Prenatal ethanol effects on reward efficacy for adult mice are gestation stage specific

Middaugh, Lawrence D.; Gentry, G. David

doi:10.1016/0892-0362(92)90044-b

Cited by 13 publications

(4 citation statements)

References 21 publications

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“…The rapid acquisition of FR responding is sensitive to developmental exposure to cadmium (Newland, et al, 1986), tetrochlorodibenzo-p-dioxin (TCDD) (Hojo, et al, 2002), ethanol (Middaugh and Gentry, 1992), and MeHg (Paletz, et al, 2006; Reed, et al, 2008). With cadmium, TCDD, and MeHg, the effect is in the direction of enhanced acquisition.…”

Section: Behavioral Effects Of Developmental Methylmercury Exposurmentioning

confidence: 99%

Methylmercury and nutrition: Adult effects of fetal exposure in experimental models

2008

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Human exposure to the life-span developmental neurotoxicant, methylmercury (MeHg), is primarily via the consumption of fish or marine mammals. Fish are also excellent sources of important nutrients, including selenium and n-3 polyunsaturated fatty acids (PUFAs), such as docosahexaenoic acid (DHA). Laboratory models of developmental MeHg exposure can be employed to assess the roles of nutrients and MeHg and to identify potential mechanisms of action if the appropriate exposure measures are used. In describing chronic exposures, relationships between daily intake and brain mercury are consistent and orderly across species, even when large differences in blood:brain ratios exist. It is well-established that low level developmental MeHg produces sensory deficits. Recent studies also show that perseveration in reversal-learning tasks occurs after gestational exposures that produce low micromolar concentrations in the brain. A no-effect level has not been identified for this effect. These exposures do not affect the acquisition or performance of discrimination learning, set shifting (extra-dimensional shift), or memory. Reversal learning deficits may be related to enhanced impact of reinforcers as measured using progressive ratio reinforcement schedules, an effect that could result in perseveration. Also reported is enhanced sensitivity to dopamine reuptake inhibitors and diminished sensitivity to pentobarbital, a GABAA agonist. Diets rich in PUFAs or selenium do not protect against MeHg's effects on reversal learning but, by themselves, may diminish variability in performance, enhance attention or psychomotor function and may confer some protection against age-related deficits in these areas. It is hypothesized that altered reward processing, dopamine and GABAergic neurotransmitter systems, and cortical regions associated with choice and perseveration are especially sensitive to developmental MeHg at low exposure levels. Human testing for MeHg's neurotoxicity should emphasize these behavioral domains.

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Section: Behavioral Effects Of Developmental Methylmercury Exposurmentioning

confidence: 99%

Methylmercury and nutrition: Adult effects of fetal exposure in experimental models

2008

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“…Both Riley et al (1980) and Middaugh and Gentry (1992) made a similar suggestion in interpreting the effects of prenatal exposure to ethanol on fixed-ratio bar pressing. In the present study, compensatory adjustments in attaining the steady-state baseline performance, i.e., responding under FR 20 for females and FR 28 for males, might have masked potential underlying functional deficits.…”

Section: Discussionmentioning

confidence: 95%

“…(3) Schedule of exposures: Exposures were conducted from GD 7-19 in the Stanton et al study; thus, in contrast to the present experiment, the rat pups were not exposed to methanol during the developmental period that is equivalent to the third trimester in the human. Postnatal exposures to ethanol in the rodent may produce effects on cell proliferation and neuronal migration that differ from those seen during prenatal only exposures (cf., Miller, 1992;Pierce and West, 1987;West et al 1986); differential prenatal vs postnatal exposure effects on behavior also have been reported (e.g., Middaugh and Gentry, 1992;Wigal and Amsel, 1990). Comparable studies for methanol have not been conducted, although, as noted earlier, there is evidence that the period of developmental exposure to methanol can determine the emergence of abnormalities (Bolon et al, 1993).…”

Section: Discussionmentioning

confidence: 95%

Perinatal Methanol Exposure in the Rat II Behavioral Effects in Neonates and Adults

Stern¹,

Cox

Preston³

et al. 1997

Toxicol Sci

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The use of methanol as a component of automobile fuel will increase perinatal exposures in the general population. Few studies have addressed questions concerning neurotoxicity stemming from such exposures. In the current study, four cohorts of pregnant Long-Evans rats, each cohort consisting of an exposure and a control group, were exposed to 4500 ppm methanol vapor in Rochester-type inhalation chambers for 6 hr daily beginning on Gestation Day 6. Exposure continued for both dams and pups through Postnatal Day 21 (PND 21) to model gestational and neonatal toxicity in humans. Several behavioral procedures were used to assess exposure effects in the offspring. Male-female littermates were studied whenever possible to examine sex differences, with one pair from a litter for each procedure. Exposure to methanol did not affect suckling latency and nipple attachment on PND 5 or performance on an aversive olfactory conditioning procedure on PND 10. Exposure to methanol did alter performances in a motor activity procedure. Methanol-exposed neonates were less active on PND 18, but more active on PND 25 than the equivalent control group pups. Two operant conditioning procedures, not used previously in this context, assayed other littermates as adults. A fixed ratio schedule required the rat to rotate a running wheel a specified number of revolutions to obtain food-pellet reinforcers. When the fixed ratio requirement changed, number of responses (revolutions) per 1-hr session displayed a complex interaction with treatment Changes in performance over the course of training differed between males and females depending on exposure to methanol. Compared to initial baseline performances, methanolexposed males showed decreases, and methanol-exposed females increases, in the rate of running. A stochastic spatial discrimination procedure permitted subjects to respond on any three levers, with the probabilities of food-pellet delivery determined by the location of the preceding response. A reinforcement matrix defined

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“…Blood was not collected after the 0.5 g/kg test (Series 1). The blood sampling and gas chromatography assay procedures to determine ethanol concentration were according to previously published techniques (Griffin et al , 2009; Middaugh et al , 1992c). …”

Section: Methodsmentioning

confidence: 99%

Effects of vigabatrin, an irreversible GABA transaminase inhibitor, on ethanol reinforcement and ethanol discriminative stimuli in mice

Griffin¹,

Nguyen²,

Deleon³

et al. 2012

Behavioural Pharmacology

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We tested the hypothesis that the irreversible gamma-amino butyric acid (GABA) transaminase inhibitor, γ-vinyl GABA (Vigabatrin; VGB) would reduce ethanol reinforcement and enhance the discriminative stimulus effect of ethanol, effectively reducing ethanol intake. The present studies used adult C57BL/6J (B6) mice in well-established operant, two-bottle choice consumption, locomotor activity and ethanol discrimination procedures, to examine comprehensively the effects of VGB on ethanol-supported behaviors. VGB dose-dependently reduced operant responding for ethanol as well as ethanol consumption for long periods of time. Importantly, a low dose (200 mg/kg) of VGB was selective for reducing ethanol responding without altering intake of food or water reinforcement. Higher VGB doses (>200 mg/kg) still reduced ethanol intake, but also significantly increased water consumption and, more modestly, increased food consumption. While not affecting locomotor activity on its own, VGB interacted with ethanol to reduce the stimulatory effects of ethanol on locomotion. Finally, VGB (200 mg/kg) significantly enhanced the discriminative stimulus effects of ethanol as evidenced by significant left-ward and up-ward shifts in ethanol generalization curves. Interestingly, VGB treatment was associated with slight increases in blood ethanol concentrations. The reduction in ethanol intake by VGB appears to be related to the ability of VGB to potentiate the pharmacological effects of ethanol.

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Prenatal ethanol effects on reward efficacy for adult mice are gestation stage specific

Cited by 13 publications

References 21 publications

Methylmercury and nutrition: Adult effects of fetal exposure in experimental models

Methylmercury and nutrition: Adult effects of fetal exposure in experimental models

Perinatal Methanol Exposure in the Rat II Behavioral Effects in Neonates and Adults

Effects of vigabatrin, an irreversible GABA transaminase inhibitor, on ethanol reinforcement and ethanol discriminative stimuli in mice

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