summary: A recent study investigated the effects of fetal alcohol exposure on brain development in neonatal mice.
In this study, we found that ethanol-induced neonatal apoptosis often causes immediate neuronal loss that persists into adulthood. Some brain regions are more vulnerable to ethanol-induced neuronal loss than others, with the anterior thalamic nucleus showing the greatest loss of neurons.
This study highlights the importance of identifying vulnerable brain regions for potential therapeutic intervention, and to prevent or reduce the long-term effects of alcohol exposure during critical periods of brain development. It may inform the strategy of
Important facts:
- Ethanol-induced neonatal apoptosis often causes immediate neuronal loss that persists into adulthood. This indicates a limited ability of the brain to compensate for early neuronal loss caused by alcohol exposure during a critical period of brain development.
- Some brain regions are more vulnerable to ethanol-induced neuronal loss than others. The anterior thalamic nucleus showed the greatest loss of neurons, followed by the medial septal/vertical diagonal band, the dorsal subiculum, and the dorsal lateral geniculate nucleus. In contrast, the entire neocortex had a relatively slight deficit in total neuron number.
- Identifying vulnerable brain regions is important for potential therapeutic interventions to prevent or reduce the long-term effects of alcohol exposure during critical periods of brain development.
sauce: neuroscience news
Recent studies have shed new light on the effects of fetal alcohol exposure on brain development.
This study focuses on specific exposure paradigms optimized to induce a spike in cell apoptosis in several regions of the forebrain of neonatal mice.
Although it is well established that alcohol exposure during this critical period can cause neuronal cell death, the local selectivity of ethanol effects and whether the brain has the ability to compensate for initial neuronal loss remain unclear. remains a question.
This study employed stereocytometric cell counting to compare cumulative neuronal loss 8 hours after ethanol treatment at postnatal day 7 (P7) with cumulative neuronal loss in animals left to adulthood (P70). Did.
Results show that the reduction in total neuron number after 8 h is as large as that in adult animals, indicating that ethanol-induced neonatal apoptosis often causes immediate neuronal loss that persists into adulthood. increase.
This study also found that some brain regions are more vulnerable to ethanol-induced neuronal loss than others. The anterior thalamic nucleus showed the greatest loss of neurons, followed by the medial septal/vertical diagonal band, the dorsal subiculum, and the dorsal lateral geniculate nucleus. In contrast, there was a relatively small loss of total number of neurons in the entire neocortex.
Interestingly, in this study, estimates of the number of apoptotic cells in Nissl-stained sections 8 h after ethanol treatment could provide a less reliable predictor of adult neuron loss than estimates of total neuron number. got it.
This suggests that while markers of apoptotic cells can confirm the presence of an apoptotic response, they are unreliable predictors of regional differences or total neuronal loss.
This study provides a reliable method to assess regional differences in neuronal loss caused by ethanol exposure in neonates and highlights the importance of identifying vulnerable brain regions for potential therapeutic intervention. I’m here.
The findings also suggest that the brain may have a limited ability to compensate for neuronal loss induced by ethanol.
Overall, this study contributes to a better understanding of the effects of fetal alcohol exposure on brain development, and strategies to prevent or mitigate the long-term effects of alcohol exposure during critical periods of brain development. may provide the
About this brain development research news
author: press office
sauce: neuroscience news
contact: Press Office – Neuroscience News
image: Image credited to Neuroscience News
Original research: open access.
“Total neuron number estimates indicate that neonatal ethanol causes immediate and sustained neuronal loss in cortical and subcortical regionsBy John F. Smiley et al. The forefront of neuroscience
overview
Total neuron number estimates indicate that neonatal ethanol causes immediate and sustained neuronal loss in cortical and subcortical regions
Neonatal brain development has periods of normal apoptotic cell death that regulate adult neuron numbers. Around the same time, ethanol exposure can trigger a dramatic spike in apoptotic cell death.
Although ethanol-induced apoptosis has been shown to reduce adult neuron numbers, questions remain about the local selectivity of ethanol effects, and whether the brain has the ability to overcome early neuronal loss.
In this study, stereoscopic cell counting was performed to compare the cumulative neuronal loss 8 h after ethanol treatment at postnatal day 7 (P7) with that of animals left to mature to adulthood (P70). used. Across several brain regions, the reduction in total neuron number after 8 hours was found to be as large as that in adult animals.
A comparison between regions showed that some regions were more vulnerable, anterior thalamic nucleus > medial septal/vertical diagonal zone, dorsal subiculum, and dorsal lateral geniculate nucleus > mammary body and cingulate cortex > neocortex It became clear that neurons were lost throughout. In contrast to estimates of total neuron numbers, estimates of apoptotic cell numbers in Nissl-stained sections 8 h after ethanol treatment provided unreliable predictors of adult neuron loss.
Findings indicate that ethanol-induced neonatal apoptosis often causes immediate neuronal loss that persists into adulthood, and may further limit the brain’s ability to compensate for ethanol-induced neuronal loss. suggests that
