scholarly journals Ethanol Exposure Induces Neonatal Neurodegeneration by Enhancing CB1R Exon1 Histone H4K8 Acetylation and Up-regulating CB1R Function causing Neurobehavioral Abnormalities in Adult Mice

2014 ◽  
Vol 18 (5) ◽  
pp. pyu028-pyu028 ◽  
Author(s):  
S. Subbanna ◽  
N. N. Nagre ◽  
N. S. Umapathy ◽  
B. S. Pace ◽  
B. S. Basavarajappa
Keyword(s):  
Ethanol Exposure ◽  
Adult Mice

scholarly journals Chronic Ethanol Exposure Enhances Facial Stimulation-Evoked Mossy Fiber–Granule Cell Synaptic Transmission via GluN2A Receptors in the Mouse Cerebellar Cortex

2021 ◽  
Vol 15 ◽  
Author(s):  
Bing-Xue Li ◽  
Guang-Hui Dong ◽  
Hao-Long Li ◽  
Jia-Song Zhang ◽  
Yan-Hua Bing ◽  
...  
Keyword(s):  
Synaptic Transmission ◽  
Cerebellar Cortex ◽  
Granule Cell ◽  
Mossy Fiber ◽  
Sensory Information ◽  
Ethanol Exposure ◽  
Chronic Ethanol ◽  
Chronic Ethanol Exposure ◽  
Adult Mice

Sensory information is transferred to the cerebellar cortex via the mossy fiber–granule cell (MF–GC) pathway, which participates in motor coordination and motor learning. We previously reported that chronic ethanol exposure from adolescence facilitated the sensory-evoked molecular layer interneuron–Purkinje cell synaptic transmission in adult mice in vivo. Herein, we investigated the effect of chronic ethanol exposure from adolescence on facial stimulation-evoked MF–GC synaptic transmission in the adult mouse cerebellar cortex using electrophysiological recording techniques and pharmacological methods. Chronic ethanol exposure from adolescence induced an enhancement of facial stimulation-evoked MF–GC synaptic transmission in the cerebellar cortex of adult mice. The application of an N-methyl-D-aspartate receptor (NMDAR) antagonist, D-APV (250 μM), induced stronger depression of facial stimulation-evoked MF–GC synaptic transmission in chronic ethanol-exposed mice compared with that in control mice. Chronic ethanol exposure-induced facilitation of facial stimulation evoked by MF–GC synaptic transmission was abolished by a selective GluN2A antagonist, PEAQX (10 μM), but was unaffected by the application of a selective GluN2B antagonist, TCN-237 (10 μM), or a type 1 metabotropic glutamate receptor blocker, JNJ16259685 (10 μM). These results indicate that chronic ethanol exposure from adolescence enhances facial stimulation-evoked MF–GC synaptic transmission via GluN2A, which suggests that chronic ethanol exposure from adolescence impairs the high-fidelity transmission capability of sensory information in the cerebellar cortex by enhancing the NMDAR-mediated components of MF–GC synaptic transmission in adult mice in vivo.

Chronic ethanol exposure during adolescence alters the behavioral responsiveness to ethanol in adult mice

2012 ◽  
Vol 229 (1) ◽  
pp. 1-9 ◽  
Author(s):  
Caroline Quoilin ◽  
Vincent Didone ◽  
Ezio Tirelli ◽  
Etienne Quertemont
Keyword(s):  
Ethanol Exposure ◽  
Chronic Ethanol ◽  
Chronic Ethanol Exposure ◽  
Adult Mice ◽  
Behavioral Responsiveness

scholarly journals Intermittent ethanol exposure during adolescence impairs cannabinoid type 1 receptor-dependent long-term depression and recognition memory in adult mice

2019 ◽  
Vol 45 (2) ◽  
pp. 309-318 ◽  
Author(s):  
Sara Peñasco ◽  
Irantzu Rico-Barrio ◽  
Nagore Puente ◽  
Christine J. Fontaine ◽  
Almudena Ramos ◽  
...  
Keyword(s):  
Recognition Memory ◽  
Ethanol Exposure ◽  
Long Term Depression ◽  
Cannabinoid Type 1 Receptor ◽  
Adult Mice

scholarly journals Postnatal Ethanol Exposure Activates HDAC-Mediated Histone Deacetylation, Impairs Synaptic Plasticity Gene Expression and Behavior in Mice

2020 ◽  
Vol 23 (5) ◽  
pp. 324-338 ◽  
Author(s):  
Madhu Shivakumar ◽  
Shivakumar Subbanna ◽  
Vikram Joshi ◽  
Balapal S Basavarajappa
Keyword(s):  
Gene Expression ◽  
Synaptic Plasticity ◽  
Cognitive Decline ◽  
Ethanol Exposure ◽  
Epigenetic Mechanism ◽  
Fetal Alcohol ◽  
Adult Mice ◽  
Epigenetic Remodeling ◽  
Factor C ◽  
Fetal Alcohol Spectrum

Abstract Background Alcohol consumption during pregnancy is widespread and contributes to pediatric neurological defects, including hippocampal and neocortex dysfunction, causing cognitive deficits termed fetal alcohol spectrum disorders. However, the critical mechanisms underlying these brain abnormalities remain poorly described. Methods Using a postnatal ethanol exposure (PEE) animal model and pharmacological, epigenetic, synaptic plasticity-related and behavioral approaches, we discovered a novel persistent epigenetic mechanism of neurodegeneration in neonatal hippocampus and neocortex brain regions and of cognitive decline in adult animals. Results PEE, which activates caspase-3 (CC3, a neurodegeneration marker), enhanced histone deacetylase (HDAC1–HDAC3) levels and reduced histone 3 (H3) and 4 (H4) acetylation (ac) in mature neurons. PEE repressed the expression of several synaptic plasticity genes, such as brain-derived neurotrophic factor, C-Fos, early growth response 1 (Egr1), and activity-regulated cytoskeleton-associated protein (Arc). Detailed studies on Egr1 and Arc expression revealed HDAC enrichment at their promoter regions. HDAC inhibition with trichostatin A (TSA) before PEE rescued H3ac/H4ac levels and prevented CC3 formation. Antagonism/null mutation of cannabinoid receptor type-1 (CB1R) before PEE to inhibit CC3 production prevented Egr1 and Arc loss via epigenetic events. TSA administration before PEE prevented postnatal ethanol-induced loss of Egr1 and Arc expression and neurobehavioral defects in adult mice via epigenetic remodeling. In adult mice, 3-day TSA administration attenuated PEE-induced behavioral defects. Conclusions These findings demonstrate that CB1R/HDAC-mediated epigenetic remodeling disrupts gene expression and is a critical step in fetal alcohol spectrum disorder-associated cognitive decline but is reversed by restoration of histone acetylation in the brain.

scholarly journals P-71ADOLESCENT ETHANOL EXPOSURE INDUCES LONG-TERM MEMORY DEFICITS AND POTENTIATES THE MEMORY IMPAIRMENT INDUCED BY COCAINE WITHDRAWAL IN ADULT MICE

2015 ◽  
Vol 50 (suppl 1) ◽  
pp. i63.2-i63
Author(s):  
J. C. Ledesma ◽  
P. Giménez-Gómez ◽  
C. Navarro-Francés ◽  
A. Mateos-García ◽  
M. Rodríguez-Arias ◽  
...  
Keyword(s):  
Memory Impairment ◽  
Memory Deficits ◽  
Ethanol Exposure ◽  
Long Term Memory ◽  
Cocaine Withdrawal ◽  
Term Memory ◽  
Adult Mice

scholarly journals Binge ethanol exposure induces endoplasmic reticulum stress in the brain of adult mice

2018 ◽  
Vol 356 ◽  
pp. 172-181 ◽  
Author(s):  
Yongchao Wang ◽  
Xin Wang ◽  
Hui Li ◽  
Mei Xu ◽  
Jacqueline Frank ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
Ethanol Exposure ◽  
Adult Mice ◽  
Binge Ethanol Exposure ◽  
The Brain ◽  
Binge Ethanol

scholarly journals Sex Differences in Photic Entrainment and Sensitivity to Ethanol-Induced Chronodisruption in Adult Mice After Adolescent Intermittent Ethanol Exposure

2018 ◽  
Vol 42 (11) ◽  
pp. 2144-2159 ◽  
Author(s):  
Christina L. Ruby ◽  
Gerneleh Paye ◽  
Jason L. Fabi ◽  
Jiawen Zhang ◽  
Megan O. Risinger ◽  
...  
Keyword(s):  
Sex Differences ◽  
Ethanol Exposure ◽  
Photic Entrainment ◽  
Adult Mice

Binucleate Spermiogenesis in the Mouse

1972 ◽  
Vol 30 ◽  
pp. 112-113
Author(s):  
John J. Wolosewick
Keyword(s):  
Electron Microscopy ◽  
Phosphate Buffer ◽  
Seminiferous Epithelium ◽  
Mouse Testis ◽  
Germinal Epithelium ◽  
Intercellular Bridges ◽  
Adult Mice ◽  
Cervical Dislocation ◽  
Human And Mouse

Classically, the male germinal epithelium is depicted as synchronously developing uninucleate spermatids conjoined by intercellular bridges. Recently, binucleate and multinucleate spermatids from human and mouse testis have been reported. The present paper describes certain developmental events in one type of binucleate spermatid in the seminiferous epithelium of the mouse.Testes of adult mice (ABP Jax) were removed from the animals after cervical dislocation and placed into 2.5% glutaraldehyde/Millonig's phosphate buffer (pH 7.2). Testicular capsules were gently split and separated, exposing the tubules. After 15 minutes the tissue was carefully cut into cubes (approx. 1mm), fixed for an additional 45 minutes and processed for electron microscopy.

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