Fixed-ratio performance and subsequent extinction in rats prenatally exposed to ethanol

Riley, Edward P.; Shapiro, Neil R.; Lochry, Elizabeth A.; Broida, John

doi:10.3758/bf03326446

Cited by 22 publications

(10 citation statements)

References 13 publications

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“…The current results, however, are in agreement with the operant literature that suggests minimal or no impairment due to prenatal ethanol or cocaine exposure (Driscoll et al, 1980;Heyser et al, 1992Heyser et al, , 1994Riley et al, 1980). To the best of our knowledge, this is the first neonatal study of ethanol and/or cocaine exposure that has investigated operant learning.…”

Section: Discussionsupporting

confidence: 92%

Acquisition of a Fixed Ratio Schedule in Adult Male Rats Neonatally Exposed to Ethanol and/or Cocaine

Segar

Klebaur

Bardo

et al. 1999

Alcoholism Clin & Exp Res

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Acquisition of an operant learning task for sucrose reinforcement was examined in rats after neonatal exposure to ethanol and/or cocaine. Subjects were raised using an artificial rearing procedure from postnatal days 4 to 11 and were intragastrically fed a milk diet containing either ethanol (6 g/kg/day), cocaine (60 mg/kg/day), the combination (6 g/kg/day + 60 mg/kg/day), or an isocaloric control diet. There was also a suckled sham control. Adult male offspring (postnatal day 65 to postnatal day 68) were shaped to lever press for sucrose reinforcement and then began daily 15-min sessions of fixed ratio (FR) training. The number of days to acquire an FR 20 was measured. Neonatal exposure to the ethanol/cocaine combination significantly increased the number of days to reach the FR 20. There was also a trend for fewer of these subjects to reach the FR 20, although this difference was not statistically significant. These results suggest that subjects neonatally exposed to the ethanol/cocaine combination have difficulty learning an operant task. This impairment was unique to the ethanol/cocaine combination group and suggests that polydrug exposure during development may have a more adverse outcome than exposure to ethanol or cocaine alone.

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Section: Discussionsupporting

confidence: 92%

Acquisition of a Fixed Ratio Schedule in Adult Male Rats Neonatally Exposed to Ethanol and/or Cocaine

Segar

Klebaur

Bardo

et al. 1999

Alcoholism Clin & Exp Res

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“…This result is remarkably consistent across multiple learning paradigms that measure adaptive response inhibition in experimental animals (Riley et al, 1979(Riley et al, , 1980Abel, 1982;Driscoll et al, 1990) and children with fetal alcohol spectrum disorder (Streissguth et al, 1984;Nanson and Hiscock, 1990;Mattson and Riley, 1998), indicating that common neuroanatomical structures and/or neurophysiological processes may be involved. Our data suggest that CPEE alters the regulation of presynaptic GABA release, resulting in increased release of this neurotransmitter, in the hippocampus during periods of high-frequency stimulation that would be consistent with deficits in the expression of synaptic plasticity in this brain region.…”

Section: Prenatal Ethanol Exposure Impairs Conditioned Responding 649supporting

confidence: 56%

“…In the rat (Blanchard et al, 1987;Reyes et al, 1989;Matthews and Simson, 1998) and the guinea pig (Richardson et al, 2002;Iqbal et al, 2003), CPEE impairs spatial learning in postnatal offspring. Similarly, in tests of operant learning, CPEE has been reported to produce impairments in performance (Riley et al, 1980;Driscoll et al, 1990), the magnitude of which may be dependent on the complexity of the task (Mihalick et al, 2001). Among brain regions adversely affected by CPEE, the hippocampus appears to be especially vulnerable (West and Pierce, 1986).…”

mentioning

confidence: 99%

Chronic Prenatal Ethanol Exposure Impairs Conditioned Responding and Enhances GABA Release in the Hippocampus of the Adult Guinea Pig

Hayward¹,

Martin²,

Brien³

et al. 2003

J Pharmacol Exp Ther

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In this study, we assessed the effects of chronic prenatal ethanol exposure (CPEE) on spatial navigation in the water maze, conditioned responding using food-reinforced lever pressing, and amino acid neurotransmitter release from the hippocampus of the adult guinea pig. Pregnant guinea pigs were treated with ethanol (3 g/kg of maternal body weight/day), isocaloric-sucrose/pair-feeding, or water throughout gestation. Adult offspring were trained in two-lever operant chambers to respond for sucrose pellets, with one lever designated as the reward lever. There were no group differences in response acquisition or lever discrimination on a fixed-ratio 1 (FR-1) schedule. During extinction sessions, CPEE offspring maintained higher levels of responding on the previously reinforced lever, suggesting that CPEE increases perseveration and/or impairs response inhibition but does not affect operant responding for an appetitive reinforcer or the ability to discriminate rewarding from nonrewarding stimuli. In contrast, there was no effect of CPEE on performance in the water maze in the maternal ethanol regimen used in this study. CPEE did not alter electrically evoked glutamate or GABA release from hippocampal brain slices. However, when slices were tested after delivery of a tetanizing stimulation (five 5-s trains at 100 Hz), post-tetanic potentiation of electrically stimulated GABA release was greater in hippocampal slices obtained from CPEE offspring, whereas posttetanic potentiation of electrically stimulated glutamate release was unaffected. These data suggest that conditioned learning is a sensitive behavioral measure of CPEE-induced brain injury. Increased activity-dependent potentiation of GABA release in the hippocampus may contribute to alterations in synaptic plasticity observed in CPEE offspring.

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“…2004). Similarly, learning deficits are also observed in animal models of prenatal alcohol exposure (Riley et al. 1980; Blanchard et al.…”

mentioning

confidence: 88%

Prenatal ethanol exposure persistently impairs NMDA receptor‐dependent activation of extracellular signal‐regulated kinase in the mouse dentate gyrus

Samudio-Ruiz

Allan

Valenzuela

et al. 2009

Journal of Neurochemistry

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The dentate gyrus (DG) is the central input region to the hippocampus and is known to play an important role in learning and memory. Previous studies have shown that prenatal alcohol is associated with hippocampal‐dependent learning deficits and a decreased ability to elicit long‐term potentiation (LTP) in the DG in adult animals. Given that activation of the extracellular signal‐regulated kinase 1/2 (ERK1/2) signaling cascade by NMDA receptors is required for various forms of learning and memory, as well as LTP, in hippocampal regions, including the DG, we hypothesized that fetal alcohol‐exposed adult animals would have deficits in hippocampal NMDA receptor‐dependent ERK1/2 activation. We used immunoblotting and immunohistochemistry techniques to detect NMDA‐stimulated ERK1/2 activation in acute hippocampal slices prepared from adult fetal alcohol‐exposed mice. We present the first evidence linking prenatal alcohol exposure to deficits in NMDA receptor‐dependent ERK1/2 activation specifically in the DG of adult offspring. This deficit may account for the LTP deficits previously observed in the DG, as well as the life‐long cognitive deficits, associated with prenatal alcohol exposure.

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Fixed-ratio performance and subsequent extinction in rats prenatally exposed to ethanol

Cited by 22 publications

References 13 publications

Acquisition of a Fixed Ratio Schedule in Adult Male Rats Neonatally Exposed to Ethanol and/or Cocaine

Acquisition of a Fixed Ratio Schedule in Adult Male Rats Neonatally Exposed to Ethanol and/or Cocaine

Chronic Prenatal Ethanol Exposure Impairs Conditioned Responding and Enhances GABA Release in the Hippocampus of the Adult Guinea Pig

Prenatal ethanol exposure persistently impairs NMDA receptor‐dependent activation of extracellular signal‐regulated kinase in the mouse dentate gyrus

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