Perinatal protein malnutrition enhances rewarding cocaine properties in adult rats

Valdomero, Analía; Bussolino, Daniela F.; Orsingher, Otto A.; Cuadra, Gabriel

doi:10.1016/j.neuroscience.2005.08.055

Cited by 21 publications

(16 citation statements)

References 37 publications

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“…These two behaviors were noted in IUGR animals (exaggerated response to cocaine and decreased sucrose preference), suggesting that the IUGR animals may represent an animal model of increased addiction risk as a result of suboptimal prenatal environment. These findings are consistent with other observations in the literature linking malnutrition and addictive behavior in rodents (Palmer et al, 2008; Valdomero et al, 2007; Valdomero et al, 2006; Shultz et al, 1999) and humans (Franzek et al, 2008). …”

Section: Discussionsupporting

confidence: 93%

Early life protein restriction alters dopamine circuitry

et al. 2010

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Adverse prenatal environment, such as intrauterine growth retardation (IUGR), increases the risk for negative neurobehavioral outcomes. IUGR, affecting approximately 10% of all US infants, is a known risk factor for ADHD, schizophrenia spectrum disorders and addiction. Mouse dams were fed a protein deficient (8.5% protein) or isocaloric control (18% protein) diet through pregnancy and lactation (a well validated rodent model of IUGR). Dopamine-related gene expression, dopamine content and behavior were examined in adult offspring. IUGR offspring have 6-8 fold overexpression of dopamine (DA)-related genes (tyrosine hydroxylase (TH) and dopamine transporter) in brain regions related to reward processing (ventral tegmental area (VTA), nucleus accumbens, Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. DISCLOSURE/CONFLICTS OF INTERESTZ Vucetic, K Totoki, H. Schoch, KW Whitaker, T. E. Hill-Smith, and TM Reyes declare no conflicts of interest, either financial or otherwise. Irwin Lucki has been on the Scientific Advisory Board for Wyeth and has received research support from AstraZeneca, Wyeth, Forest and Epix pharmaceutical companies during the past 3 years. NIH Public Access Author ManuscriptNeuroscience. Author manuscript; available in PMC 2011 June 30. NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author Manuscript prefrontal cortex (PFC)) and homeostatic control (hypothalamus), as well as increased number of TH-ir neurons in the VTA and increased dopamine in the PFC. Cyclin-dependent kinase inhibitor 1C (Cdkn1c) is critical for dopaminergic neuron development. Methylation of the promoter region of Cdkn1c was decreased by half and there was a resultant 2-7 fold increase in Cdkn1c mRNA expression across brain regions. IUGR animals demonstrated alterations in dopamine-dependent behaviors, including altered reward-processing, hyperactivity and exaggerated locomotor response to cocaine.These data describe significant dopamine-related molecular and behavioral abnormalities in a mouse model of IUGR. This animal model, with both face validity (behavior) and construct validity (link to IUGR and dopamine dysfunction) may prove useful in identifying underlying mechanisms linking IUGR and adverse neurobehavioral outcomes such as ADHD. Keywordsdopamine; neurodevelopmental programming; epigenetics; addiction; perinatal nutrition A suboptimal prenatal environment, typically indicated by low birth weight or being small for gestational age (SGA), can increase the risk for adverse neurobehavioral outcomes, including ADHD (Hultman et al., 2007;Lahti et al., 2006), schizophr...

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Section: Discussionsupporting

confidence: 93%

Early life protein restriction alters dopamine circuitry

et al. 2010

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“…This neurochemical sensitization is focused mainly on the DA and opioids transmissions (Cadoni and Di Chiara, 1999; Barbano et al, 2009). Our results corroborate those of Valdomero et al (2006), who reported increased expression of FosB after stimulation of areas particularly involved in neural reward circuits and suggested that this increased expression could have been a consequence of perinatal undernutrition. This differential response in neuronal activity in brain areas that coordinate the sensation of pleasure parallels the reactivity to stimuli such as drugs of abuse (Velazquez et al, 2010).…”

Section: Discussionsupporting

confidence: 92%

Perinatal undernutrition stimulates seeking food reward

Silva

Borba

Lira

et al. 2013

Intl J of Devlp Neuroscience

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Experiments in animals have revealed that perinatal nutritional restriction, which manifests in adulthood, increases food intake and preference for palatable foods. Considering this, we aimed to evaluate the effects of perinatal malnutrition on hedonic control of feeding behavior. In this study, we divided Wistar rats into two groups according to the diet provided to their mothers during pregnancy and lactation: the control group (diet with 17% casein) and low-protein group (diet with 8% casein). We assessed the animals' motivational behavior in adulthood by giving them a stimulus of food reward. We also assessed their neuronal activation triggered by the stimulus of palatable food using FOS protein labeling of neurons activated in the caudate putamen, paraventricular, dorsomedial, ventromedial, and lateral hypothalamic nuclei and amygdala. Evaluation of body weight in malnourished animals showed reduction from the 6th day of life until adulthood. Analysis of feeding behavior revealed that these animals were more motivated by food reward, but they had delays during learning of the task. This finding correlated with the number of c-FOS-immunoreactive neurons, which indicated that malnourished animals had an increase in the number of neurons activated in response to the palatable diet, especially in the amygdala and caudate putamen. The study therefore confirmed our hypothesis that early nutritional insults promote changes in encephalic control mechanisms, especially those related to food intake and search for reward.

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“…Previous studies suggest an association between a deficient nutritional status during early life and an increased responsiveness to psychoactive substances later in life (Franzek et al, 2008; Valdomero et al, 2006; Velazquez et al, 2010). Here, undernutrition during lactation did not elicit an increase in nicotine susceptibility in adolescent mice.…”

Section: Discussionmentioning

confidence: 97%

“…Of note, an association between early undernutrition and the response to psychoactive drugs has been reported in humans: a case‐control study indicates a relationship between the prenatal famine during the Dutch hunger winter of 1944–45 and addiction later in life (Franzek et al, 2008). In parallel, animal models of perinatal undernutrition indicate an increased response of the mesocorticolimbic dopaminergic pathway to the rewarding effects of cocaine (Valdomero et al, 2006) and morphine (Velazquez et al, 2010).…”

Section: Introductionmentioning

confidence: 99%

Locomotor response to acute nicotine in adolescent mice is altered by maternal undernutrition during lactation

Dutra-Tavares

Manhães

Silva

et al. 2015

Intl J of Devlp Neuroscience

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Undernutrition during brain development causes long lasting alterations in different neurotransmitter systems that may alter responses to psychoactive drugs. Despite the recognized effects of early undernutrition on the cholinergic system, no evidence that demonstrates the influence of this insult on nicotine susceptibility has been reported. We investigated the effects of protein/calorie restriction during lactation on the susceptibility to nicotine in adolescent mice. Dams were randomly assigned to one of the following groups: Control (C, 20 litters)—free access to standard laboratory diet (23% protein); Protein Restricted (PR, 12 litters)—free access to a isoenergetic, 8% protein diet; Calorie Restricted (CR, 12 litters)—access to standard laboratory diet in restricted quantities (mean ingestion of PR: pair‐fed group). Undernutrition extended from postnatal day 2 (PN2) to weaning (PN21). At PN30, animals either received an i.p. injection of nicotine (0.5 mg/Kg) or saline and were immediately placed in open field (OF). After the OF, adrenal glands and serum were collected for the analyses of stress‐related endocrine parameters and leptin concentration. PR and CR offspring showed less body mass gain and visceral fat mass. PR offspring presented reduced serum leptin concentration. In the OF, nicotine increased locomotor activity of C and PR, but not of CR. CR and PR offspring showed decreased adrenal catecholamine content, which was not dependent on nicotine exposure. Our results indicate that early undernutrition interferes with nicotine‐elicited locomotor effects in adolescent mice and suggest that endocrine parameters alterations in malnourished animals do not influence the behavioral response to nicotine.

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Perinatal protein malnutrition enhances rewarding cocaine properties in adult rats

Cited by 21 publications

References 37 publications

Early life protein restriction alters dopamine circuitry

Early life protein restriction alters dopamine circuitry

Perinatal undernutrition stimulates seeking food reward

Locomotor response to acute nicotine in adolescent mice is altered by maternal undernutrition during lactation

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