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Age-specific locomotor response to nicotine in yellow and mottled yellow A(vy)/a mice.

Dingman MA, Gyekis JP, Whetzel CA, Klein LC, Vandenbergh DJ - BMC Res Notes (2013)

Bottom Line: We investigated the influence of excessive agouti expression on open-field locomotor response to daily 0.5 mg/kg (-)-freebase nicotine injections in 27 early adolescent and 27 young adult male Avy/a and a/a mice, and assessed the effects of nicotine administration (0.5 mg/kg) followed by open-field testing on serum corticosterone levels in a separate group of 25 young adult male Avy/a and a/a mice.Overall, the results suggest an age- and epigenotype- or genotype-specific response to nicotine administration in young adult male Avy/a mice.It appears the Avy/a locomotor and thigmotaxic responses to acute nicotine administration are not mediated solely by hypothalamic-pituitary-adrenal (HPA) axis stimulation.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Biobehavioral Health, The Pennsylvania State University, 219 Biobehavioral Health Building, 16802 University Park, PA, USA. djv4@psu.edu.

ABSTRACT

Background: Most Agouti viable yellow (Avy) mice display constitutive expression of agouti protein, which acts as an inverse agonist at the melanocortin receptor 4 (Mc4r), resulting in adult-onset obesity as well as an altered sensitivity to some drugs of abuse. We investigated the influence of excessive agouti expression on open-field locomotor response to daily 0.5 mg/kg (-)-freebase nicotine injections in 27 early adolescent and 27 young adult male Avy/a and a/a mice, and assessed the effects of nicotine administration (0.5 mg/kg) followed by open-field testing on serum corticosterone levels in a separate group of 25 young adult male Avy/a and a/a mice.

Findings: Young adult Avy/a mice displayed pronounced nicotine-induced hypolocomotion (a 24% reduction in distance traveled) compared to their a/a littermates. Early adolescent Avy/a mice did not differ from their a/a littermates or saline-matched controls in locomotion following nicotine administration. Young adult Avy/a mice also displayed increased thigmotaxis (a 5% increase in time spent outside the center of the apparatus) on the first day of nicotine administration as compared to saline-matched controls, while a/a mice did not. An increase in serum corticosterone levels 20 minutes after nicotine injection in a separate group of young adult male mice (n = 25) was proportionally similar between Avy/a and a/a mice.

Conclusions: Overall, the results suggest an age- and epigenotype- or genotype-specific response to nicotine administration in young adult male Avy/a mice. It appears the Avy/a locomotor and thigmotaxic responses to acute nicotine administration are not mediated solely by hypothalamic-pituitary-adrenal (HPA) axis stimulation.

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Adolescent locomotion following nicotine administration. Nicotine (0.5 mg/kg) was administered for 5 consecutive days to a/a mice (a), and Avy/a mice (b). Data are presented as mean distance traveled in meters ± SE; n = 6–8 per group.
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Figure 1: Adolescent locomotion following nicotine administration. Nicotine (0.5 mg/kg) was administered for 5 consecutive days to a/a mice (a), and Avy/a mice (b). Data are presented as mean distance traveled in meters ± SE; n = 6–8 per group.

Mentions: Overall 4-way repeated measures ANOVA showed a significant effect of Age x Genotype x Treatment (F1, 46 = 6.21, p < 0.05) on locomotor activity. Nicotine administration had no noticeable effect on locomotion in adolescent mice (Figure 1). In young adult mice, a/a mouse locomotion was not influenced by nicotine administration (Figure 2a) while Avy/a mice displayed hypolocomotion after nicotine treatment throughout the course of testing period (Figure 2b). Nicotine-treated young adult Avy/a mice were significantly different than their saline-matched controls on Day 1 (t10 = -4.06, p < 0.01), Day 2 (t10 = -2.26, p < 0.05), Day 3 (t10 = -2.52, p < 0.05), Day 4 (t10 = -3.44, p < 0.01), and Day 5 (t10 = -2.35, p < 0.05).


Age-specific locomotor response to nicotine in yellow and mottled yellow A(vy)/a mice.

Dingman MA, Gyekis JP, Whetzel CA, Klein LC, Vandenbergh DJ - BMC Res Notes (2013)

Adolescent locomotion following nicotine administration. Nicotine (0.5 mg/kg) was administered for 5 consecutive days to a/a mice (a), and Avy/a mice (b). Data are presented as mean distance traveled in meters ± SE; n = 6–8 per group.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4222098&req=5

Figure 1: Adolescent locomotion following nicotine administration. Nicotine (0.5 mg/kg) was administered for 5 consecutive days to a/a mice (a), and Avy/a mice (b). Data are presented as mean distance traveled in meters ± SE; n = 6–8 per group.
Mentions: Overall 4-way repeated measures ANOVA showed a significant effect of Age x Genotype x Treatment (F1, 46 = 6.21, p < 0.05) on locomotor activity. Nicotine administration had no noticeable effect on locomotion in adolescent mice (Figure 1). In young adult mice, a/a mouse locomotion was not influenced by nicotine administration (Figure 2a) while Avy/a mice displayed hypolocomotion after nicotine treatment throughout the course of testing period (Figure 2b). Nicotine-treated young adult Avy/a mice were significantly different than their saline-matched controls on Day 1 (t10 = -4.06, p < 0.01), Day 2 (t10 = -2.26, p < 0.05), Day 3 (t10 = -2.52, p < 0.05), Day 4 (t10 = -3.44, p < 0.01), and Day 5 (t10 = -2.35, p < 0.05).

Bottom Line: We investigated the influence of excessive agouti expression on open-field locomotor response to daily 0.5 mg/kg (-)-freebase nicotine injections in 27 early adolescent and 27 young adult male Avy/a and a/a mice, and assessed the effects of nicotine administration (0.5 mg/kg) followed by open-field testing on serum corticosterone levels in a separate group of 25 young adult male Avy/a and a/a mice.Overall, the results suggest an age- and epigenotype- or genotype-specific response to nicotine administration in young adult male Avy/a mice.It appears the Avy/a locomotor and thigmotaxic responses to acute nicotine administration are not mediated solely by hypothalamic-pituitary-adrenal (HPA) axis stimulation.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Biobehavioral Health, The Pennsylvania State University, 219 Biobehavioral Health Building, 16802 University Park, PA, USA. djv4@psu.edu.

ABSTRACT

Background: Most Agouti viable yellow (Avy) mice display constitutive expression of agouti protein, which acts as an inverse agonist at the melanocortin receptor 4 (Mc4r), resulting in adult-onset obesity as well as an altered sensitivity to some drugs of abuse. We investigated the influence of excessive agouti expression on open-field locomotor response to daily 0.5 mg/kg (-)-freebase nicotine injections in 27 early adolescent and 27 young adult male Avy/a and a/a mice, and assessed the effects of nicotine administration (0.5 mg/kg) followed by open-field testing on serum corticosterone levels in a separate group of 25 young adult male Avy/a and a/a mice.

Findings: Young adult Avy/a mice displayed pronounced nicotine-induced hypolocomotion (a 24% reduction in distance traveled) compared to their a/a littermates. Early adolescent Avy/a mice did not differ from their a/a littermates or saline-matched controls in locomotion following nicotine administration. Young adult Avy/a mice also displayed increased thigmotaxis (a 5% increase in time spent outside the center of the apparatus) on the first day of nicotine administration as compared to saline-matched controls, while a/a mice did not. An increase in serum corticosterone levels 20 minutes after nicotine injection in a separate group of young adult male mice (n = 25) was proportionally similar between Avy/a and a/a mice.

Conclusions: Overall, the results suggest an age- and epigenotype- or genotype-specific response to nicotine administration in young adult male Avy/a mice. It appears the Avy/a locomotor and thigmotaxic responses to acute nicotine administration are not mediated solely by hypothalamic-pituitary-adrenal (HPA) axis stimulation.

Show MeSH
Related in: MedlinePlus