Amphetamine sensitization in mice is sufficient to produce both manic- and depressive-related behaviors as well as changes in the functional connectivity of corticolimbic structures

Pathak, Geetanjali; Ibrahim, Baher A.; McCarthy, Sheryl A.; Baker, Kevin B.; Kelly, Michy P.

doi:10.1016/j.neuropharm.2015.04.026

Cited by 33 publications

(39 citation statements)

References 106 publications

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“…Nest building is considered an ethologically-relevant “activity of daily living” for healthy rodents [31] which is positively correlated to fitness [32]. Increasing activity levels via pharmacological treatment or selective breeding also reduces nest building behavior [33, 34]. However, failure to build sleeping nests differs from the failure of pregnant dams to build brooding nests.…”

Section: Discussionmentioning

confidence: 99%

The impact of maternal neglect on genetic hyperactivity

Majdak

Grogan

Gogola

et al. 2016

Behavioural Brain Research

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Early environmental conditions are increasingly appreciated as critical in shaping behavior and cognition. Evidence suggests that stressful rearing environments can have an enduring impact on behaviors in adulthood, but few studies have explored the possibility that rearing environment could exacerbate genetic hyperactivity disorders. Uncovering a strong environmental influence on the transmission of hyperactivity could provide novel avenues for translational research. Recently we developed a selectively bred High-Active line of mice to model ADHD, providing a unique resource to address the question of environmental transmission. The High-Active line demonstrates transgenerational hyperactivity, but the influence of the postnatal environment (i.e. maternal care provided by dams) on hyperactivity had not been systemically quantified. This study employed a cross-fostering method to simultaneously address 1) whether High-Active and Control pups are provided with similar levels of care in the early environment, and 2) whether any differences in rearing environment influence hyperactive behavior. High-Active dams demonstrated impairment in all measures of maternal competence relative to Controls, which reduced survival rates and significantly reduced the body mass of offspring in early life and at weaning. While the deteriorated postnatal environment provided by High-Active dams was ultimately sufficient to depress Control activity, the hyperactivity of High-Active offspring remained unaffected by fostering condition. These data not only confirm the power of genetics to influence hyperactivity across generations, but also provide evidence that early rearing environments may not have a significant impact on the extreme end of hyperactive phenotypes.

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Section: Discussionmentioning

confidence: 99%

The impact of maternal neglect on genetic hyperactivity

Majdak

Grogan

Gogola

et al. 2016

Behavioural Brain Research

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“…As previously described (Kelly et al, 2010; Kelly, 2014; Pathak et al, 2015), to mitigate non-specific effects related to transfer efficiencies, film exposures, etc. across gels, Western blot data on a given gel were normalized to a reference group (e.g., GH).…”

Section: Methodsmentioning

confidence: 99%

“…In cases of significant ANOVAs, post hoc analyses were conducted using the Student–Newman–Keuls Method. As previously described (Kelly et al, 2008, 2010; Kelly, 2014; Pathak et al, 2015), statistical outliers >2 standard deviations from the mean were removed from analyses (outliers/total data points: Fig. 1C Left, 2/62; Fig.…”

Section: Methodsmentioning

confidence: 99%

PDE11A regulates social behaviors and is a key mechanism by which social experience sculpts the brain

et al. 2016

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Despite the fact that appropriate social behaviors are vital to thriving in one’s environment, little is understood of the molecular mechanisms controlling social behaviors or how social experience sculpts these signaling pathways. Here, we determine if Phosphodiesterase 11A (PDE11A), an enzyme that is restricted to the ventral hippocampal formation (VHIPP) and that breaks down cAMP and cGMP, regulates social behaviors. PDE11 wild-type (WT), heterozygous (HT), and knockout (KO) mice were tested in various social approach assays and gene expression differences were measured by RNA sequencing. The effect of social isolation on PDE11A4 compartmentalization and subsequent social interactions and social memory was also assessed. Deletion of PDE11A triggered age- and sex-dependent deficits in social approach in specific social contexts but not others. Mice appear to detect altered social behaviors of PDE11A KO mice, because C57BL/6J mice prefer to spend time with a sex-matched PDE11A WT vs. its KO littermate; whereas, a PDE11A KO prefers to spend time with a novel PDE11A KO vs. its WT littermate. Not only is PDE11A required for intact social interactions, we found that 1 month of social isolation vs. group housing decreased PDE11A4 protein expression specifically within the membrane fraction of VHIPP. This isolation-induced decrease in PDE11A4 expression appears functional because social isolation impairs subsequent social approach behavior and social memory in a PDE11A genotype-dependent manner. Pathway analyses following RNA sequencing suggests PDE11A is a key regulator of the oxytocin pathway and membrane signaling, consistent with its pivotal role in regulating social behavior.

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“…Increases in anxiety and depression are frequently observed in those who abuse AMPHs, especially during early stage of withdrawal (London, 2004; Thompson et al 2004; Zorick et al, 2010; Leventhal et al, 2010). In adult rodents, withdrawal from chronic exposure to AMPHs is associated with increases in anxiety-like behavior (Barr et al, 2010) and a transient anhedonic state (Barr and Phillips, 1999; Che et al, 2013; Pathak et al, 2015). To date, few studies have examined affective behavior following exposure to AMPH in adolescence and the available results are mixed (Labonte et al, 2012; Kolyaduke and Hughes, 2013).…”

Section: Introductionmentioning

confidence: 99%

Timing of amphetamine exposure in relation to puberty onset determines its effects on anhedonia, exploratory behavior, and dopamine D1 receptor expression in young adulthood

Kang

Galvez

et al. 2016

Neuroscience

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Non-medical use of amphetamine (AMPH) among adolescents is prevalent, which is problematic given the potential consequences of developmental drug exposure on brain function and behavior. Previously we found in adult male rats that AMPH exposure starting before puberty induces a persistent decrease in dopamine D1 receptor (D1R) function in the medial prefrontal cortex (mPFC). Here we investigated if this dysfunction was associated with changes in D1R expression in the mPFC and nucleus accumbens (NAc). We also determined if starting drug exposure well before or near the onset of puberty would influence AMPH-induced changes in D1R expression and behavior. Male and female Sprague-Dawley rats were treated once every other day (10 injections total) with saline or 3 mg/kg AMPH (i.p.) from either postnatal day (P) 27 to 45 (pre-puberty groups; pre-P) or P37 to 55 (peri-puberty groups; peri-P). After 1, 7 and 21 days of withdrawal, sucrose preference tests were performed to assess anhedonia. Exploratory behavior was studied in an open-field arena and on an elevated plus maze (EPM). Rats were then sacrificed for western blot analysis of D1R expression. We found that AMPH withdrawal induced decreases in sucrose preference that persisted in rats with peri-P onset treatment. Pre-P onset AMPH exposure led to increased open arm exploration in the EPM test, as well as a decreased D1R level in the mPFC but not NAc. Our results demonstrated that AMPH exposure starting at different developmental stages resulted in distinct neurobehavioral abnormalities, suggesting an important role of exposure timing in drug-induced plasticity.

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Amphetamine sensitization in mice is sufficient to produce both manic- and depressive-related behaviors as well as changes in the functional connectivity of corticolimbic structures

Cited by 33 publications

References 106 publications

The impact of maternal neglect on genetic hyperactivity

The impact of maternal neglect on genetic hyperactivity

PDE11A regulates social behaviors and is a key mechanism by which social experience sculpts the brain

Timing of amphetamine exposure in relation to puberty onset determines its effects on anhedonia, exploratory behavior, and dopamine D1 receptor expression in young adulthood

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