Effect of acute ethanol exposure during pregnancy on dentate gyrus synaptic plasticity in 45-day-old rats

1992 ◽  
Vol 42 (1) ◽  
pp. 85-89 ◽  
Author(s):  
Raúl A. Gómez ◽  
Susana Fulginiti ◽  
Oscar A. Ramírez
Keyword(s):  
Synaptic Plasticity ◽  
Dentate Gyrus ◽  
Ethanol Exposure ◽  
Acute Ethanol ◽  
Old Rats ◽  
Exposure During Pregnancy

Acute ethanol exposure during pregnancy in rats: Effects upon a multiple learning task

Alcohol ◽  
1989 ◽  
Vol 6 (5) ◽  
pp. 363-368 ◽  
Author(s):  
Nora Silvana Vigliecca ◽  
Susana Fulginiti ◽  
Silvia Alejandra Minetti
Keyword(s):  
Learning Task ◽  
Ethanol Exposure ◽  
Acute Ethanol ◽  
Exposure During Pregnancy

scholarly journals Acute Ethanol Exposure Enhances Synaptic Plasticity in the Dorsal Striatum in Adult Male and Female Rats

2020 ◽  
Vol 6 (1) ◽  
pp. 113-122 ◽  
Author(s):  
Yosef Avchalumov ◽  
Juan C. Piña-Crespo ◽  
John J. Woodward ◽  
Chitra D. Mandyam
Keyword(s):  
Sex Differences ◽  
Synaptic Plasticity ◽  
Synaptic Transmission ◽  
Ex Vivo ◽  
Dorsal Striatum ◽  
Ethanol Exposure ◽  
Female Rats ◽  
Male And Female ◽  
Male And Female Rats ◽  
Acute Ethanol

Background: Acute (ex vivo) and chronic (in vivo) alcohol exposure induces neuroplastic changes in the dorsal striatum, a critical region implicated in instrumental learning. Objective: Sex differences are evident in alcohol reward and reinforcement, with female rats consuming higher amount of alcohol in operant paradigms compared to male rats. However, sex differences in the neuroplastic changes produced by acute alcohol in the dorsal striatum have been unexplored. Methods: Using electrophysiological recordings from dorsal striatal slices obtained from adult male and female rats, we investigated the effects of ex vivo ethanol exposure on synaptic transmission and synaptic plasticity. Ethanol (44 mM) enhanced basal synaptic transmission in both sexes. Ethanol also enhanced long-term potentiation in both sexes. Other measures of synaptic plasticity including paired-pulse ratio were unaltered by ethanol in both sexes. Results: The results suggest that alterations in synaptic plasticity induced by acute ethanol, at a concentration associated with intoxication, could play an important role in alcohol-induced experience-dependent modification of corticostriatal circuits underlying the learning of goal-directed instrumental actions and formation of habits mediating alcohol seeking and taking. Conclusions: Taken together, understanding the mechanism(s) underlying alcohol induced changes in corticostriatal function may lead to the development of more effective therapeutic agents to reduce habitual drinking and seeking associated with alcohol use disorders.

scholarly journals Synaptic plasticity in the hippocampus shows resistance to acute ethanol exposure in transgenic mice with astrocyte-targeted enhanced CCL2 expression

2013 ◽  
Vol 67 ◽  
pp. 115-125 ◽  
Author(s):  
Jennifer G. Bray ◽  
Kenneth C. Reyes ◽  
Amanda J. Roberts ◽  
Richard M. Ransohoff ◽  
Donna L. Gruol
Keyword(s):  
Synaptic Plasticity ◽  
Transgenic Mice ◽  
Ethanol Exposure ◽  
Ccl2 Expression ◽  
Acute Ethanol

scholarly journals Acute ethanol exposure disrupts VEGF receptor cell signaling in endothelial cells

2008 ◽  
Vol 295 (1) ◽  
pp. H174-H184 ◽  
Author(s):  
Katherine A. Radek ◽  
Elizabeth J. Kovacs ◽  
Richard L. Gallo ◽  
Luisa A. DiPietro
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
Cell Signaling ◽  
Network Formation ◽  
Ethanol Exposure ◽  
Capillary Network ◽  
Ethanol Metabolism ◽  
Vegf Receptor ◽  
Acute Ethanol

Physiological angiogenesis is regulated by various factors, including signaling through vascular endothelial growth factor (VEGF) receptors. We previously reported that a single dose of ethanol (1.4 g/kg), yielding a blood alcohol concentration of 100 mg/dl, significantly impairs angiogenesis in murine wounds, despite adequate levels of VEGF, suggesting direct effects of ethanol on endothelial cell signaling (40). To examine the mechanism by which ethanol influences angiogenesis in wounds, we employed two different in vitro angiogenesis assays to determine whether acute ethanol exposure (100 mg/dl) would have long-lasting effects on VEGF-induced capillary network formation. Ethanol exposure resulted in reduced VEGF-induced cord formation on collagen and reduced capillary network structure on Matrigel in vitro. In addition, ethanol exposure decreased expression of endothelial VEGF receptor-2, as well as VEGF receptor-2 phosphorylation in vitro. Inhibition of ethanol metabolism by 4-methylpyrazole partially abrogated the effect of ethanol on endothelial cell cord formation. However, mice treated with t-butanol, an alcohol not metabolized by alcohol dehydrogenase, exhibited no change in wound vascularity. These results suggest that products of ethanol metabolism are important factors in the development of ethanol-induced changes in endothelial cell responsiveness to VEGF. In vivo, ethanol exposure caused both decreased angiogenesis and increased hypoxia in wounds. Moreover, in vitro experiments demonstrated a direct effect of ethanol on the response to hypoxia in endothelial cells, as ethanol diminished nuclear hypoxia-inducible factor-1α protein levels. Together, the data establish that acute ethanol exposure significantly impairs angiogenesis and suggest that this effect is mediated by changes in endothelial cell responsiveness to both VEGF and hypoxia.

Effects of Adult Neurogenesis on Synaptic Plasticity in the Rat Dentate Gyrus

2001 ◽  
Vol 85 (6) ◽  
pp. 2423-2431 ◽  
Author(s):  
J. S. Snyder ◽  
N. Kee ◽  
J. M. Wojtowicz
Keyword(s):  
Synaptic Plasticity ◽  
Dentate Gyrus ◽  
Adult Neurogenesis ◽  
Long Term Potentiation ◽  
Receptor Blocker ◽  
Granule Neurons ◽  
Term Potentiation ◽  
Cell Recording ◽  
Similar Preparation ◽  
Nmda Receptor Blocker

Ongoing neurogenesis in the adult hippocampal dentate gyrus (DG) generates a substantial population of young neurons. This phenomenon is present in all species examined thus far, including humans. Although the regulation of adult neurogenesis by various physiologically relevant factors such as learning and stress has been documented, the functional contributions of the newly born neurons to hippocampal functions are not known. We investigated possible contributions of the newly born granule neurons to synaptic plasticity in the hippocampal DG. In the standard hippocampal slice preparation perfused with artificial cerebrospinal fluid (ACSF), a small (10%) long-term potentiation (LTP) of the evoked field potentials is seen after tetanic stimulation of the afferent medial perforant pathway (MPP). The induction of this ACSF-LTP is resistant to a N-methyl-d-aspartate (NMDA) receptor blocker,d,l-2-amino-5-phosphonovaleric acid (APV), but is completely prevented by ifenprodil, a blocker of NR2B subtype of NMDA receptors. In contrast, slices perfused with picrotoxin (PICRO), a GABA-receptor blocker, revealed a larger (40–50%), APV-sensitive but ifenprodil-insensitive LTP. The ACSF-LTP required lower frequency of stimulation and fewer stimuli for its induction than the PICRO-LTP. All these characteristics of ACSF-LTP are in agreement with the properties of the putative individual new granule neurons examined previously with the use of the whole cell recording technique in a similar preparation. A causal relationship between neurogenesis and ACSF-LTP was confirmed in experiments using low dose of gamma radiation applied to the brain 3 wk prior to the electrophysiological experiments. In these experiments, the new cell proliferation was drastically reduced and ACSF-LTP was selectively blocked. We conclude that the young, adult-generated granule neurons play a significant role in synaptic plasticity in the DG. Since DG is the major source of the afferent inputs into the hippocampus, the production and the plasticity of new neurons may have an important role in the hippocampal functions such as learning and memory.

scholarly journals A STEREOLOGICAL ANALYSIS OF THE EFFECT OF EARLY POSTNATAL ETHANOL EXPOSURE ON NEURONAL NUMBERS IN RAT DENTATE GYRUS

2011 ◽  
Vol 19 (2) ◽  
pp. 99 ◽  
Author(s):  
Takanori Miki ◽  
Simon J Harris ◽  
Peter Wilce ◽  
Yoshiki Takeuchi ◽  
Kuldip S Bedi
Keyword(s):  
Dentate Gyrus ◽  
Hippocampal Formation ◽  
Ethanol Exposure ◽  
Learning Ability ◽  
Ethanol Ingestion ◽  
High Dose ◽  
Postnatal Life ◽  
Numerical Density ◽  
Rat Pups ◽  
Early Postnatal Life

Maternal ethanol ingestion during pregnancy can cause fetal alcohol syndrome (FAS) in their offspring. Among the symptoms of FAS, damage to the central nervous system has emerged as one of the most serious problems. We have previously shown that a relatively high dose of ethanol exposure during early postnatal life can cause alterations in spatial learning ability. This ability is controlled, at least in part, by the hippocampal formation. The purpose of the present study was to determine whether exposure of rat pups to ethanol during early postnatal life had effects on the total number of the dentate gyrus neurons. Wistar rats were exposed to a relatively high daily dose of ethanol between postnatal days 10 to 15. Ethanol exposure was achieved by placing rat pups in a chamber containing ethanol vapour for 3 hours a day. The blood ethanol concentration was found to be about 430 mg/dL at the end of the exposure period. Groups of ethanol treated (ET), separation controls (SC) and mother reared controls (MRC) were anaesthetised and killed at 16-days-of-age by perfusion with phosphate-buffered 2.5% glutaraldehyde. The Cavalieri principle was used to determine the volume of subdivisions of the dentate gyrus, and the physical disector method was used to estimate the numerical densities of neurons within each subdivision. The total number of neurons was calculated by multiplying estimates of the numerical density with the volume. There was, on average, about 421,000 granule cells in all three treatment groups. In the hilus region, ET rats had about 27,000 neuronal cells. This value was significantly smaller than the average of 38,000 such neurons estimated to be present in both MRC and SC animals. It is concluded that neurons in the hilus region of the dentate gyrus may be particularly vulnerable to the effects of a high dose of ethanol exposure during PND 10-15. It is likely that this deficit was due to neuronal death induced by some mechanisms related to the ethanol exposure.

scholarly journals Induction of autophagy by zinc during acute ethanol exposure (122.1)

2014 ◽  
Vol 28 (S1) ◽  
Author(s):  
Juan Liuzzi ◽  
Lorenzo Menzel ◽  
Changwon Yoo
Keyword(s):  
Ethanol Exposure ◽  
Acute Ethanol

scholarly journals Acute ethanol stress induces sumoylation of conserved chromatin structural proteins in Saccharomyces cerevisiae

2021 ◽  
pp. mbc.E20-11-0715
Author(s):  
Amanda I. Bradley ◽  
Nicole M. Marsh ◽  
Heather R. Borror ◽  
Kaitlyn E. Mostoller ◽  
Amber I. Gama ◽  
...  
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Ethanol Exposure ◽  
S Phase ◽  
Structural Proteins ◽  
Ethanol Stress ◽  
Post Translational Modification ◽  
Yeast Saccharomyces Cerevisiae ◽  
Cycle Arrest ◽  
Chromatin Structural ◽  
Acute Ethanol

Stress is ubiquitous to life and can irreparably damage essential biomolecules and organelles in cells. To survive, organisms must sense and adapt to stressful conditions. One highly conserved adaptive stress response is through the post-translational modification of proteins by the small ubiquitin-like modifier (SUMO). Here, we examine the effects of acute ethanol stress on protein sumoylation in the budding yeast Saccharomyces cerevisiae . We found that cells exhibit a transient sumoylation response after acute exposure to ≤ 7.5% ethanol. By contrast, the sumoylation response becomes chronic at 10% ethanol exposure. Mass spectrometry analyses identified 18 proteins that are sumoylated after acute ethanol exposure, with 15 known to associate with chromatin. Upon further analysis, we found that the chromatin structural proteins Smc5 and Smc6 undergo ethanol-induced sumoylation that depends on the activity of the E3 SUMO ligase Mms21. Using cell-cycle arrest assays, we observed that Smc5 and Smc6 ethanol-induced sumoylation occurs during G1 and G2/M phases but not S phase. Acute ethanol exposure also resulted in the formation of Rad52 foci at levels comparable to Rad52 foci formation after exposure to the DNA alkylating agent methyl methanesulfonate (MMS). MMS exposure is known to induce the intra-S phase DNA damage checkpoint via Rad53 phosphorylation, but ethanol exposure did not induce Rad53 phosphorylation. Ethanol abrogated the effect of MMS on Rad53 phosphorylation when added simultaneously. From these studies, we propose that acute ethanol exposure induces a change in chromatin leading to sumoylation of specific chromatin-structural proteins.

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