neural reward system
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Although mechanisms of mate preference are thought to be relatively hard-wired, experience with appetitive and consummatory sexual reward has been shown to condition preferences for partner related cues and even objects that predict sexual reward. Here, we reviewed evidence from laboratory species and humans on sexually conditioned place, partner, and ejaculatory preferences in males and females, as well as the neurochemical, molecular, and epigenetic mechanisms putatively responsible. From a comprehensive review of the available data, we concluded that opioid transmission at μ opioid receptors forms the basis of sexual pleasure and reward, which then sensitizes dopamine, oxytocin, and vasopressin systems responsible for attention, arousal, and bonding, leading to cortical activation that creates awareness of attraction and desire. First experiences with sexual reward states follow a pattern of sexual imprinting, during which partner- and/or object-related cues become crystallized by conditioning into idiosyncratic "types" that are found sexually attractive and arousing. These mechanisms tie reward and reproduction together, blending proximate and ultimate causality in the maintenance of variability within a species.
- Klíčová slova
- conditioned partner preference, conditioned place preference, dopamine, first sexual experiences, mate preference, opioids, oxytocin, paraphilias, reward, vasopressin,
- MeSH
- ejakulace fyziologie MeSH
- lidé MeSH
- odměna MeSH
- opioidní analgetika * MeSH
- sexuální chování zvířat * fyziologie MeSH
- sexuální chování MeSH
- zvířata MeSH
- Check Tag
- lidé MeSH
- mužské pohlaví MeSH
- ženské pohlaví MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- přehledy MeSH
- Názvy látek
- opioidní analgetika * MeSH
Animals and humans share similar reactions to the effects of addictive substances, including those of their brain networks to drugs. Our review focuses on simple invertebrate models, particularly the honeybee (Apis mellifera), and on the effects of drugs on bee behaviour and brain functions. The drug effects in bees are very similar to those described in humans. Furthermore, the honeybee community is a superorganism in which many collective functions outperform the simple sum of individual functions. The distribution of reward functions in this superorganism is unique - although sublimated at the individual level, community reward functions are of higher quality. This phenomenon of collective reward may be extrapolated to other animal species living in close and strictly organised societies, i.e. humans. The relationship between sociality and reward, based on use of similar parts of the neural network (social decision-making network in mammals, mushroom body in bees), suggests a functional continuum of reward and sociality in animals.
- Klíčová slova
- Addiction, Brain reward system, Collective reward, Drosophila brain, Honeybee brain, Insect brain, Insect model of addiction,
- MeSH
- Drosophila * MeSH
- hmyz MeSH
- lidé MeSH
- mozek MeSH
- odměna * MeSH
- savci MeSH
- sociální chování MeSH
- včely MeSH
- zvířata MeSH
- Check Tag
- lidé MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- přehledy MeSH
A substantive literature has drawn a compelling case for the functional involvement of mesolimbic/prefrontal cortical neural reward systems in normative control of eating and in the etiology and persistence of severe eating disorders that affect diverse human populations. Presently, we provide a short review that develops an equally compelling case for the importance of dysregulated frontal cortical cognitive neural networks acting in concert with regional reward systems in the regulation of complex eating behaviors and in the presentation of complex pathophysiological symptoms associated with major eating disorders. Our goal is to highlight working models of major eating disorders that incorporate complementary approaches to elucidate functionally interactive neural circuits defined by their regulatory neurochemical phenotypes. Importantly, we also review evidence-based linkages between widely studied psychiatric and neurodegenerative syndromes (e.g., autism spectrum disorders and Parkinson's disease) and co-morbid eating disorders to elucidate basic mechanisms involving dopaminergic transmission and its regulation by endogenously expressed morphine in these same cortical regions.
- MeSH
- fenotyp MeSH
- kognice fyziologie MeSH
- lidé MeSH
- nervový přenos fyziologie MeSH
- odměna * MeSH
- poruchy příjmu potravy patofyziologie MeSH
- prefrontální mozková kůra patofyziologie MeSH
- Check Tag
- lidé MeSH
- Publikační typ
- časopisecké články MeSH
- přehledy MeSH
In classical neuroscience, Dale´s principle postulates that neuronal identity is conferred by the specific neurotransmitter that it releases. However, the brain might be more tractable to specific situations regardless of specific specialisation which may contradict this principle. Hence, this constrained approach of how we perceive and study the nervous system must be revisited and revised, specifically by studying the dopaminergic system. We presume a relatively flexible change in the dopaminergic system due to neuronal activity or environmental changes. While the parallel between the reward system of mammals and insects is generally well accepted, herein, we extend the idea that the insect nervous system might also possess incredible plasticity, similar to the mammalian system. In this review, we critically evaluate the available information about the reward system in vertebrates and invertebrates, emphasising the dopaminergic neuronal plasticity, a challenge to the classical Dale's principle. Thus, neurotransmitter switching significantly disrupts the static idea of neural network organisation and suggests greater possibilities for a dynamic response to the current life context of organisms.
- Klíčová slova
- Brain reward system, Co-transmission, Dopaminergic function, Insect brain, Neural plasticity, Neurotransmitter switching, Universality of neural function,
- MeSH
- dopamin MeSH
- dopaminergní neurony fyziologie MeSH
- Drosophila melanogaster fyziologie MeSH
- Drosophila * fyziologie MeSH
- houbová tělesa * fyziologie MeSH
- lidé MeSH
- neurotransmiterové látky fyziologie MeSH
- savci MeSH
- zvířata MeSH
- Check Tag
- lidé MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- přehledy MeSH
- Názvy látek
- dopamin MeSH
- neurotransmiterové látky MeSH
Autism spectrum disorder (ASD) is a neurodevelopmental disorder accompanied by narrow interests, difficulties in communication and social interaction, and repetitive behavior. In addition, ASD is frequently associated with eating and feeding problems. Although the symptoms of ASD are more likely to be observed in boys, the prevalence of eating disorders is more common in females. The ingestive behavior is regulated by the integrative system of the brain, which involves both homeostatic and hedonic neural circuits. Sex differences in the physiology of food intake depend on sex hormones regulating the expression of the ASD-associated Shank genes. Shank3 mutation leads to ASD-like traits and Shank3B -/- mice have been established as an animal model to study the neurobiology of ASD. Therefore, the long-lasting neuronal activity in the central neural circuit related to the homeostatic and hedonic regulation of food intake was evaluated in both sexes of Shank3B mice, followed by the evaluation of the food intake and preference. In the Shank3B +/+ genotype, well-preserved relationships in the tonic activity within the homeostatic neural network together with the relationships between ingestion and hedonic preference were observed in males but were reduced in females. These interrelations were partially or completely lost in the mice with the Shank3B -/- genotype. A decreased hedonic preference for the sweet taste but increased total food intake was found in the Shank3B -/- mice. In the Shank3B -/- group, there were altered sex differences related to the amount of tonic cell activity in the hedonic and homeostatic neural networks, together with altered sex differences in sweet and sweet-fat solution intake. Furthermore, the Shank3B -/- females exhibited an increased intake and preference for cheese compared to the Shank3B +/+ ones. The obtained data indicate altered functional crosstalk between the central homeostatic and hedonic neural circuits involved in the regulation of food intake in ASD.
- Klíčová slova
- Autism spectrum disorders, Food intake, Food selectivity, FosB/delta FosB, Reward system, Shank3B mice,
- MeSH
- homeostáza * fyziologie MeSH
- mikrofilamentové proteiny * genetika metabolismus MeSH
- modely nemocí na zvířatech MeSH
- myši inbrední C57BL MeSH
- myši knockoutované MeSH
- myši MeSH
- pohlavní dimorfismus * MeSH
- poruchy autistického spektra * genetika metabolismus MeSH
- preference v jídle fyziologie MeSH
- přijímání potravy * fyziologie genetika MeSH
- proteiny nervové tkáně * genetika MeSH
- protoonkogenní proteiny c-fos metabolismus biosyntéza MeSH
- zvířata MeSH
- Check Tag
- mužské pohlaví MeSH
- myši MeSH
- ženské pohlaví MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- Názvy látek
- mikrofilamentové proteiny * MeSH
- proteiny nervové tkáně * MeSH
- protoonkogenní proteiny c-fos MeSH
- Shank3 protein, mouse MeSH Prohlížeč
RATIONALE AND OBJECTIVES: In addition to dopamine, endocannabinoids are thought to participate in neural reward mechanisms of opioids. Number of recent studies suggests crucial involvement of ghrelin in some addictive drugs effects. Our previous results showed that ghrelin participates in morphine-induced changes in the mesolimbic dopaminergic system associated with reward processing. The goal of the present study was to test whether the growth hormone secretagogue receptor (GHS-R1A) antagonist JMV2959 was able to influence morphine-induced effects on anandamide (N-arachidonoylethanolamine, AEA) and 2-arachidonoylglycerol (2-AG) in the nucleus accumbens shell (NACSh). METHODS: We used in vivo microdialysis to determine changes in levels of AEA and 2-AG in the NACSh in rats following (i) an acute morphine dose (5, 10 mg/kg s.c.) with and without JMV2959 pretreatment (3, 6 mg/kg i.p.) or (ii) a morphine challenge dose (5 mg/kg s.c.) with and without JMV2959 (3, 6 mg/kg i.p.) pretreatment, administered during abstinence following repeated doses of morphine (5 days, 10-40 mg/kg). Co-administration of ghrelin (40 ug/kg i.p.) was used to verify the ghrelin mechanisms involvement. RESULTS: Pretreatment with JMV2959 significantly and dose-dependently reversed morphine-induced anandamide increases in the NACSh in both the acute and longer-term models, resulting in a significant AEA decrease. JMV2959 significantly intensified acute morphine-induced decreases in accumbens 2-AG levels and attenuated morphine challenge-induced 2-AG decreases. JMV2959 pretreatment significantly reduced concurrent morphine challenge-induced behavioral sensitization. JMV2959 pretreatment effects were abolished by co-administration of ghrelin. CONCLUSIONS: Our results indicate significant involvement of ghrelin signaling in morphine-induced endocannabinoid changes in the NACSh.
- Klíčová slova
- 2-Arachidonoylglycerol, Acute, Anandamide, Challenge during abstinence, Endocannabinoids, Ghrelin, Microdialysis, Morphine, Neural reward system, Nucleus accumbens shell, Stereotyped behavior,
- MeSH
- endokanabinoidy metabolismus fyziologie MeSH
- extracelulární prostor účinky léků metabolismus MeSH
- ghrelin fyziologie MeSH
- glyceridy metabolismus MeSH
- glycin analogy a deriváty farmakologie MeSH
- krysa rodu Rattus MeSH
- kyseliny arachidonové metabolismus MeSH
- morfin farmakologie MeSH
- narkotika farmakologie MeSH
- nucleus accumbens účinky léků metabolismus MeSH
- polynenasycené alkamidy metabolismus MeSH
- potkani Wistar MeSH
- receptory ghrelinu antagonisté a inhibitory MeSH
- receptory somatotropinu antagonisté a inhibitory MeSH
- stereotypní chování účinky léků MeSH
- triazoly farmakologie MeSH
- vztah mezi dávkou a účinkem léčiva MeSH
- zvířata MeSH
- Check Tag
- krysa rodu Rattus MeSH
- mužské pohlaví MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- Názvy látek
- anandamide MeSH Prohlížeč
- endokanabinoidy MeSH
- ghrelin MeSH
- glyceridy MeSH
- glyceryl 2-arachidonate MeSH Prohlížeč
- glycin MeSH
- kyseliny arachidonové MeSH
- morfin MeSH
- N-(1-(4-(4-methoxybenzyl)-5-phenethyl-4H-1,2,4-triazol-3-yl)-2-(1H-indol-3-yl)ethyl)-2-aminoacetamide MeSH Prohlížeč
- narkotika MeSH
- polynenasycené alkamidy MeSH
- receptory ghrelinu MeSH
- receptory somatotropinu MeSH
- triazoly MeSH
RATIONALE AND OBJECTIVES: Ghrelin, an orexigenic (appetite stimulating) peptide activates binding sites in the ventral tegmental area (a structure linked with the neural reward system) allowing it to participate in reward-seeking behavior. An increasing number of studies over the past few years have demonstrated ghrelin's role in alcohol, cocaine, and nicotine abuse. However, the role of ghrelin, in opioid effects, has rarely been examined. The aim of the present study was to ascertain whether a ghrelin antagonist (JMV2959) was able to inhibit markers of morphine-induced activation of the neural reward system, namely morphine-induced increase of dopamine in the nucleus accumbens and behavioral changes in rats. METHODS: We used in vivo microdialysis to determine changes of dopamine and its metabolites in the nucleus accumbens shell in rats following morphine (MO, 5, 10 mg/kg s.c.) administration with and without ghrelin antagonist pretreatment (JMV2959, 3, 6 mg/kg i.p., 20 min before MO). Induced behavioral changes were simultaneously monitored. RESULTS: JMV2959 significantly and dose dependently reduced MO-induced dopamine release in the nucleus accumbens shell and affected concentration of by-products associated with dopamine metabolism: 3-methoxytyramine (3-MT), 3,4-dihydroxyphenylacetic acid (DOPAC), and homovanillic acid (HVA). JMV2959 pretreatment also significantly reduced MO-induced behavioral stimulation, especially stereotyped behavior. CONCLUSIONS: Ghrelin secretagogue receptors (GHS-R1A) appear to be involved in the opioid-induced changes in the mesolimbic dopaminergic system associated with the reward processing.
- MeSH
- chování zvířat účinky léků MeSH
- dopamin analogy a deriváty metabolismus farmakologie MeSH
- ghrelin metabolismus MeSH
- glycin aplikace a dávkování analogy a deriváty farmakologie MeSH
- krysa rodu Rattus MeSH
- kyselina 3,4-dihydroxyfenyloctová metabolismus MeSH
- kyselina homovanilová farmakologie MeSH
- mikrodialýza MeSH
- morfin aplikace a dávkování farmakologie MeSH
- nucleus accumbens účinky léků metabolismus MeSH
- odměna MeSH
- opioidní analgetika aplikace a dávkování farmakologie MeSH
- potkani Wistar MeSH
- receptory ghrelinu antagonisté a inhibitory metabolismus MeSH
- stereotypní chování účinky léků MeSH
- triazoly aplikace a dávkování farmakologie MeSH
- vztah mezi dávkou a účinkem léčiva MeSH
- zvířata MeSH
- Check Tag
- krysa rodu Rattus MeSH
- mužské pohlaví MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- Názvy látek
- 3-methoxytyramine MeSH Prohlížeč
- dopamin MeSH
- ghrelin MeSH
- glycin MeSH
- kyselina 3,4-dihydroxyfenyloctová MeSH
- kyselina homovanilová MeSH
- morfin MeSH
- N-(1-(4-(4-methoxybenzyl)-5-phenethyl-4H-1,2,4-triazol-3-yl)-2-(1H-indol-3-yl)ethyl)-2-aminoacetamide MeSH Prohlížeč
- opioidní analgetika MeSH
- receptory ghrelinu MeSH
- triazoly MeSH
The opioid-induced rise of extracellular dopamine, endocannabinoid anandamide and γ-aminobutyric acid (GABA) concentrations triggered by opioids in the nucleus accumbens shell (NACSh) most likely participate in opioid reward. We have previously demonstrated that systemic administration of ghrelin antagonist (JMV2959) significantly decreased morphine-induced dopamine and anandamide (N-arachidonoylethanolamine, AEA) increase in the NACSh. Fentanyl is considered as a µ-receptor-selective agonist. The aim of this study was to test whether JMV2959, a growth hormone secretagogue receptor (GHS-R1A) antagonist, can influence the fentanyl-induced effects on anandamide, 2-arachidonoylglycerol (2-AG) and GABA in the NACSh and specify the involvement of GHS-R1A located in the ventral tegmental area (VTA) and nucleus accumbens (NAC). Using in vivo microdialysis in rats, we have found that pre-treatment with JMV2959 reversed dose dependently fentanyl-induced anandamide increases in the NACSh, resulting in a significant AEA decrease and intensified fentanyl-induced decreases in accumbens 2-AG levels, with both JMV2959 effects more expressed when administered into the NACSh in comparison to the VTA. JMV2959 pre-treatment significantly decreased the fentanyl-evoked accumbens GABA efflux and reduced concurrently monitored fentanyl-induced behavioural stimulation. Our current data encourage further investigation to assess if substances affecting GABA or endocannabinoid concentrations and action, such as GHS-R1A antagonists, can be used to prevent opioid-seeking behaviour.
- Klíčová slova
- 2-arachidonoylglycerol, GABA, anandamide, endocannabinoids, fentanyl, ghrelin, microdialysis, neural reward system, nucleus accumbens shell, ventral tegmental area,
- MeSH
- chování zvířat MeSH
- endokanabinoidy metabolismus MeSH
- extracelulární prostor metabolismus MeSH
- fentanyl farmakologie MeSH
- GABA metabolismus MeSH
- ghrelin farmakologie MeSH
- glycin analogy a deriváty farmakologie MeSH
- krysa rodu Rattus MeSH
- nucleus accumbens účinky léků metabolismus MeSH
- receptory ghrelinu metabolismus MeSH
- tegmentum mesencephali - area ventralis účinky léků metabolismus MeSH
- triazoly farmakologie MeSH
- zvířata MeSH
- Check Tag
- krysa rodu Rattus MeSH
- mužské pohlaví MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- Názvy látek
- endokanabinoidy MeSH
- fentanyl MeSH
- GABA MeSH
- ghrelin MeSH
- glycin MeSH
- N-(1-(4-(4-methoxybenzyl)-5-phenethyl-4H-1,2,4-triazol-3-yl)-2-(1H-indol-3-yl)ethyl)-2-aminoacetamide MeSH Prohlížeč
- receptory ghrelinu MeSH
- triazoly MeSH
Morphine plays a critical regulatory role in both simple and complex plant species. Dopamine is a critical chemical intermediate in the morphine biosynthetic pathway and may have served as a primordial agonist in developing catecholamine signaling pathways. While dopamine remains the preeminent catecholamine in invertebrate neural systems, epinephrine is the major product of catecholamine synthetic pathways in vertebrate species. Given that the enzymatic steps leading to the generation of morphine are similar to those constraining the evolutionary adaptation of the biosynthesis of catecholamines, we hypothesize that the emergence of these more advanced signaling pathways was based on conservation and selective "retrofitting" of pre-existing enzyme activities. This is consistent with observations that support the recruitment of enzymatically synthesized tetrahydrobiopterin (BH4), which is a cofactor for tyrosine hydroxylase, the enzyme responsible for dopamine production. BH4 is also an electron donor involved in the production of nitric oxide (NO). The links that coordinate BH4-mediated NO and catecholaminergic-mediated processes provide these systems with the capacity to regulate numerous downstream signaling pathways. We hypothesize that the evolution of catecholamine signaling pathways in animal species depends on the acquisition of a mobile lifestyle and motivationally driven feeding, sexual, and self-protective responses.
- Klíčová slova
- behavior, catecholamines, cognition, dopamine, evolution, mobility, morphine, motivation, reward, stress, μ3 receptor,
- Publikační typ
- časopisecké články MeSH
- přehledy MeSH
Behavioral sensitization is defined as augmented psychomotor activity, which can be observed after drug re-administration following withdrawal of repeated drug exposure. It has been shown that abuse of one drug can lead to increased sensitivity to certain other drugs. This effect of developed general drug sensitivity is called cross-sensitization and has been reported between drugs with similar as well as different mechanisms of action. There is growing evidence that exposure to drugs in utero not only causes birth defects and delays in infant development, but also impairs the neural reward pathways, in the brains of developing offspring, in such a way that it can increase the tendency for drug addiction later in life. This review summarizes the results of preclinical studies that focused on testing behavioral cross-sensitization, after prenatal Methamphetamine exposure, to drugs administered in adulthood, with both similar and different mechanisms of action. Traditionally, behavioral sensitization has been examined using the Open field or the Laboras Test to record locomotor activity, and the Conditioned Place Preference and Self-administration test to examine drug-seeking behavior. However, it seems that prenatal drug exposure can sensitize animals not only to the locomotor-stimulating and conditioning effects of drugs, but may also be responsible for modified responses to various drug effects.
- MeSH
- lidé MeSH
- lokomoce účinky léků fyziologie MeSH
- methamfetamin aplikace a dávkování škodlivé účinky MeSH
- modely u zvířat * MeSH
- poruchy spojené s užíváním psychoaktivních látek etiologie metabolismus psychologie MeSH
- stimulanty centrálního nervového systému aplikace a dávkování MeSH
- těhotenství MeSH
- zpožděný efekt prenatální expozice chemicky indukované metabolismus psychologie MeSH
- zvířata MeSH
- Check Tag
- lidé MeSH
- těhotenství MeSH
- ženské pohlaví MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- přehledy MeSH
- Názvy látek
- methamfetamin MeSH
- stimulanty centrálního nervového systému MeSH