Differential effects of ethanol ingestion on somatostatin content, somatostatin receptors and adenylyl cyclase activity in the frontoparietal cortex of virgin and parturient rats

Barrios, Vicente; Puebla‐Jiménez, L.; Boyano‐Adánez, María del Carmen; Sanz, Manuel; Soriano‐Guillén, Leandro; Arilla‐Ferreiro, Eduardo

doi:10.1016/j.lfs.2005.01.019

Cited by 5 publications

(2 citation statements)

References 41 publications

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“…Sstr4 is expressed in the nAc where increased DA release has been observed following somatostatin administration (presumably via glutamate stimulation) (Hathway et al, 1998). EtOH consumption has also been shown to affect somatostatin release and receptor numbers (Barrios et al, 2005;Rage et al, 1998), probably in a region-dependent manner. A decrease in Sstr4 mRNA, as observed here in EtOH consumers, and in general after 10 months, may be an adjustment to higher somatostatin levels induced by EtOH.…”

Section: Discussionmentioning

confidence: 99%

Modest Long‐Term Ethanol Consumption Affects Expression of Neurotransmitter Receptor Genes in the Rat Nucleus Accumbens

Jönsson

Ericson

Söderpalm

2013

Alcoholism Clin & Exp Res

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Background: Over 100 million people worldwide are affected by alcohol use disorders. These conditions usually take years to develop where an initial, voluntary consumption is gradually replaced by a compulsive intake of alcohol. The exact mechanisms behind this transition remain unknown. However, ethanol (EtOH) is known to interact with several neurotransmitters and receptors in the central nervous system, and chronic EtOH consumption causes alterations in these neurotransmitter systems, proposed to contribute to the development of dependence. This study aimed to repeat previous findings that animals after long-term voluntary EtOH consumption spontaneously increase their intake. That the initial encounter with EtOH causes an elevation of dopamine in the nucleus accumbens (nAc), inducing feelings of well-being and creating an incentive to continue the behavior, has been repeatedly reported in both animals and humans. The effects of chronic EtOH consumption on this region are not as well investigated.Methods: We examined both long-term EtOH consumption behavior and its consequences on expression of neurotransmitter-related genes in the nAc of the Wistar rat using quantitative polymerase chain reaction.Results: In general, the EtOH consumption of the animals in this study was modest with an average intake of 0.9 g/kg/d, and only 1 of the 24 rats consuming EtOH for 10 months drastically increased its intake in line with the results of Wolffgramm and Heyne (1995). Expression of the genes for dopamine receptor 2, l-opioid receptor, and somatostatin receptor 4 were down-regulated in animals after 2 and/ or 4, but not 10, months of EtOH consumption.Conclusions: Chronic consumption even of modest amounts of alcohol seems to affect regulation of expression of these genes, possibly leading to changes in neurotransmitter signaling. Studies are ongoing to investigate whether these alterations are specific for the nAc.

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Section: Discussionmentioning

confidence: 99%

Modest Long‐Term Ethanol Consumption Affects Expression of Neurotransmitter Receptor Genes in the Rat Nucleus Accumbens

Jönsson

Ericson

Söderpalm

2013

Alcoholism Clin & Exp Res

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“…pig might be more predictive in studying the possible role of somatostatin in the human AUD brain (Barrios et al, 2005).…”

Section: Prefrontal Cortex and Corticolimbic Systemmentioning

confidence: 99%

Alcohol Induced Brain and Liver Damage: Advantages of a Porcine Alcohol Use Disorder Model

2021

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Alcohol is one of the most commonly abused intoxicants with 1 in 6 adults at risk for alcohol use disorder (AUD) in the United States. As such, animal models have been extensively investigated with rodent AUD models being the most widely studied. However, inherent anatomical and physiological differences between rodents and humans pose a number of limitations in studying the complex nature of human AUD. For example, rodents differ from humans in that rodents metabolize alcohol rapidly and do not innately demonstrate voluntary alcohol consumption. Comparatively, pigs exhibit similar patterns observed in human AUD including voluntary alcohol consumption and intoxication behaviors, which are instrumental in establishing a more representative AUD model that could in turn delineate the risk factors involved in the development of this disorder. Pigs and humans also share anatomical similarities in the two major target organs of alcohol- the brain and liver. Pigs possess gyrencephalic brains with comparable cerebral white matter volumes to humans, thus enabling more representative evaluations of susceptibility and neural tissue damage in response to AUD. Furthermore, similarities in the liver result in a comparable rate of alcohol elimination as humans, thus enabling a more accurate extrapolation of dosage and intoxication level to humans. A porcine model of AUD possesses great translational potential that can significantly advance our current understanding of the complex development and continuance of AUD in humans.

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Chronic intermittent ethanol exposure selectively alters the expression of Gα subunit isoforms and RGS subtypes in rat prefrontal cortex

et al. 2017

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Chronic alcohol exposure induces pronounced changes in GPCR-mediated G-protein signaling. Recent microarray and RNA-seq analyses suggest associations between alcohol abuse and the expression of genes involved in G-protein signaling. The activity of G-proteins (e.g. Gαi/o and Gαq) is negatively modulated by regulator of G-protein signaling (RGS) proteins which are implicated in drugs of abuse including alcohol. The present study used 7 days of chronic intermittent ethanol exposure followed by 24 hour withdrawal (CIE) to investigate changes in mRNA and protein levels of G-protein subunit isoforms and RGS protein subtypes in rat prefrontal cortex, a region associated with cognitive deficit attributed to excessive alcohol drinking. We found that this ethanol paradigm induced differential expression of Gα subunits and RGS subtypes. For example, there were increased mRNA and protein levels of Gαi1/3 subunits and no changes in the expression of Gαs and Gαq subunits in ethanol-treated animals. Moreover, CIE increased the mRNA but not the protein levels of Gαo. Additionally, a modest increase in Gαi2 mRNA level by CIE was accompanied by a pronounced increase in its protein level. Interestingly, we found that CIE increased mRNA and protein levels of RGS2, RGS4, RGS7 and RGS19 but had no effect on the expression of RGS5, RGS6, RGS8, RGS12 or RGS17. Changes in the expression of Gα subunits and RGS subtypes could contribute to the functional alterations of certain GPCRs following chronic ethanol exposure. The present study suggests that RGS proteins may be potential new targets for intervention of alcohol abuse via modification of Gα-mediated GPCR function.

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Differential effects of ethanol ingestion on somatostatin content, somatostatin receptors and adenylyl cyclase activity in the frontoparietal cortex of virgin and parturient rats

Cited by 5 publications

References 41 publications

Modest Long‐Term Ethanol Consumption Affects Expression of Neurotransmitter Receptor Genes in the Rat Nucleus Accumbens

Modest Long‐Term Ethanol Consumption Affects Expression of Neurotransmitter Receptor Genes in the Rat Nucleus Accumbens

Alcohol Induced Brain and Liver Damage: Advantages of a Porcine Alcohol Use Disorder Model

Chronic intermittent ethanol exposure selectively alters the expression of Gα subunit isoforms and RGS subtypes in rat prefrontal cortex

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