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Distribution and Characteristics of Brain Dopamine
Published in Nira Ben-Jonathan, Dopamine, 2020
The mesolimbic dopaminergic pathway transmits DA from the VTA to the ventral striatum [10]. In histological preparations, the striatum is seen as stripes of gray and white matter and hence its name. In primates, the striatum is divided into a ventral sector, which consists of the nucleus accumbens and the olfactory tubercle, and a dorsal sector, which comprises the caudate nucleus and putamen. The major cells that populate the striatum are medium spiny GABAergic neurons that express DA receptors and are intermixed with inhibitory cholinergic interneurons. The ventral striatum, especially the nucleus accumbens, is associated with reward-related cognition, pleasure, and positive reinforcement. Dysfunctions of the mesolimbic dopaminergic system result in disorders similar to those listed above for the mesocortical system.
The Hungry Brain
Published in Emily Crews Splane, Neil E. Rowland, Anaya Mitra, Psychology of Eating, 2019
Emily Crews Splane, Neil E. Rowland, Anaya Mitra
To demonstrate this, Castro and Berridge (2014) used previous observations that neurons in the nucleus accumbens have receptors for opioid peptide transmitters that are released both from local interneurons (consequent to dopamine stimulation) or input from other brain regions. Stimulation of opioid receptors in the nucleus accumbens by micro-injections of opioid agonist (mimicking) drugs is known to increase food intake. In their experiments, rats were surgically implanted with bilateral cannulas (small injection tubes) that, in different rats, were aimed at different parts of the nucleus accumbens. After full recovery from surgery, hedonic liking was assessed by slowly infusing a palatable sucrose solution into the rats’ mouths and recording appetitive (swallowing) responses. On separate days, these responses were measured after injection of vehicle (or placebo), or after a single dose of agonists of three subtypes of opioid receptor (mu, kappa, delta). The principal result is that injections into an approximately 1 mm3 region (about 10% of the total size of the nucleus) of the medio-frontal part of the nucleus accumbens produced a large increase in liking responses when treated with any of the three agents, relative to vehicle. This region was termed a hedonic hotspot. Identical injections into more posterior parts of the nucleus accumbens decreased the liking responses, and this region was termed a hedonic coldspot.
The Mesocorticolimbic Circuit in Drug Dependence and Reward — a Role for the Extended Amygdala?
Published in Peter W. Kalivas, Charles D. Barnes, Limbic Motor Circuits and Neuropsychiatry, 2019
George F. Koob, Patricia Robledo, Athina Markou, S. Barak Caine
The other important issue involves understanding the circuitry with which the mesocorticolimbic DA system interacts to produce such hypothesized functional attributes. As discussed above, the region of the nucleus accumbens is a heterogenous structure, subregions of which receive important limbic system afferents (e.g., amygdala, hippocampal formation, frontal cortex, lateral septum, lateral hypothalamus) that may be critically involved in reward. Studies of the reward function of these subregions (both drug and non-drug), and how they are related to the ventral striatopallidal/extended amygdala distinction may be the key to understanding the relationship of rewarding stimuli to the subjective feelings of pleasure or emotion in humans.
Cocaine induced heart failure: report and literature review
Published in Journal of Community Hospital Internal Medicine Perspectives, 2021
Sherif Elkattawy, Ramez Alyacoub, Abraham Al-Nassarei, Islam Younes, Sarah Ayad, Mirette Habib
Cocaine is a highly addictive stimulant that alters human behavior through the limbic system’s activity, a structure in the brain involved in motivation, emotion, learning, and memory. The nucleus accumbens (NA) is a specific area within the limbic system that receives connections through dopaminergic neurons. When stimulated, the accumulation of dopamine at the NA causes euphoria, conditioning the brain to establish a reward pathway in association with a stimulant. Cocaine inhibits dopamine transport protein (DAT) embedded within presynaptic neurons of the NA, forming a reward pathway; thus, explaining the drug’s highly addictive nature and potential for abuse [1, 5]. Although the overall incidence of recreational cocaine use has been declining over the years within the United States, the global prevalence of cocaine is still approximately 0.4%. Many studies have provided significant evidence explaining the relationship between cocaine use and the onset of cocaine-induced morbidity (including cardiovascular, neurovascular, psychiatric, and infectious illnesses) and mortality over time.[2,3,4,6,7]
Chronic stress in adolescence differentially affects cocaine vulnerability in adulthood in a selectively bred rat model of individual differences: role of accumbal dopamine signaling
Published in Stress, 2021
Cigdem Aydin, Karla Frohmader, Michael Emery, Peter Blandino Jr, Huda Akil
The role of dopaminergic signaling in the nucleus accumbens (Nacc) in addiction-related behaviors has been widely demonstrated (see (Chen et al., 2017) for a recent review). Notably, the Nacc is also highly susceptible to stress and is altered by stressful stimuli (Cabib and Puglisi-Allegra, 1996; Krishnan et al., 2007) due to the ability of cortisol and corticosterone to modulate dopamine release (Oswald et al., 2005; Wand et al., 2007), making it an important structure for the interaction of stress and drugs of abuse. In the Nacc, the two main dopamine receptor types, D1R and D2R, have been widely implicated in drug sensitization (Cabib et al., 1991; Kai et al., 2015) as well as in stress-related disorders (Francis and Lobo, 2017). However, their contribution to the interaction of these behaviors remain unclear. Previous studies from our laboratory have shown that the levels of D1R and D2R differ basally in the Nacc of the bHR\bLR rats (Clinton et al., 2012; Flagel et al., 2010). Specifically, lower D2R (Clinton et al., 2012; Flagel et al., 2010) but higher D1R (Clinton et al., 2012) mRNA levels are observed in the Nacc in bHRs compared to bLRs, indicating innate differences in the accumbal dopamine signaling. These differences may be associated with differences in addiction vulnerability, and possibly the differential responsivity to chronic stress observed in these animals. However, whether these differences in accumbal dopamine signaling influence the interaction of chronic stress and drugs of abuse has not been investigated.
Bridging inhaled aerosol dosimetry to physiologically based pharmacokinetic modeling for toxicological assessment: nicotine delivery systems and beyond
Published in Critical Reviews in Toxicology, 2019
A. R. Kolli, A. K. Kuczaj, F. Martin, A. W. Hayes, M. C. Peitsch, J. Hoeng
Nicotine, one of the most abundant tobacco alkaloids, has been reported to exert several pharmacological effects on the brain and GI system (Benowitz et al. 2009). Nicotine permeates the blood-brain barrier, and its effects are mediated through binding to nicotinic acetylcholine receptor (nAChR) subtypes, particularly those located on dopaminergic neurons in the ventral tegmental area. Upon stimulation, dopamine is released in the shell of the nucleus accumbens, which is an important mechanism in drug-induced reward-motivated behavior. Changes in dopamine levels are also supported by nicotine-induced release of other neurotransmitters, such as glutamate (that facilitates the release of dopamine) and γ-aminobutyric acid (that inhibits dopamine release), in these brain areas. The absorption, distribution, metabolism, and excretion (ADME) properties of nicotine have been studied in humans and pre-clinical species (Benowitz et al. 2009). Nicotine has a very low plasma protein binding and is rapidly metabolized by the liver, primarily by the cytochrome P450 (CYP) 2A6 (and to a lesser extent by CYP2B6 and CYP2E1), to cotinine, its main metabolite (80% of nicotine conversion) (Benowitz et al. 2009).