Early Postnatal Ethanol Exposure: Glutamatergic Excitotoxic Cell Death During Acute Withdrawal

Clements, K.M.; Smith, L.; Reynolds, John N. J.; Overton, Paul G.; Thomas, Jennifer D.; Napper, Ruth M. A.

doi:10.1007/s11062-012-9308-7

Cited by 3 publications

(3 citation statements)

References 64 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Once the ethanol is metabolized, this receptor increase can result in excitotoxicity. Early postnatal ethanol exposure in rodents has been shown to increase markers for glutamatergic activity (NMDA1 receptor) in the prefrontal cortex, dorsal striatum, somatosensory cortex, and motor cortex during acute withdrawal (22 or 26 h post ethanol administration) [ 41 ]. During normal development, there is a sharp increase in vulnerability to NMDA receptor-mediated excitotoxicity in the third trimester equivalent (P6–P7 in rats), and the associated behavioral deficits can be ameliorated with the administration of an NMDA antagonist 21–33 h after ethanol administration.…”

Section: Discussionmentioning

confidence: 99%

Acute Ethanol Exposure during Synaptogenesis Rapidly Alters Medium Spiny Neuron Morphology and Synaptic Protein Expression in the Dorsal Striatum

Clabough

Ingersoll

Reekes

et al. 2021

IJMS

View full text Add to dashboard Cite

Fetal alcohol spectrum disorders are caused by the disruption of normal brain development in utero. The severity and range of symptoms is dictated by both the dosage and timing of ethanol administration, and the resulting developmental processes that are impacted. In order to investigate the effects of an acute, high-dose intoxication event on the development of medium spiny neurons (MSNs) in the striatum, mice were injected with ethanol on P6, and neuronal morphology was assessed after 24 h, or at 1 month or 5 months of age. Data indicate an immediate increase in MSN dendritic length and branching, a rapid decrease in spine number, and increased levels of the synaptic protein PSD-95 as a consequence of this neonatal exposure to ethanol, but these differences do not persist into adulthood. These results demonstrate a rapid neuronal response to ethanol exposure and characterize the dynamic nature of neuronal architecture in the MSNs. Although differences in neuronal branching and spine density induced by ethanol resolve with time, early changes in the caudate/putamen region have a potential impact on the execution of complex motor skills, as well as aspects of long-term learning and addictive behavior.

show abstract

Section: Discussionmentioning

confidence: 99%

Acute Ethanol Exposure during Synaptogenesis Rapidly Alters Medium Spiny Neuron Morphology and Synaptic Protein Expression in the Dorsal Striatum

Clabough

Ingersoll

Reekes

et al. 2021

IJMS

View full text Add to dashboard Cite

show abstract

“…The liver alcohol dehydrogenase metabolizes the acetaldehyde of alcohol making this organ particularly susceptible to lesion ( 2 ). Alcohol intake during pregnancy can result in damage in newborns with detrimental effects on memory ( 3 ) due to hippocampal and prefrontal cortical alteration ( 3 , 4 ). In addition, alcohol use commonly starts during adolescence disrupting brain maturation and key processes of development.…”

Section: Introductionmentioning

confidence: 99%

The effect of omega-3 fatty acids on alcohol-induced damage

2023

View full text Add to dashboard Cite

Alcohol is the most widely consumed psychoactive substance in the world that has a severe impact on many organs and bodily systems, particularly the liver and nervous system. Alcohol use during pregnancy roots long-lasting changes in the newborns and during adolescence has long-term detrimental effects especially on the brain. The brain contains docosahexaenoic acid (DHA), a major omega-3 (n-3) fatty acid (FA) that makes up cell membranes and influences membrane-associated protein function, cell signaling, gene expression and lipid production. N-3 is beneficial in several brain conditions like neurodegenerative diseases, ameliorating cognitive impairment, oxidative stress, neuronal death and inflammation. Because alcohol decreases the levels of n-3, it is timely to know whether n-3 supplementation positively modifies alcohol-induced injuries. The aim of this review is to summarize the state-of-the-art of the n-3 effects on certain conditions caused by alcohol intake, focusing primarily on brain damage and alcoholic liver disease.

show abstract

“…JPEG files were processed for cell counts using MBF-Image J software as previously described (Clements et al, 2012).…”

Section: Confirmation Of Lesion Extent Using Tyrosine Hydroxylase Immmentioning

confidence: 99%

Striatal mRNA expression patterns underlying peak dose l-DOPA-induced dyskinesia in the 6-OHDA hemiparkinsonian rat

et al. 2016

View full text Add to dashboard Cite

L-DOPA is the primary pharmacological treatment for relief of the motor symptoms of ParkinsonÕs disease. With prolonged treatment (≥5 years) the majority of patients will develop abnormal involuntary movements as a result of L-DOPA treatment, known as L-DOPA-induced dyskinesia. Understanding the underlying mechanisms of dyskinesia is a crucial step towards developing treatments for this debilitating side effect. We used the 6-OHDA rat model of ParkinsonÕs disease treated with a three week dosing regimen of L-DOPA plus the dopa decarboxylase inhibitor benserazide (4 mg/kg and 7.5 mg/kg s.c., respectively) to induce dyskinesia in 50% of individuals. We then used RNA-seq to investigate the differences in mRNA expression in the striatum of dyskinetic animals, nondyskinetic animals, and untreated parkinsonian controls at the peak of dyskinesia expression, 60 minutes after L-DOPA administration. Overall, 255 genes were differentially expressed; with significant differences in mRNA expression observed between all three groups. In dyskinetic animals 129 genes were more highly expressed and 14 less highly expressed when compared with non-dyskinetic and untreated parkinsonian controls. In L-DOPA treated animals 42 genes were more highly expressed and 95 less highly expressed when compared with untreated parkinsonian controls. Gene set cluster analysis revealed an increase in expression of genes associated with the cytoskeleton and phosphoproteins in dyskinetic animals compared with non-dyskinetic animals, which is consistent with recent studies documenting an increase in synapses in dyskinetic animals. These genes may be potential targets for drugs to ameliorate L-DOPA-induced dyskinesia or as an adjunct treatment to prevent their occurrence. ¥ Cytoskeletal elements present a potential target for treatments to prevent or ameliorate L-DOPA-induced dyskinesia.

show abstract

Early Postnatal Ethanol Exposure: Glutamatergic Excitotoxic Cell Death During Acute Withdrawal

Cited by 3 publications

References 64 publications

Acute Ethanol Exposure during Synaptogenesis Rapidly Alters Medium Spiny Neuron Morphology and Synaptic Protein Expression in the Dorsal Striatum

Acute Ethanol Exposure during Synaptogenesis Rapidly Alters Medium Spiny Neuron Morphology and Synaptic Protein Expression in the Dorsal Striatum

The effect of omega-3 fatty acids on alcohol-induced damage

Striatal mRNA expression patterns underlying peak dose l-DOPA-induced dyskinesia in the 6-OHDA hemiparkinsonian rat

Contact Info

Product

Resources

About