How does the brain's reward system play a role in the etiology of alcohol use disorder?5 answersThe development and maintenance of Alcohol Use Disorder (AUD) involve complex interactions within the brain's reward system. Research suggests that alterations in dopaminergic neurotransmission due to chronic alcohol consumption impact reward processing. Additionally, individuals with AUD exhibit decreased activation in reward-related brain regions during both anticipation and outcome stages of reward processing, indicating a changed sensitivity to monetary rewards. Furthermore, individuals with AUD show neural reward tolerance in the medial orbitofrontal cortex and ventral striatum, alongside enhanced neural responses in supplementary motor and inferior frontal gyrus regions, contributing to sustained alcohol motivation. These findings highlight the crucial role of the brain's reward system in driving compulsive alcohol-seeking behavior and the development of AUD.
What are the neurobiological mechanisms underlying alcohol dependence and addiction?4 answersThe neurobiological mechanisms underlying alcohol dependence and addiction involve alterations in neurotransmitter systems and brain circuitries that are involved in learning and memory. Dopamine and norepinephrine play a significant role in alcohol dependence, and recent research using animal models and optogenetics has helped identify the specific changes in neurotransmission within dopaminergic and noradrenergic neural circuits that govern ethanol-addictive behavior. Brain nicotinic acetylcholine receptors (nAChRs) and cholinergic nicotinic mechanisms also play important roles in alcohol use disorders, including alcohol dependence. Dual dependence, where individuals are dependent on more than one drug and/or alcohol, is an understudied area in addiction research, but studies have shown that the use of multiple drugs can produce neuroadaptations that are distinct from single drug use. Alcohol's addictive property is associated with its ability to increase the activity of dopaminergic neurons in the ventral tegmental area (VTA) in the brain, and the rostromedial tegmental nucleus (RMTg) is a major GABAergic afferent to these neurons, playing a key role in MOR-dependent regulation of DA neurons.
What are the neurobiological mechanisms especially in cortex underlying alcohol dependence and addiction?5 answersAlcohol dependence and addiction involve neurobiological mechanisms in the cortex. Chronic alcohol intake leads to neuroadaptive changes in neurotransmitter systems and brain circuitries involved in learning and memory. Neuroimaging studies have identified neural correlates of addiction-related behaviors, such as cue-induced craving and automatic action tendencies. Alterations in reward anticipation and processing, as well as learning mechanisms, are implicated in alcohol dependence. Additionally, genetic variants associated with alcohol use traits have been found to impact key pathways involved in drug metabolism and neuronal apoptosis. These risk genes are highly expressed in cortical glutamatergic neurons, suggesting their relevance in understanding the neurobiological mechanisms of alcohol use disorders. Dysregulation of Corticotropin Releasing Factor (CRF) systems, particularly in the extended amygdala, also contributes to the vulnerability for escalated alcohol drinking and dependence. Overall, these findings highlight the importance of cortical processes and genetic factors in the neurobiology of alcohol dependence and addiction.
How does alcohol influence brain?5 answersAlcohol affects the brain in various ways. It can cause damage during intoxication, withdrawal, and from the toxicity of alcohol and its metabolites, leading to altered brain structure and function. Prenatal alcohol exposure can also result in irreversible changes and fetal alcohol syndrome. Genetic studies have identified specific polymorphisms associated with altered risks of alcoholism. Metabolomic studies have shown that alcohol affects energy metabolism, oxidation, and the production of certain substances, which can impact brain energy production/utilization and cytotoxicity. Proteomic studies have identified altered expression of proteins involved in brain energy metabolism. Alcohol also affects neurotransmitter systems in the brain, leading to changes in brain function. Chronic alcohol consumption can cause neurodegenerative effects, compromising cognitive abilities. Overall, alcohol has a significant impact on brain structure, function, and development, contributing to the risks and consequences of alcoholism.
How does craving affect learning in the brain?4 answersCravings have been found to impair memory performance, specifically on cued-recall and recognition tasks. They also affect the accuracy of judgments of learning (JOLs) and feeling-of-knowing (FOK) judgments. Cravings impair resolution for FOK judgments but not JOLs, and reduce calibration for JOLs but not FOK judgments. Additionally, cravings reduce the ability to monitor the likely accuracy of answers during a cued-recall test. Momentary craving biases learning during addictive decision-making, leading to faster learning in addictive domains. Habitual food cravers direct limited cognitive resources to craving-related cues, at the cost of competing cognitive demands. Craving is embedded within a network of cognitive processes that influence drug use and relapse.
How does prenatal exposure to ethanol affect striatum?5 answersPrenatal exposure to ethanol has been shown to have significant effects on the striatum. Studies have found that prenatal ethanol exposure leads to persistent abnormal synaptic plasticity in the dorsolateral (DL) striatum, which is involved in hyperlocomotion in offspring. Additionally, prenatal exposure to ethanol has been found to alter dopaminergic regulation in the striatum, resulting in long-lasting effects on dopamine release and metabolism. Furthermore, prenatal ethanol exposure has been associated with hyperactive, inattentive, and impulsive behaviors in rodent offspring, which may be related to changes in dopamine transporter and MeCP2 expression in the prefrontal cortex and striatum. The striatum has been identified as a pivotal brain structure in the neuroalterations induced by prenatal alcohol exposure, and further research is needed to understand the morphological and functional changes at the circuit, neuronal, synaptic, and molecular levels.