Selective effects of perinatal ethanol exposure in medial prefrontal cortex and nucleus accumbens

Lawrence, R. Charles; Otero, Nicha K. H.; Kelly, Sandra J.

doi:10.1016/j.ntt.2011.08.002

Cited by 54 publications

(47 citation statements)

References 81 publications

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“…Such damage may contribute to the impaired impulse control and social deficits observed in children with FASD throughout life. In particular, rodent models of developmental alcohol exposure result in increased caspase-3 expression in the central nucleus of the amygdala (Mitchell & Snyder-Keller, 2003), long-term reductions to amygdalar opioid signaling (Lugo, Wilson, & Kelly, 2006), and altered synaptic connectivity and neuronal loss in the amygdala (Balaszczuk, Bender, Pereno, & Beltramino, 2011; Cullen et al, 2013; Zhou et al, 2010) and the prefrontal cortex (Hamilton, Whitcher, & Klintsova, 2010; Ikonomidou et al, 2000; Lawrence, Otero, & Kelly, 2012; Whitcher & Klintsova, 2008). Dysfunction of these brain areas could contribute to disruptions in social and play behavior observed in AE rats.…”

Section: Discussionmentioning

confidence: 99%

Activity and social behavior in a complex environment in rats neonatally exposed to alcohol

Boschen

Hamilton

Delorme

et al. 2014

Alcohol

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Environmental complexity (EC) is a powerful, stimulating paradigm that engages animals through a variety of sensory and motor pathways. Exposure to EC (30 days) following 12 days of wheel running preserves hippocampal neuroplasticity in male rats neonatally exposed to alcohol during the third-trimester equivalent (binge-like exposure on postnatal days [PD] 4–9). The current experiment investigates the importance of various components of EC (physical activity, exploration, social interaction, novelty) and examines whether neonatal alcohol exposure affects how male rats interact with their environment and other male rats. Male pups were assigned to 1 of 3 neonatal conditions from PD 4–9: suckle control (SC), sham-intubated (SI), or alcohol-exposed (AE, 5.25 g/kg/day). From PD 30–42 animals were housed with 24-h access to a voluntary running wheel. The animals were then placed in EC from PD 42–72 (9 animals/cage, counterbalanced by neonatal condition). During EC, the animals were filmed for five 30-min sessions (PD 42, 48, 56, 64, 68). For the first experiment, the videos were coded for distance traveled in the cage, overall locomotor activity, time spent near other animals, and interaction with toys. For the second experiment, the videos were analyzed for wrestling, mounting, boxing, grooming, sniffing, and crawling over/under. AE animals were found to be less active and exploratory and engaged in fewer mounting behaviors compared to control animals. Results suggest that after exposure to wheel running, AE animals still have deficits in activity and social behaviors while housed in EC compared to control animals with the same experience.

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Section: Discussionmentioning

confidence: 99%

Activity and social behavior in a complex environment in rats neonatally exposed to alcohol

Boschen

Hamilton

Delorme

et al. 2014

Alcohol

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“…Two studies showed decreased spine density in OFC and either no change (66) or a decrease (67) in mPFC in adult brains.…”

Section: Factors Influencing Prefrontal Developmentmentioning

confidence: 99%

Experience and the developing prefrontal cortex

Kolb

Mychasiuk

Muhammad

et al. 2012

Proc. Natl. Acad. Sci. U.S.A.

475

321

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The prefrontal cortex (PFC) receives input from all other cortical regions and functions to plan and direct motor, cognitive, affective, and social behavior across time. It has a prolonged development, which allows the acquisition of complex cognitive abilities through experience but makes it susceptible to factors that can lead to abnormal functioning, which is often manifested in neuropsychiatric disorders. When the PFC is exposed to different environmental events during development, such as sensory stimuli, stress, drugs, hormones, and social experiences (including both parental and peer interactions), the developing PFC may develop in different ways. The goal of the current review is to illustrate how the circuitry of the developing PFC can be sculpted by a wide range of pre-and postnatal factors. We begin with an overview of prefrontal functioning and development, and we conclude with a consideration of how early experiences influence prefrontal development and behavior.neural plasticity | dendritic spines | prenatal stress | psychoactive drugs | metaplasticity T he development of the cerebral cortex reflects more than a simple unfolding of a genetic blueprint; rather, it represents a complex dance of experiential and genetic factors that mold the emerging cerebrum. Pre-and postnatal environmental events, such as sensory stimuli, hormones, parent-child relationships, stress, and psychoactive drugs, modify cerebral development and, ultimately, adult behavior. Although all cerebral regions are influenced by early experience, the effects of experience are significantly different in specific cortical regions. The goal of this article is to review the ways in which one specific region, the prefrontal cortex (PFC), is sculpted by a wide range of pre-and postnatal factors. We begin with an overview of the nature and function of the PFC, followed by a review of experience-dependent modification of prefrontal organization and function. What Is the PFC?Kaas (1) proposed that a few basic areas of cerebral cortex are present in all mammals. These include primary and secondary visual and somatosensory areas (i.e., V1, V2, S1, S2), at least one auditory area and one taste area, a motor area, a transitional strip of cortex that relates the amygdala and hippocampus to other cortical areas (i.e., perirhinal cortex, entorhinal cortex), and a region referred to as the PFC. The definition of the sensory regions is relatively straightforward insofar as they receive unimodal input from the sensory receptor systems (e.g., eye, ear, tongue), and the outputs of the motor cortex are ultimately directed via polysynaptic pathways to effector organs. The outputs of all cortical regions are also components of feedback loops through which the cortex and subcortical regions of the brain mutually influence each other. Although there is no universally acceptable definition of the PFC, it can be regarded to be the region of the cortex that receives its principal thalamic inputs from the mediodorsal nucleus of the thalamus (e.g., 2). This cor...

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“…In some models, histological studies showed that these volume reductions corresponded to reduced neuron numbers (Berman & Hannigan, 2000; Ieraci & Herrera, 2007; Miller, 2006; Olney, 2004). More detailed examinations found evidence of altered dendritic length and spine density (Berman & Hannigan, 2000; Cui et al, 2010; Lawrence, Otero, & Kelly, 2012; Susick, Lowing, Provenzano, Hildebrandt, & Conti, 2014), and found evidence of disrupted organization of cortical sensory areas (Margret et al, 2006; Medina, Krahe, & Ramoa, 2005; Miller & Potempa, 1990). Additionally, in several cortical and subcortical brain regions there are findings of reduced GABAergic cell density, suggesting that inhibitory circuits in the cerebral cortex may be especially vulnerable to ethanol toxicity (Coleman et al, 2012; Sadrian, Lopez-Guzman, Wilson, & Saito, 2014; Sadrian et al, 2013).…”

Section: Introductionmentioning

confidence: 99%

Selective reduction of cerebral cortex GABA neurons in a late gestation model of fetal alcohol spectrum disorder

Smiley

Saito

Bleiwas

et al. 2015

Alcohol

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Fetal alcohol spectrum disorders (FASD) are associated with cognitive and behavioral deficits, and decreased volume of the whole brain and cerebral cortex. Rodent models have shown that early postnatal treatments, which mimic ethanol toxicity in the third trimester of human pregnancy, acutely induce widespread apoptotic neuronal degeneration and permanent behavioral deficits. However, the lasting cellular and anatomical effects of early ethanol treatments are still incompletely understood. This study examined changes in neocortex volume, thickness, and cellular organization that persist in adult mice after postnatal day 7 (P7) ethanol treatment. Post mortem brain volumes, measured by both MRI within the skull and by fluid displacement of isolated brains, were reduced 10–13% by ethanol treatment. The cerebral cortex showed a similar reduction (12%) caused mainly by lower surface area (9%). In spite of these large changes, several features of cortical organization showed little evidence of change, including cortical thickness, overall neuron size, and laminar organization. Estimates of total neuron number showed a trend level reduction of about 8%, due mainly to reduced cortical volume but unchanged neuron density. However, counts of calretinin (CR) and parvalbumin (PV) subtypes of GABAergic neurons showed a striking >30% reduction of neuron number. Similar ethanol effects were found in male and female mice, and in C57BL/6By and BALB/cJ mouse strains. Our findings indicate that the cortex has substantial capacity to develop normal cytoarchitectonic organization after early postnatal ethanol toxicity, but there is a selective and persistent reduction of GABA cells that may contribute to the lasting cognitive and behavioral deficits in FASD.

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Selective effects of perinatal ethanol exposure in medial prefrontal cortex and nucleus accumbens

Cited by 54 publications

References 81 publications

Activity and social behavior in a complex environment in rats neonatally exposed to alcohol

Activity and social behavior in a complex environment in rats neonatally exposed to alcohol

Experience and the developing prefrontal cortex

Selective reduction of cerebral cortex GABA neurons in a late gestation model of fetal alcohol spectrum disorder

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