Prenatal ethanol exposure and enkephalinergic neurotransmission.

Endogenous opioids (enkephalins, endorphins and dynorphins) are small peptides that play a main role in pain perception and analgesia, as well as in alcohol (ethanol) reinforcement and reward. Alcohol reinforcement involves the ethanol-induced activation of the endogenous opioid system, a process that may augment the hedonic value and the reinforcing properties of the drug, which in turn increases substance consumption. Changes in opioidergic transmission may contribute to alcohol intoxication and to the neuroadaptive responses produced by the long-lasting exposure to ethanol.

Impact of a novel environment on alcohol-induced locomotor activity in Wistar rats.

Clinical studies have shown a positive correlation between novelty-seeking behavior and the susceptibility to consume drugs of abuse. Although several animal studies have demonstrated this correlation with psychostimulants or morphine, studies with alcohol have shown conflicting results. The aim of this work was to investigate alcohol-induced motor effects in Wistar rats with different responses to novelty.

Comparative proteomic analysis of growth hormone secretagogue A233 treatment of murine macrophage cells J774A.2 indicates it has a role in antiviral innate response.

Background: Growth hormone secretagogues (GHS), among other factors, regulate the release of GH. The biological activity of the secretagogue peptide A233 as a promoter of growth and innate immunity in teleost fish has previously been demonstrated, but its role in the immune system of mammals is not well understood.

Methods: The effect of the peptide was investigated in J774A.

Acute ethanol administration differentially alters enkephalinase and aminopeptidase N activity and mRNA levels in regions of the nigrostriatal pathway.

Opioid peptides play a key role in ethanol reinforcement and may also represent important determinants in brain sensitivity to ethanol through modulation of nigrostriatal dopaminergic activity. Regulation of opioid levels by peptidase-degrading enzymes could be relevant in ethanol's actions. The aim of this work was to study the acute ethanol (2.

Activity and expression of enkephalinase and aminopeptidase N in regions of the mesocorticolimbic system are selectively modified by acute ethanol administration.

Opioid peptides play a key role in ethanol reinforcement and alcohol drinking behavior. However, regulation of opioid levels by peptidase-degrading activities in ethanol's actions in brain is still unclear. The aim of this work was to study the acute effects of ethanol (2.

Behavioral and neurochemical studies in distinct animal models of ethanol's motivational effects.

In the last decades, the goal of creating a unique and complete model of alcohol use and alcoholism has been replaced by a myriad of different animal models, each addressing a specific feature of problematic alcohol consumption. This mini-review highlights selected findings in the field of alcohol abuse and dependence, as found through the use of animal models. There are models (e.

Role of mu and delta opioid receptors in alcohol drinking behaviour.

The dopaminergic mesolimbic system plays a key role in the mechanisms of reinforcement elicited by alcohol (ethanol) and other drugs of abuse. Numerous lines of evidence indicate that ethanol reinforcement mechanisms involve, at least partially, the ethanol-induced activation of the endogenous opioid system. Ethanol may alter opioidergic transmission at different levels, including the biosynthesis, release, and degradation of opioid peptides, as well as binding of endogenous ligands to opioid receptors.

Developing partnerships to advance youth violence prevention in Puerto Rico: the role of an academic center of excellence.

This article presents and discusses strategies implemented by the University of Puerto Rico Center for Hispanic Youth Violence Prevention (CHYVP) to facilitate community mobilization to reduce youth violence in a high-risk Latino community. Participatory communication strategies were used to enhance mobilization and to develop community partnerships. Short-term outcomes included overcoming resistance and distrust, active community dialogue and consensus building, the development of a school-community task force, the identification of priorities, the negotiation of conflicts, the implementation of a common action plan, and the commitment of government officials to adopt community recommendations.

Ethanol-induced changes in proenkephalin mRNA expression in the rat nigrostriatal pathway.

Endogenous opioid systems have been suggested to play a key role in ethanol reinforcement mechanisms and alcohol-drinking behavior. Ethanol induces differential alterations in opioid peptide expression in brain areas of the reward circuits, which may be linked to the reinforcing effects of ethanol. In addition, ethanol-induced alterations in opioidergic nigrostriatal transmission could be involved in brain sensitivity to ethanol and play a role in addictive processes.

Presence of pro-opiomelanocortin mRNA in the rat medial prefrontal cortex, nucleus accumbens and ventral tegmental area: studies by RT-PCR and in situ hybridization techniques.

Pro-opiomelanocortin (POMC) is a large proteic precursor which originates several biologically actives neuropeptides, such as beta-lipotropin (beta-LPH), beta-endorphin (beta-END), adenocorticotropic hormone (ACTH) and alpha-melanocyte-stimulating hormone (alpha-MSH). The arcuate nucleus of the hypothalamus is the main POMC producing cell group in brain and innervates several areas of the limbic system and brainstem. POMC-derived neuropeptides have been related to several motivated and rewarding behaviours, including sexual facilitation, feeding, and drug addiction.

Changes in Proenkephalin mRNA expression in forebrain areas after amphetamine-induced behavioural sensitization.

Acute and repeated psychostimulant administration induces a long-lasting enhanced behavioural response to a subsequent drug challenge, known as behavioural sensitization. This phenomenon involves persistent neurophysiological adaptations, which may lead to drug addiction. Brain dopaminergic pathways have been implicated as the main neurobiological substrates of behavioural sensitization, although other neurotransmitters and neuromodulators may also participate.

Ethanol exposure differentially alters pro-enkephalin mRNA expression in regions of the mesocorticolimbic system.

Rationale: Opioid peptides have been suggested to play a major role in ethanol reinforcement mechanisms and alcohol drinking behaviour. However, in non-selected strains of rodents, it is not known whether opioid biosynthesis is a critical event in these processes.

Objective: The aim of this work was to study the effects of a high dose of ethanol (2.

[3H]DPDPE binding to delta opioid receptors in the rat mesocorticolimbic and nigrostriatal pathways is transiently increased by acute ethanol administration.

Dopaminergic transmission in the mesolimbic and nigrostriatal pathways plays a key role in the reinforcement mechanisms and brain sensitivity to ethanol, respectively. Ethanol reinforcement and high alcohol drinking behaviour have been postulated to be partially mediated by a neurobiological mechanism involving the ethanol-induced activation of the endogenous opioid system. Activation of opioid neural pathways by ethanol may include alterations in the processing, release and/or the receptor binding of opioid peptides.

Acute ethanol administration transiently decreases [3H]-DAMGO binding to mu opioid receptors in the rat substantia nigra pars reticulata but not in the caudate-putamen.

Ethanol's actions in brain have been suggested to be partially mediated by a mechanism involving the ethanol-induced activation of the endogenous opioid system. Opioid systems, which are closely linked with dopamine transmission, are thought to be affected by ethanol through alterations in the processing, release, and/or receptor binding of opioid peptides. We studied the effects of a single acute dose of ethanol on rat nigrostriatal mu opioid receptors by quantitative receptor autoradiography, using [3H] [D-Ala(2),MePhe(4),Gly-ol(5)]-enkephalin ([3H]-DAMGO) as radioligand.