1994
DOI: 10.1007/s004010050082
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Long-term effects of intermittent versus continuous ethanol exposure on hippocampal synapses of the rat

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Cited by 3 publications
(6 citation statements)
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“…Investigation of IAA/CAA in other than adult animals is limited : Few articles have explored possible age dependency of IAA/CAA effects, although intermittency has been suggested to be important in fetal exposure studies (see Lundquist et al, 1994, for discussion) and intermittency effects have been reported to be more pronounced in adolescent than adult C57 mice (Melendez, 2011). There is also some initial evidence that consequences of IAA and CAA may differ in the aged brain from that of the adult brain (Reynolds et al, 2015).…”
Section: Discussionmentioning
confidence: 99%
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“…Investigation of IAA/CAA in other than adult animals is limited : Few articles have explored possible age dependency of IAA/CAA effects, although intermittency has been suggested to be important in fetal exposure studies (see Lundquist et al, 1994, for discussion) and intermittency effects have been reported to be more pronounced in adolescent than adult C57 mice (Melendez, 2011). There is also some initial evidence that consequences of IAA and CAA may differ in the aged brain from that of the adult brain (Reynolds et al, 2015).…”
Section: Discussionmentioning
confidence: 99%
“…A couple of other studies have focused on regions of the nervous system differentially affected by IAA and CAA. Lundquist and colleagues (1994) gave male W rats IAA (3 g/kg EtOH intraperitoneally 2 times/d for ~1 month) or CAA (20% EtOH in drinking water [1 bottle only available] for ~1 month). In this study, only rats exposed to IAA exhibited a reduction in number of synapses in the CA3 region of the hippocampus (HPC) , even though total EtOH exposure was greater in the CAA than IAA group (Lundquist et al, 1994).…”
Section: Potential Neurobiological Contributors To Iaa/caa Differencesmentioning
confidence: 99%
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“…The ethanol-withdrawal syndrome and excitotoxic mechanisms related to it may contribute to ethanolinduced neurodegeneration. Intermittent ethanol exposure with repeated withdrawal periods has been suggested to be more damaging to neurons than continuous exposure (Lundqvist et al, 1994(Lundqvist et al, , 1995Lundqvist, 1997). Previously, ageing has been reported to increase the severity of the ethanol withdrawal syndrome (Maier and Pohorecky, 1989).…”
Section: Discussionmentioning
confidence: 99%
“…A key feature of alcohol use disorders (AUDs) is the transition from recreational to escalated use that persists despite adverse consequences. 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 which are often treated as aversive in naïve rats (Carnicella et al, 2014, Simms et al, 2008, Rosenwasser et al, 2013, Lundqvist et al, 1994). 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 (Tomie et al, 2006, Loney and Meyer, 2018).…”
Section: Introductionmentioning
confidence: 89%