Loss of Nicotine-Induced Effects on Locomotor Activity in Fetal Alcohol-Exposed Rats

doi:10.1016/S0892-0362(99)00040-9

Neurotoxicology and Teratology

Volume 21, Issue 6, November–December 1999, Pages 647-652

https://doi.org/10.1016/S0892-0362(99)00040-9 Get rights and content

Abstract

Previous evidence from our laboratory showed that systemic injection of nicotine enhanced attention and memory in control rats, but not fetal alcohol–exposed (FAE) rats. The present study examined the effects of nicotine on two measures of locomotor activity in FAE rats. Subjects were 2-month-old male offspring of Sprague–Dawley rats fed a 35% ethanol-derived caloric diet, a pair-fed sucrose diet, or a chow-fed diet during the last 2 weeks of gestation. The two experiments examined the effects of intraperitoneal injection of saline or nicotine (0.25 or 0.75 mg/kg) on rearing in an operant chamber and locomotor activity in an open field for 60 min. The high dose of nicotine produced a decrease in rearing in the first 10-min period, followed by a later increase in rearing in the pair-fed and chow-fed groups, but not the FAE group. Nicotine also produced an elevation of locomotor activity in the open field in only the two control groups. These findings provide additional evidence that FAE rats show less behavioral responsiveness to nicotine.

Section snippets

Subjects

Male Sprague–Dawley rats were used in the present study. The subjects were offspring of dams given different feeding treatments during the last 2 weeks of gestation. Rats (Charles River, Portage MI) were received on the fourth day of pregnancy, and fetal dietary treatment began on the seventh day of pregnancy. The alcohol-treated dams received a diet consisting of ethanol, chocolate-flavored Sustacal (Mead Johnson, Evansville, IN) supplemented with vitamins (Vitamin Diet Fortifications Mixture;

Dam and Litter Data

In the rearing experiment, dams in the FAE group (n = 7) consumed a daily average of 4.05 g of ETOH with an average of 3.01 g and 4.50 g of ETOH consumed on first day (GD7) and last day (G20) of feeding, respectively. The average body weight of these dams on the first day of feeding (GD7) was 249 g. The average body weights on day 0 for all of the pups in the FAE group (5.88 ± 0.05 g) and pair-fed group (5.92 ± 0.05 g) were significantly lower than for the chow-fed group (6.30 ± 0.07g).

In the

Discussion

The findings of the present study indicate that nicotine induced a change in locomotor activity in the control groups, but not the FAE group. In the first experiment, rats in both control groups exhibited a decrease in rearing activity followed by an elevation in rearing following nicotine treatment. This pattern of locomotor activity has been reported in rodents following nicotine administration in a few studies 10, 14, 59. However, FAE rats did not show an initial depression or later

Acknowledgements

This study was supported by National Institute on Alcohol Abuse and Alcoholism grants K21AA00192 (to A.H.N.) and AA08696 (to R.J.H.). We thank Jennifer Dowd and Fatema Rehman Mirza for their technical assistance.

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Prenatal exposure to nicotine in varied rodent models is known to: perturb early brain morphogenesis through excessive neuroepithelial cell apoptosis (Roy et al., 1998; Zhao and Reece, 2005); elicit shortfalls in neuronal cell numbers through decreased cell proliferation or enhanced apoptosis (Jang et al., 2002; Navarro et al., 1989; Slotkin, 1999; Slotkin et al., 1986, 1987, 1997); alter cell size, packing density or cortical thickness (Gospe et al., 1996; Roy et al., 2002); promote abnormal gliosis at the expense of neurogenesis (Roy et al., 2002); and interfere with the development of neural circuitry (Levin and Slotkin, 1998; Levin et al., 1996; Slawecki and Ehlers, 2002; Slawecki et al., 2000) (Slotkin, 1992, 1999) – all in the developing brain. The nicotine-induced “structural” alterations in the brain, noted above, correlate with neurobehavioral/cognitive “functional” deficits in exposed animals which mimic deficits seen in children whose mothers smoked during pregnancy (Cornelius and Day, 2000; DiFranza et al., 2004; Ernst et al., 2001) including: increased locomotor activity (Fung, 1988; Koehl et al., 2000; Nagahara and Handa, 1999; Shacka et al., 1997), hyperactivity (Ajarem and Ahmad, 1998; Newman et al., 1999; Sobrian et al., 2003; Vaglenova et al., 2004), impulsivity (Sobrian et al., 2003), and anxiety (Vaglenova et al., 2004). In addition, long-term impairments in attention, learning, and memory in smoke exposed animals have been observed through the aid of various paradigms such as, avoidance acquisition (Genedani et al., 1983; Peters and Ngan, 1982; Vaglenova et al., 2004), radial arm maze tasks (Levin et al., 1993; Sorenson et al., 1991), and operant learning behaviors (Martin and Becker, 1971).
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ArticlesLoss of Nicotine-Induced Effects on Locomotor Activity in Fetal Alcohol-Exposed Rats

Abstract

Section snippets

Subjects

Dam and Litter Data

Discussion

Acknowledgements

Brain Res.

Am. J. Obstet. Gynecol.

Neurotoxicol. Teratal.

Neurotoxicol. Teratol.

Neurotoxicol. Teratol.

Eur. J. Pharmacol.

Biol. Psychiatry

Neurotoxicol. Teratol.

Alcohol

Brain Res. Dev. Brain Res.

Alcohol

Brain Res.

Neuroscience

Drug Alcohol Depend.

Neurotoxicol. Teratol.

Pharmacol. Biochem. Behav.

Pharmacol. Biochem. Behav.

Neuropsychologia

Pharmacol. Biochem. Behav.

Pharmacol. Biochem. Behav.

Effects of prenatal ethanol exposure in C57BL mice on locomotor activity and passive avoidance behavior

Psychopharmacology (Berl.)

The effects of acute and repeated nicotine treatment on nucleus accumbens dopamine and locomotor activity

Br. J. Pharmacol.

Prenatal alcohol exposure and offspring hyperactivityEffects of scopolamine and methylscopolamine

Neurobehav. Toxicol. Teratol.

Effect of prenatal alcohol consumption on open-field and alcohol preference in rats

Psychopharmacolgia

Quantitative brain magnetic resonance imaging in attentional-deficit hyperactivity disorder

Arch. Gen. Psychiatry

Chronic central nicotinic blockade after a single administration of the bisquaternary ganglion-blocking drug chlorisondamine

Br. J. Pharmacol.

A comparison of children affected by prenatal alcohol exposure and attention deficit, hyperactivity disorder

Alcohol. Clin. Exp. Res.

Is the dopaminergic system involved in the central effects of nicotine in mice?

Psychopharmacology (Berl.)

Effects of in utero ethanol exposure on the developing dopaminergic system in rats

J. Neurosci. Res.

DOPA decarboxylase activity in attention deficit hyperactivity disorder adults. A [fluroine-18]flurodopa positron emission tomographic study

J. Neurosci.

Articles
Loss of Nicotine-Induced Effects on Locomotor Activity in Fetal Alcohol-Exposed Rats