Alcohol‐induced neuronal death in central extended amygdala and pyriform cortex during the postnatal period of the rat

Balaszczuk, Verónica; Bender, Crhistian Luis; Pereno, Germán Leandro; Beltramino, C.

doi:10.1016/j.ijdevneu.2011.05.011

Cited by 12 publications

(13 citation statements)

References 77 publications

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“…Therefore, this stage of development remains a window of plasticity during which structures remain vulnerable to cytotoxic insults that can destabilize subsequent circuit performance. Our observations in olfacto-hippocampal circuit dysfunction may be associated with the immediate wave of neurodegeneration observed throughout this circuit following acute ethanol exposure, as detected by caspase-3 and caspase-9a activation [116]. Just as with our studies, Criado and Ehlers [36] found that hippocampal event related oscillations in adult rats exposed to ethanol as adolescents were elevated at specific frequency ranges, again suggesting a possible shift in excitation/inhibition balance.…”

Section: Findings Of Neuropathology In Acute Ethanol Exposure Animsupporting

confidence: 76%

Long-Lasting Neural Circuit Dysfunction Following Developmental Ethanol Exposure

2013

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Fetal Alcohol Spectrum Disorder (FASD) is a general diagnosis for those exhibiting long-lasting neurobehavioral and cognitive deficiencies as a result of fetal alcohol exposure. It is among the most common causes of mental deficits today. Those impacted are left to rely on advances in our understanding of the nature of early alcohol-induced disorders toward human therapies. Research findings over the last decade have developed a model where ethanol-induced neurodegeneration impacts early neural circuit development, thereby perpetuating subsequent integration and plasticity in vulnerable brain regions. Here we review our current knowledge of FASD neuropathology based on discoveries of long-lasting neurophysiological effects of acute developmental ethanol exposure in animal models. We discuss the important balance between synaptic excitation and inhibition in normal neural network function, and relate the significance of that balance to human FASD as well as related disease states. Finally, we postulate that excitation/inhibition imbalance caused by early ethanol-induced neurodegeneration results in perturbed local and regional network signaling and therefore neurobehavioral pathology.

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Section: Findings Of Neuropathology In Acute Ethanol Exposure Animsupporting

confidence: 76%

Long-Lasting Neural Circuit Dysfunction Following Developmental Ethanol Exposure

2013

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“…There was also a main effect of age, ([age] PCX F [1,24] =4.75, p=0.0394) with no significant interaction between treatment and age. Neurodegeneration in the PCX has been detected before immediately following acute ethanol exposure in early postnatal rats (Balaszczuk et al, 2011) and in adult rats (Leasure and Nixon, 2010). The identity of the affected cell populations and long-term effects however, had not previously been identified.…”

Section: Resultsmentioning

confidence: 99%

Distinct neurobehavioral dysfunction based on the timing of developmental binge-like alcohol exposure

et al. 2014

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Gestational exposure to alcohol can result in long-lasting behavioral deficiencies generally described as fetal alcohol spectrum disorder (FASD). FASD-modeled rodent studies of acute ethanol exposure typically select one developmental window to simulate a specific context equivalent of human embryogenesis, and study consequences of ethanol exposure within that particular developmental epoch. Exposure timing is likely a large determinant in the neurobehavioral consequence of early ethanol exposure, as each brain region is variably susceptible to ethanol cytotoxicity and has unique sensitive periods in their development. We made a parallel comparison of the long-term effects of single-day binge ethanol at either embryonic day 8 (E8) or postnatal day 7 (P7) in male and female mice, and here demonstrate the differential long-term impacts on neuroanatomy, behavior and in vivo electrophysiology of two systems with very different developmental trajectories. The significant long-term differences in odor-evoked activity, local circuit inhibition, and spontaneous coherence between brain regions in the olfacto-hippocampal pathway that were found as a result of developmental ethanol exposure, varied based on insult timing. Long-term effects on cell proliferation and interneuron cell density were also found to vary by insult timing as well as by region. Finally, spatial memory performance was affected in P7-exposed mice, but not E8-exposed mice. Our physiology and behavioral results are conceptually coherent with the neuroanatomical data attained from these same mice. Our results recognize both variable and shared effects of ethanol exposure timing on long-term circuit function and their supported behavior.

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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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Alcohol‐induced neuronal death in central extended amygdala and pyriform cortex during the postnatal period of the rat

Cited by 12 publications

References 77 publications

Long-Lasting Neural Circuit Dysfunction Following Developmental Ethanol Exposure

Long-Lasting Neural Circuit Dysfunction Following Developmental Ethanol Exposure

Distinct neurobehavioral dysfunction based on the timing of developmental binge-like alcohol exposure

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

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