A diet promoting sugar dependency causes behavioral cross-sensitization to a low dose of amphetamine

doi:10.1016/S0306-4522(03)00502-5

Neuroscience

Volume 122, Issue 1, 20 November 2003, Pages 17-20

https://doi.org/10.1016/S0306-4522(03)00502-5 Get rights and content

Abstract

Previous research in this laboratory has shown that a diet of intermittent excessive sugar consumption produces a state with neurochemical and behavioral similarities to drug dependency. The present study examined whether female rats on various regimens of sugar access would show behavioral cross-sensitization to a low dose of amphetamine. After a 30-min baseline measure of locomotor activity (day 0), animals were maintained on a cyclic diet of 12-h deprivation followed by 12-h access to 10% sucrose solution and chow pellets (12 h access starting 4 h after onset of the dark period) for 21 days. Locomotor activity was measured again for 30 min at the beginning of days 1 and 21 of sugar access. Beginning on day 22, all rats were maintained on ad libitum chow. Nine days later locomotor activity was measured in response to a single low dose of amphetamine (0.5 mg/kg). The animals that had experienced cyclic sucrose and chow were hyperactive in response to amphetamine compared with four control groups (ad libitum 10% sucrose and chow followed by amphetamine injection, cyclic chow followed by amphetamine injection, ad libitum chow with amphetamine, or cyclic 10% sucrose and chow with a saline injection). These results suggest that a diet comprised of alternating deprivation and access to a sugar solution and chow produces bingeing on sugar that leads to a long lasting state of increased sensitivity to amphetamine, possibly due to a lasting alteration in the dopamine system.

Section snippets

Animals and equipment

Sixty female Sprague–Dawley rats weighing 225–250 g were obtained from Taconic Farms (Germantown, NY, USA) and housed individually on a reversed 12-h light/dark cycle. Water was available ad libitum throughout the experiment. Locomotor activity was measured in a computerized 43.2×43.2 cm, open-field activity chamber with 30.5 cm high acrylic sidewalls and 16 infrared photocells on each of the three axes (MED Associates, Georgia, VT, USA). All procedures were carried out in accordance with the

Results

All rats in the experiment tasted the sugar or chow during the period prior to the locomotor activity tests (for the cyclic groups, this was when the sugar and/or chow were first presented that day). There was no difference between groups that would receive amphetamine or saline in the time spent drinking sucrose or eating chow prior to locomotor activity tests on day 1 (F(3,29)=0.24, n.s., F(3,29)=0.54, n.s., respectively) nor on day 21 (F(3,29)=0.16, n.s., F(3,29)=0.28, n.s., respectively).

Discussion

The results of this experiment suggest that sugar and amphetamine may be working via the same neural systems, as evidenced by cross-sensitization. These results are similar to those obtained with drugs of abuse Greenberg and Segal, 1985, Kalivas and Weber, 1988, Schenk et al., 1991, Pierce and Kalivas, 1995, Itzhak and Martin, 1999, Itzhak et al., 1999, Pontieri et al., 2001. This concept has been previously demonstrated in our laboratory with animals first sensitized to amphetamine becoming

Acknowledgements

This research was supported by USPHS grants MH-65024 and DA-10608 and Wyeth Research.

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View full text

A diet promoting sugar dependency causes behavioral cross-sensitization to a low dose of amphetamine

Abstract

Section snippets

Animals and equipment

Results

Discussion

Acknowledgements

Norepinephrine-dopamine interactions and behavior

Science

Naltrexone suppresses hyperphagia induced in the rat by a highly palatable diet

Pharmacol Biochem Behav

Amphetamine-sensitized rats show sugar-induced hyperactivity (cross-sensitization) and sugar hyperphagia

Pharmacol Biochem Behav

Sensitization and conditioning of feeding following multiple morphine microinjections into the nucleus accumbens

Brain Res

Comorbidity of axis I psychiatric disorders in bulimia nervosa

J Clin Psychiatry

Excessive sugar intake alters binding to dopamine and mu-opioid receptors in the brain

Neuroreport

Evidence that intermittent, excessive sugar intake causes endogenous opioid dependence

Obes Res

Repeated social-defeat stress, cocaine or morphineeffects on behavioral sensitization and intravenous cocaine self-administration “binges”

Psychopharmacology (Berl)

Self-administration of intravenous amphetamine is predicted by individual differences in sucrose feeding in rats

Psychopharmacology (Berl)

Taste responses and preferences for sweet high-fat foodsevidence for opioid involvement

Physiol Behav

Facilitation of sexual behavior in male rats following d-amphetamine-induced behavioral sensitization

Psychopharmacology (Berl)

Facilitation of sexual behavior and enhanced dopamine efflux in the nucleus accumbens of male rats after d-amphetamine-induced behavioral sensitization

J Neurosci

The nutrient intake of women with bulimia nervosa

Int J Eat Disord

Acute and chronic behavioral interactions between phencyclidine (PCP) and amphetamineevidence for a dopaminergic role in some PCP induced behaviors

Pharmacol Biochem Behav

Repeated cocaine administration causes persistent enhancement of D1 dopamine receptor sensitivity within the rat nucleus accumbens

J Pharmacol Exp Ther

The persistence of behavioral sensitization to cocaine parallels enhanced inhibition of nucleus accumbens neurons

J Neurosci

Feeding and hypothalamic stimulation increase dopamine turnover in the accumbens

Physiol Behav

Food reward and cocaine increase extracellular dopamine in the nucleus accumbens as measured by microdialysis

Life Sci

Reduction of dopamine release and synthesis by repeated amphetamine treatmentrole in behavioral sensitization

Eur J Pharmacol

Effects of cocaine, nicotine, dizocipline and alcohol on mice locomotor activitycocaine-alcohol cross-sensitization involves upregulation of striatal dopamine transporter binding sites

Brain Res

Effect of the dopaminergic neurotoxin MPTP on cocaine-induced locomotor sensitization

Pharmacol Biochem Behav