Special Issue "Ethanol Neurotoxicity"
A special issue of Brain Sciences (ISSN 2076-3425).
Deadline for manuscript submissions: closed (28 February 2013)
Dr. D. Blaine Moore
Department of Biology, Kalamazoo College, Kalamazoo, MI 49006, USA
Phone: +269 337 7301
Fax: +269 337 7508
Interests: ethanol toxicity mechanism; particularly the role of Bcl-2 family members and caspases
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
Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. Papers will be published continuously (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.
Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are refereed through a peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Brain Sciences is an international peer-reviewed Open Access quarterly journal published by MDPI.
Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 500 CHF (Swiss Francs). English correction and/or formatting fees of 250 CHF (Swiss Francs) will be charged in certain cases for those articles accepted for publication that require extensive additional formatting and/or English corrections.
- 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
Review: Drug-Induced Apoptosis: Mechanism by which Alcohol and Many Other Drugs Can Disrupt Brain Development
Brain Sci. 2013, 3(3), 1153-1181; doi:10.3390/brainsci3031153
Received: 25 May 2013; in revised form: 8 July 2013 / Accepted: 11 July 2013 / Published: 31 July 2013| Cited by 2 | PDF Full-text (5703 KB) | HTML Full-text | XML Full-text
Article: Developmental Neurotoxicity of Alcohol and Anesthetic Drugs Is Augmented by Co-Exposure to Caffeine
Brain Sci. 2013, 3(3), 1128-1152; doi:10.3390/brainsci3031128
Received: 22 April 2013; in revised form: 6 July 2013 / Accepted: 11 July 2013 / Published: 30 July 2013| PDF Full-text (8968 KB) | HTML Full-text | XML Full-text
Article: Effects of Ethanol Exposure during Distinct Periods of Brain Development on Hippocampal Synaptic Plasticity
Brain Sci. 2013, 3(3), 1076-1094; doi:10.3390/brainsci3031076
Received: 15 May 2013; in revised form: 15 June 2013 / Accepted: 29 June 2013 / Published: 19 July 2013| PDF Full-text (349 KB) | HTML Full-text | XML Full-text
Review: Fetal Alcohol Spectrum Disorder (FASD) Associated Neural Defects: Complex Mechanisms and Potential Therapeutic Targets
Brain Sci. 2013, 3(2), 964-991; doi:10.3390/brainsci3020964
Received: 1 April 2013; in revised form: 3 June 2013 / Accepted: 4 June 2013 / Published: 19 June 2013| Cited by 2 | PDF Full-text (2180 KB) | HTML Full-text | XML Full-text
Brain Sci. 2013, 3(2), 941-963; doi:10.3390/brainsci3020941
Received: 11 April 2013; in revised form: 8 May 2013 / Accepted: 4 June 2013 / Published: 14 June 2013| PDF Full-text (453 KB) | HTML Full-text | XML Full-text
Article: Effects of Lifelong Ethanol Consumption on Brain Monoamine Transmitters in Alcohol-Preferring Alko Alcohol (AA) Rats
Brain Sci. 2013, 3(2), 790-799; doi:10.3390/brainsci3020790
Received: 1 March 2013; in revised form: 2 May 2013 / Accepted: 7 May 2013 / Published: 15 May 2013| PDF Full-text (217 KB) | HTML Full-text | XML Full-text
Article: Differential Effects of Chronic and Chronic-Intermittent Ethanol Treatment and Its Withdrawal on the Expression of miRNAs
Brain Sci. 2013, 3(2), 744-756; doi:10.3390/brainsci3020744
Received: 27 February 2013; in revised form: 11 April 2013 / Accepted: 25 April 2013 / Published: 3 May 2013| Cited by 1 | PDF Full-text (372 KB) | HTML Full-text | XML Full-text
Brain Sci. 2013, 3(2), 704-727; doi:10.3390/brainsci3020704
Received: 27 February 2013; in revised form: 10 April 2013 / Accepted: 23 April 2013 / Published: 29 April 2013| Cited by 2 | PDF Full-text (554 KB) | HTML Full-text | XML Full-text
Brain Sci. 2013, 3(2), 670-703; doi:10.3390/brainsci3020670
Received: 21 February 2013; in revised form: 30 March 2013 / Accepted: 12 April 2013 / Published: 26 April 2013| PDF Full-text (382 KB) | HTML Full-text | XML Full-text
Brain Sci. 2013, 3(2), 615-626; doi:10.3390/brainsci3020615
Received: 14 March 2013; in revised form: 12 April 2013 / Accepted: 16 April 2013 / Published: 23 April 2013| Cited by 1 | PDF Full-text (373 KB) | HTML Full-text | XML Full-text
Brain Sci. 2013, 3(1), 396-414; doi:10.3390/brainsci3010396
Received: 24 December 2012; in revised form: 5 February 2013 / Accepted: 12 March 2013 / Published: 22 March 2013| Cited by 1 | PDF Full-text (591 KB) | HTML Full-text | XML Full-text
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:firstname.lastname@example.org
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.
Last update: 5 December 2012