittent access; psychophysics; self‐administration; taste

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