Special Issue "Ethanol Neurotoxicity"
A special issue of Brain Sciences (ISSN 2076-3425).
Deadline for manuscript submissions: closed (28 February 2013)
Alcohol abuse is a worldwide public health concern resulting in significant morbidity, mortality and financial burden. Decades of research have pinpointed the pathological consequences of ethanol and have focused considerable attention on neurotoxicity. Indeed, ethanol is known to induce structural changes and neuronal cell death in the nervous system of humans and animals, and significant progress is being made in unraveling the mechanisms and neural consequences of ethanol exposure. Several important questions related to ethanol neurotoxicity remain unanswered: What is the precise cellular mechanism of ethanol induced neuronal cell death? What is the role of support cells such as glia in neurotoxicity, and are glia themselves targets of ethanol? What are the developmental consequences of ethanol exposure culminating in Fetal Alcohol Spectrum Disorders (FASD)? How does ethanol affect neuronal membrane proteins such as receptors and transporters? Are synaptic connections between neurons affected by ethanol? What are the pathological consequences of long-term ethanol exposure in alcoholics? What structural changes are noted in brain imaging studies of chronic alcoholics or children with FASD?
This special issue will collect a series of articles which document the important strides being made towards understanding the basis for and consequences of ethanol neurotoxicity. It is meant to be inclusive of the major questions indicated above, and it is my hope that the ethanol research community will greatly benefit from this anthology.
Dr. D. Blaine Moore
Manuscript Submission Information
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- ethanol-induced neuronal apoptosis
- fetal alcohol spectrum disorder
- ethanol and membrane proteins
- ethanol and signal transduction
- ethanol and glia
- ethanol and synapses/circuitry
- neuropathology in chronic alcoholism
- ethanol and neuro-imaging
- ethanol and cognition
The below list represents only planned manuscripts. Some of these manuscripts have not been received by the Editorial Office yet. Papers submitted to MDPI journals are subject to peer-review.
Type of paper: Article
Title: Ethanol Modulates Spontaneous Calcium Waves in Axonal Growth Cones in Vitro
Authors: Tara A. Lindsley and Jessica Donnelly
Affiliation: Center for Neuropharmacology & Neuroscience, Albany Medical College (MC-136), 47 New Scotland Ave., Albany, NY 12208, USA; E-Mail:email@example.com
Abstract: In developing neurons the frequency of spontaneous, transient calcium elevations localized to the growth cone is inversely related to the rate of axon elongation and increases several fold when axons pause. Here we report that these growth cone calcium waves are modulated by conditions of ethanol exposure that alter axonal growth dynamics. Using time-series Fluo-3 confocal imaging we found that acute treatment of fetal rat hippocampal neurons with 43 or 87 mM ethanol at an early stage of development in culture dramatically decreased percent of axonal growth cones showing at least one Ca2+ transient during 10 min of recording, from 18% in controls to 5% in cultures exposed to ethanol. Chronic exposure to 43 mM ethanol also reduced the frequency of Ca2+ transients in growth cones to 8%, but 87 mM ethanol increased their frequency to 40%. Neither chronic nor acute ethanol affected the peak amplitude, time to peak or total duration of transients. In some experiments, we determined the correlation between rate of axon elongation (or retraction) and frequency of transients. As expected, increases in transient frequency were correlated with pausing in control and ethanol treated growth cones, except in cultures exposed chronically to 87mM ethanol. Thus, the relationship between growth cone Ca2+ wave frequency and axon growth dynamics is disrupted by ethanol.