The Effects of Prenatal Protein Malnutrition and Cocaine on the Development of the Rat<sup>a</sup>

Galler, Janina R.; Tonkiss, John

doi:10.1111/j.1749-6632.1998.tb09724.x

Cited by 11 publications

(5 citation statements)

References 46 publications

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“…By weaning the weight deficit has declined but remains significant but, by the time the rats reach adulthood (>P90), the 6/25 rats catch up with the 25/25 and their weights are similar. (Galler and Tonkiss, 1998; Fischer et al, 2014). A student’s t-test comparing the body weight of all subjects in breeding B (n=8 25/25, n=8 6/25) at the time of tissue harvest shows that there is no difference between the two nutritional groups (t(14)=0.216, p=0.832).…”

Section: Resultsmentioning

confidence: 99%

Prenatal protein malnutrition decreases KCNJ3 and 2DG activity in rat prefrontal cortex

et al. 2015

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Prenatal protein malnutrition (PPM) in rats causes enduring changes in brain and behavior including increased cognitive rigidity and decreased inhibitory control. A preliminary gene microarray screen of PPM rat prefrontal cortex (PFC) identified alterations in KCNJ3 (GIRK1/Kir3.1), a gene important for regulating neuronal excitability. Follow-up with polymerase chain reaction and Western blot showed decreased KCNJ3 expression in PFC, but not hippocampus or brainstem. To verify localization of the effect to the PFC, baseline regional brain activity was assessed with 14C-2-deoxyglucose. Results showed decreased activation in PFC but not hippocampus. Together these findings point to the unique vulnerability of the PFC to the nutritional insult during early brain development, with enduring effects in adulthood on KCNJ3 expression and baseline metabolic activity.

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Section: Resultsmentioning

confidence: 99%

Prenatal protein malnutrition decreases KCNJ3 and 2DG activity in rat prefrontal cortex

et al. 2015

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“…This lack of effect is not due to generalized behavioral suppression, as the locomotor activity of SPF40 mice is not significantly different than either SAL or cocaine-exposed mice. It has been shown that prenatal malnutrition independently impairs spatial learning in adulthood, and that this impairment is associated with deficits in long-term but not short-term memory (Galler and Tonkiss, 1998). It is therefore possible that failure to associate the non-contingent delivery of a reward (UCS) with a specific set of environmental cues (CS) could result in impaired placeconditioning to cocaine.…”

Section: Discussionmentioning

confidence: 99%

Prenatal exposure to cocaine alters the development of conditioned place-preference to cocaine in adult mice

Malanga

Pejchal

Kosofsky

2007

Pharmacology Biochemistry and Behavior

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As addiction is increasingly formulated as a developmental disorder, identifying how early developmental exposures influence later responses to drugs of abuse is important to our understanding of substance abuse neurobiology. We have previously identified behavioral changes in adult mice following gestational exposure to cocaine that differ when assessed with methods employing contingent and non-contingent drug administration. We sought to clarify this distinction using a Pavlovian behavioral measure, conditioned place-preference. Adult mice exposed to cocaine in utero (40 or 20 mg/kg/day), vehicle and pair-fed controls were place-conditioned to either cocaine (5 mg/kg or 20 mg/kg, i.p.) or saline injections. The development of conditioned place-preference to cocaine was impaired in mice exposed to cocaine in utero, and was abolished by fetal malnutrition. A context-specific place-aversion to vehicle but not cocaine injection was observed in prenatally cocaine-exposed mice. Locomotor behavior did not differ among prenatal treatment groups. We conclude that early developmental exposure to cocaine may diminish the subsequent rewarding effects of cocaine in adulthood measured with classical conditioning techniques, and that this is not due to changes in locomotor behavior. Sensitivity to acute stress is also altered by prenatal cocaine exposure, consistent with earlier findings in this model.

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“…Such attentional deficits may contribute to deleterious cognitive effects following PCE. While some researchers have found little to no evidence of cognitive deficits (Morris et al, ; Paule et al, ; Galler and Tonkiss, ; Markowski et al, ), the majority of findings suggest the opposite. These deficits are apparent at a very early age, as prenatally cocaine‐exposed neonatal rats were significantly impaired in the acquisition and retention of milk‐odor associations relative to controls (Spear et al, ), and demonstrated an initial inability to develop associations in a test of Pavlovian conditioning (Kosofsky and Wilkins, ).…”

Section: Animal Modelsmentioning

confidence: 99%

Cocaine‐induced neurodevelopmental deficits and underlying mechanisms

Martin

Graham

McCarthy

et al. 2016

Birth Defects Research Pt C

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Exposure to drugs early in life has complex and long-lasting implications for brain structure and function. This review summarizes work to date on the immediate and long-term effects of prenatal exposure to cocaine. In utero cocaine exposure produces disruptions in brain monoamines, particularly dopamine, during sensitive periods of brain development, and leads to permanent changes in specific brain circuits, molecules, and behavior. Here, we integrate clinical studies and significance with mechanistic preclinical studies, to define our current knowledge base and identify gaps for future investigation.

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The Effects of Prenatal Protein Malnutrition and Cocaine on the Development of the Rat^a

Cited by 11 publications

References 46 publications

Prenatal protein malnutrition decreases KCNJ3 and 2DG activity in rat prefrontal cortex

Prenatal protein malnutrition decreases KCNJ3 and 2DG activity in rat prefrontal cortex

Prenatal exposure to cocaine alters the development of conditioned place-preference to cocaine in adult mice

Cocaine‐induced neurodevelopmental deficits and underlying mechanisms

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The Effects of Prenatal Protein Malnutrition and Cocaine on the Development of the Rata

Cited by 11 publications

References 46 publications

Prenatal protein malnutrition decreases KCNJ3 and 2DG activity in rat prefrontal cortex

Prenatal protein malnutrition decreases KCNJ3 and 2DG activity in rat prefrontal cortex

Prenatal exposure to cocaine alters the development of conditioned place-preference to cocaine in adult mice

Cocaine‐induced neurodevelopmental deficits and underlying mechanisms

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The Effects of Prenatal Protein Malnutrition and Cocaine on the Development of the Rat^a