Maternal separation altered behavior and neuronal spine density without influencing amphetamine sensitization

Muhammad, Arif; Kolb, Bryan

doi:10.1016/j.bbr.2011.04.015

Cited by 91 publications

(74 citation statements)

References 60 publications

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“…These findings are consistent with previous work showing that exposure to early life stress is associated with poor hippocampal function (Aisa et al, 2007;Fabricius et al, 2008;Kalinichev et al, 2002;Murgatroyd et al, 2009;Rice et al, 2008) and increased anxiety-like behavior in rodents Muhammad and Kolb, 2011;Romeo et al, 2003). …”

Section: Discussionsupporting

confidence: 93%

“…In addition, deletion of similar members of the innate immune system is associated with impairment in synaptic pruning (Stevens et al, 2007). Second, disruption of dam-pup interactions (eg, handling or maternal separation) during the postnatal period is known to increase corticosterone and work from several groups has shown that these manipulations are associated with increased spine density in limbic areas that persist into adulthood (Helmeke et al, 2001;Muhammad and Kolb, 2011;Norrholm and Ouimet, 2001;Ovtscharoff et al, 2006;Poeggel et al, 2003). These data are consistent with the notion that early life stress may interfere with normal synaptic pruning.…”

Section: Lbp and The Behavioral Consequences Of Early Life Stresssupporting

confidence: 62%

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Early Life Stress Inhibits Expression of a Novel Innate Immune Pathway in the Developing Hippocampus

Lan

Simen

Mane

et al. 2011

Neuropsychopharmacol

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Childhood maltreatment represents a major risk factor for the development of numerous childhood psychopathologies that in many cases linger as chronic mental illnesses in adulthood. Exposing rodents or non-human primates to early life stress increases anxiety-like behaviors and impairs cognitive function in adulthood, suggesting that animal models may provide important insights into parallel developmental processes in humans. Using an unbiased genomic screen, we found that expression of lipopolysaccharide binding protein (LBP), a member of the innate immune system, is dramatically decreased in the hippocampus of pups exposed to early life stress. LBP levels peak in the normally developing hippocampus at a period of intense synaptic pruning, during which LBP is colocalized with the synaptic marker PSD95 and is found in close proximity to processes of microglia cells. Expression of LBP declines to low levels seen in adulthood at around postnatal day 30. Importantly, 30-day-old LBP knockout (k.o.) mice show increased spine density and abnormal spine morphology, suggesting that peak levels of LBP during the second and third weeks of life are necessary for normal synaptic pruning in the hippocampus. Finally, LBP k.o. mice show impaired hippocampal-dependent memory and increased anxiety-like behaviors in a manner that resembles that seen in animals exposed to early life stress. These findings describe a novel role for LBP in normal hippocampal development and raise the possibility that at least some of the behavioral sequelae of early life stress are mediated by reduced expression of LBP during a critical period of neurodevelopment.

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Section: Discussionsupporting

confidence: 93%

Section: Lbp and The Behavioral Consequences Of Early Life Stresssupporting

confidence: 62%

Early Life Stress Inhibits Expression of a Novel Innate Immune Pathway in the Developing Hippocampus

Lan

Simen

Mane

et al. 2011

Neuropsychopharmacol

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“…Recent studies have reported that early-life stress alters dendritic morphology and spine density of prefrontal pyramidal neurons (Chocyk et al, 2013;Monroy et al, 2010;Muhammad and Kolb, 2011). However, the results are variable.…”

Section: Discussionmentioning

confidence: 99%

Stress during a Critical Postnatal Period Induces Region-Specific Structural Abnormalities and Dysfunction of the Prefrontal Cortex via CRF1

Yang

Liao

Uribe-Mariño

et al. 2014

Neuropsychopharmacol

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During the early postnatal period, environmental influences play a pivotal role in shaping the development of the neocortex, including the prefrontal cortex (PFC) that is crucial for working memory and goal-directed actions. Exposure to stressful experiences during this critical period may disrupt the development of PFC pyramidal neurons and impair the wiring and function of related neural circuits. However, the molecular mechanisms of the impact of early-life stress on PFC development and function are not well understood. In this study, we found that repeated stress exposure during the first postnatal week hampered dendritic development in layers II/III and V pyramidal neurons in the dorsal agranular cingulate cortex (ACd) and prelimbic cortex (PL) of neonatal mice. The deleterious effects of early postnatal stress on structural plasticity persisted to adulthood only in ACd layer V pyramidal neurons. Most importantly, concurrent blockade of corticotropin-releasing factor receptor 1 (CRF 1 ) by systemic antalarmin administration (20 mg/g of body weight) during early-life stress exposure prevented stress-induced apical dendritic retraction and spine loss in ACd layer V neurons and impairments in PFC-dependent cognitive tasks. Moreover, the magnitude of dendritic regression, especially the shrinkage of apical branches, of ACd layer V neurons predicted the degree of cognitive deficits in stressed mice. Our data highlight the region-specific effects of early postnatal stress on the structural plasticity of prefrontal pyramidal neurons, and suggest a critical role of CRF 1 in modulating early-life stress-induced prefrontal abnormalities.

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“…Factors that likely account for these differences are drug history before acute stimulant administration, doses of stimulant tested, and sex. Effects of repeated stimulant administration are also mixed, although most studies have found that maternal separation either decreases (Matthews et al, 1996b;Li et al, 2003) or has no effect (Weiss et al, 2001;Planeta and Marin, 2002;Brake et al, 2004;Muhammad and Kolb, 2011) on locomotor sensitization, whereas one study found enhanced sensitization . The age at which animals are tested for sensitization may contribute to differences observed across these studies as Weiss et al (2001) and Kikusui et al (2005) tested animals during adolescence, and in fact, the latter study found that the sensitized response did not persist into adulthood in female mice, although it did persist in male mice.…”

Section: B Social Influencesmentioning

confidence: 99%

Individual Differences and Social Influences on the Neurobehavioral Pharmacology of Abused Drugs

2013

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Maternal separation altered behavior and neuronal spine density without influencing amphetamine sensitization

Cited by 91 publications

References 60 publications

Early Life Stress Inhibits Expression of a Novel Innate Immune Pathway in the Developing Hippocampus

Early Life Stress Inhibits Expression of a Novel Innate Immune Pathway in the Developing Hippocampus

Stress during a Critical Postnatal Period Induces Region-Specific Structural Abnormalities and Dysfunction of the Prefrontal Cortex via CRF1

Individual Differences and Social Influences on the Neurobehavioral Pharmacology of Abused Drugs

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