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      Effects of Age and Acute Ethanol on Glutamatergic Neurotransmission in the Medial Prefrontal Cortex of Freely Moving Rats Using Enzyme-Based Microelectrode Amperometry

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          Abstract

          Ethanol abuse during adolescence may significantly alter development of the prefrontal cortex which continues to undergo structural remodeling into adulthood. Glutamatergic neurotransmission plays an important role during these brain maturation processes and is modulated by ethanol. In this study, we investigated glutamate dynamics in the medial prefrontal cortex of freely moving rats, using enzyme-based microelectrode amperometry. We analyzed the effects of an intraperitoneal ethanol injection (1 g/kg) on cortical glutamate levels in adolescent and adult rats. Notably, basal glutamate levels decreased with age and these levels were found to be significantly different between postnatal day (PND) 28-38 vs PND 44-55 (p<0.05) and PND 28-38 vs adult animals (p<0.001). We also observed spontaneous glutamate release (transients) throughout the recordings. The frequency of transients (per hour) was significantly higher in adolescent rats (PND 28-38 and PND 44-55) compared to those of adults. In adolescent rats, post-ethanol injection, the frequency of glutamate transients decreased within the first hour (p<0.05), it recovered slowly and in the third hour there was a significant rebound increase of the frequency (p<0.05). Our data demonstrate age-dependent differences in extracellular glutamate levels in the medial prefrontal cortex and suggest that acute ethanol injections have both inhibitory and excitatory effects in adolescent rats. These effects of ethanol on the prefrontal cortex may disturb its maturation and possibly limiting individuals´ control over addictive behaviors.

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          Most cited references 25

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          The adolescent brain and age-related behavioral manifestations.

          To successfully negotiate the developmental transition between youth and adulthood, adolescents must maneuver this often stressful period while acquiring skills necessary for independence. Certain behavioral features, including age-related increases in social behavior and risk-taking/novelty-seeking, are common among adolescents of diverse mammalian species and may aid in this process. Reduced positive incentive values from stimuli may lead adolescents to pursue new appetitive reinforcers through drug use and other risk-taking behaviors, with their relative insensitivity to drugs supporting comparatively greater per occasion use. Pubertal increases in gonadal hormones are a hallmark of adolescence, although there is little evidence for a simple association of these hormones with behavioral change during adolescence. Prominent developmental transformations are seen in prefrontal cortex and limbic brain regions of adolescents across a variety of species, alterations that include an apparent shift in the balance between mesocortical and mesolimbic dopamine systems. Developmental changes in these stressor-sensitive regions, which are critical for attributing incentive salience to drugs and other stimuli, likely contribute to the unique characteristics of adolescence.
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            Glutamate uptake.

             Niels Danbolt (2001)
            Brain tissue has a remarkable ability to accumulate glutamate. This ability is due to glutamate transporter proteins present in the plasma membranes of both glial cells and neurons. The transporter proteins represent the only (significant) mechanism for removal of glutamate from the extracellular fluid and their importance for the long-term maintenance of low and non-toxic concentrations of glutamate is now well documented. In addition to this simple, but essential glutamate removal role, the glutamate transporters appear to have more sophisticated functions in the modulation of neurotransmission. They may modify the time course of synaptic events, the extent and pattern of activation and desensitization of receptors outside the synaptic cleft and at neighboring synapses (intersynaptic cross-talk). Further, the glutamate transporters provide glutamate for synthesis of e.g. GABA, glutathione and protein, and for energy production. They also play roles in peripheral organs and tissues (e.g. bone, heart, intestine, kidneys, pancreas and placenta). Glutamate uptake appears to be modulated on virtually all possible levels, i.e. DNA transcription, mRNA splicing and degradation, protein synthesis and targeting, and actual amino acid transport activity and associated ion channel activities. A variety of soluble compounds (e.g. glutamate, cytokines and growth factors) influence glutamate transporter expression and activities. Neither the normal functioning of glutamatergic synapses nor the pathogenesis of major neurological diseases (e.g. cerebral ischemia, hypoglycemia, amyotrophic lateral sclerosis, Alzheimer's disease, traumatic brain injury, epilepsy and schizophrenia) as well as non-neurological diseases (e.g. osteoporosis) can be properly understood unless more is learned about these transporter proteins. Like glutamate itself, glutamate transporters are somehow involved in almost all aspects of normal and abnormal brain activity.
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              Age at first alcohol use: a risk factor for the development of alcohol disorders.

              This study aimed to describe the natural course of DSM-III-R alcohol disorders as a function of age at first alcohol use and to investigate the influence of early use as a risk factor for progression to the development of alcohol disorders, exclusive of the effect of confounding influences. Data were obtained from a community sample (N=5,856) of lifetime drinkers participating in the 1990-1991 Mental Health Supplement of the Ontario Health Survey. Survival analyses revealed a rapid progression to alcohol-related harm among those who reported having their first drink at ages 11-14. After 10 years, 13.5% of the subjects who began to drink at ages 11 and 12 met the criteria for a diagnosis of alcohol abuse, and 15.9% had a diagnosis of dependence. Rates for subjects who began to drink at ages 13 and 14 were 13.7% and 9.0%, respectively. In contrast, rates for those who started drinking at ages 19 and older were 2.0% and 1.0%. Unexpectedly, a delay in progression to harm was observed for the youngest drinkers (ages 10 and under). Hazard regression analyses revealed a nonlinear effect of age at first alcohol use, marked by an elevated risk of developing disorders among subjects first using alcohol at ages 11-14. First use of alcohol at ages 11-14 greatly heightens the risk of progression to the development of alcohol disorders and therefore is a reasonable target for intervention strategies that seek to delay first use as a means of averting problems later in life.
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                Author and article information

                Contributors
                Role: Academic Editor
                Journal
                PLoS One
                PLoS ONE
                plos
                plosone
                PLoS ONE
                Public Library of Science (San Francisco, CA USA )
                1932-6203
                30 April 2015
                2015
                : 10
                : 4
                Affiliations
                [1 ]Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden
                [2 ]Department of Neuroscience and Physiology, Section of Neuropsychiatry, Gothenburg University, Gothenburg, Sweden
                [3 ]Department of Neuroscience, Karolinska Institutet, Stockholm, Sweden
                Radboud University, NETHERLANDS
                Author notes

                Competing Interests: The recording equipment used in this study was borrowed from H. Lundbeck. This does not alter the authors' adherence to PLOS ONE policies on sharing data and materials.

                Conceived and designed the experiments: DM BS ÅKG. Performed the experiments: DM ÅKG. Analyzed the data: DM. Contributed reagents/materials/analysis tools: DM ÅKG. Wrote the paper: DM BS ÅKG. Assisted in supporting methodology (sensor building and calibration, histology): NRH CBG.

                Article
                PONE-D-14-52398
                10.1371/journal.pone.0125567
                4416039
                25927237

                This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited

                Page count
                Figures: 7, Tables: 1, Pages: 15
                Product
                Funding
                Support was provided by: Alcohol Research Council of the Swedish Alcohol Retailing Monopoly (Centralförbundet för alkohol och narkotikaupplysning CAN-SRA) [ www.can.se]; H. Lundbeck A/S: lent us the glutamate recording unit. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
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                Research Article
                Custom metadata
                All relevant data are within the paper.

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