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Biological Basis of Behavior
Published in Mohamed Ahmed Abd El-Hay, Understanding Psychology for Medicine and Nursing, 2019
When the brain’s reward system is activated, dopamine is released, which creates a pleasing, enjoyable sensation. Thus, we are likely to repeat these behaviors that are necessary for survival. This is because dopamine rewards us with a pleasurable feeling. The mesolimbic dopamine pathway is thought to play a primary role in the reward system. It connects the ventral tegmental area (VTA), one of the principal dopamine-producing areas in the brain, with the nucleus accumbens, an area found in the ventral striatum that is strongly associated with motivation and reward. The mesocortical pathway travels from the VTA to the cerebral cortex and is also considered part of the reward system.
Pharmaceutical interventions
Published in Jane Hanley, Mark Williams, Fathers and Perinatal Mental Health, 2019
These drugs are used for the manic episodes of bipolar disorder and severe depression. There are complex mechanisms of the role of dopamine in the development of psychosis, and it is thought the neurotransmitter dopamine plays a key role. It is argued that the unusual experiences and behaviours which are associated with psychosis are associated with the function of dopamine in the brain. There are four major pathways: the first is the mesolimbic pathway which mediates the symptoms of paranoia and hallucinations. The blockage of dopamine receptors here reduces the symptoms of delusions and hallucinations. The second, the mesocortical pathway, mediates the symptoms of withdrawal and loss of motivation. The blockage of the dopamine receptors can contribute to the lack of motivation and to an exacerbation of fatigue. The third, the nigrostriatal pathway controls movement whereby a blockage of the dopamine receptor may cause excess movements. The last pathway is the tuberoinfundibular pathway which controls the secretion of prolactin. The blockage of the dopamine receptor in this pathway can result in high levels of prolactin in the blood, which can lead to sexual dysfunction (Kapur & Remington 2001).
Neurodysfunction in Addiction and Overeating as Assessed by Brain Imaging
Published in Joan Ifland, Marianne T. Marcus, Harry G. Preuss, Processed Food Addiction: Foundations, Assessment, and Recovery, 2017
Randall J. Ellis, Michael Michaelides, Gene-Jack Wang
The mesocortical pathway, mainly implicated in modulating decision-making and executive function, carries projections from the VTA to the frontal cortex. All drugs of abuse as well as food increase dopamine production in the NAc (Volkow et al., 2013). Mesolimbic pathway dopamine neurons become desensitized after the repeated administration of initially novel rewards, highlighting a mechanism for reward tolerance accompanied by self-administering larger amounts of the reward observed in both food and drug addiction (Volkow et al., 2013).
Potassium channel modulators and schizophrenia: an overview of investigational drugs
Published in Expert Opinion on Investigational Drugs, 2023
Meghan Musselman, Eric Huynh, Rachana Kelshikar, Eric Lee, Mohammed Malik, Justin Faden
In-depth reviews about prominent hypotheses of schizophrenia symptom development have been explored elsewhere and are beyond the scope of this review [13–15]. The most pervasive theory regarding the development of schizophrenia is the dopamine hypothesis, which holds that dopamine hyperactivity in the mesolimbic pathway from the ventral tegmental area to the ventral striatum contributes to positive symptoms of schizophrenia, whereas dopamine deficit in the mesocortical pathway contributes to negative symptoms [13,14,16]. Most available antipsychotic medications are dopamine antagonists thought to exert efficacy in treating the positive symptoms of schizophrenia by blocking D2 receptors in the mesolimbic pathway. The extrapyramidal side effects associated with these medications result from the blockade of D2 receptors in the nigrostriatal pathway from the substantia nigra to the dorsal striatum [9]. Evidence supporting the dopamine hypothesis includes the observation that stimulants, such as methamphetamine and cocaine, increase the release of dopamine and induce positive symptoms like that of schizophrenia [17]. Additionally, [18F]-FDOPA PET imaging studies have consistently demonstrated an increase in dopamine synthesis capacity in the associative striatum of patients with schizophrenia [18–20]. Moreover, greater striatal dopamine synthesis capacity corresponds with greater symptom severity and yet also predicts a greater response to antipsychotic dopamine D2 receptor antagonists [18,21].
Lurasidone in adolescents and adults with schizophrenia: from clinical trials to real-world clinical practice
Published in Expert Opinion on Pharmacotherapy, 2022
Andrea Fiorillo, Alessandro Cuomo, Gaia Sampogna, Umberto Albert, Paola Calò, Giancarlo Cerveri, Sergio De Filippis, Gabriele Masi, Maurizio Pompili, Gianluca Serafini, Antonio Vita, Alessandro Zuddas, Andrea Fagiolini
Full antagonism at the D2 receptors in the mesolimbic pathway is believed to be correlated to the beneficial effects on positive symptoms of schizophrenia, such as hallucinations and delusions. Moreover, lurasidone is an antagonist for serotonin 5-HT2A receptor. By this activity, it disinhibits the dopamine neuron, and therefore increases the release of dopamine, which competes with the antipsychotic in the D2 antagonistic action at D2 receptors. This mechanism of action reduces the antagonistic binding in several dopaminergic pathways and it is associated with the better tolerability profile of lurasidone [18–22]. In particular, by targeting the nigrostriatal pathway, it reduces extrapyramidal symptoms. In the tuberoinfundibular pathway, this reduces hyperprolactinemia. In the mesocortical pathway and in the prefrontal cortex, it improves the negative, affective, and cognitive symptoms. Also, the antagonism at 5-HT2A receptors mitigates the serotonergic excitation of the cortical pyramidal cells. This results in a reduction of glutamate release, which in turn may reduce the dopaminergic activity in the mesolimbic pathway and thereby the positive symptoms of schizophrenia [18–22]. LUR’s antagonism at the 5-HT7 receptor may contribute to the favorable effects in learning and memory and, more in general, improve the cognitive deficits and the depressive symptoms [23,24]. The partial agonism at the 5-HT1A may contribute, as well, to the antidepressant properties of LUR [16].
Quetiapine attenuates the acquisition of morphine-induced conditioned place preference and reduces ERK phosphorylation in the hippocampus and cerebral cortex
Published in The American Journal of Drug and Alcohol Abuse, 2022
Ali Khezri, Mahdieh Sadat Mohsenzadeh, Elnaz Mirzayan, Nima Bagherpasand, Mohammad Fathi, Khalil Abnous, Mohsen Imenshahidi, Soghra Mehri, Hossein Hosseinzadeh
In the present study, we observed a significant reduction in the total locomotion of morphine-treated rats, which was evaluated in the open field. This result is in accordance with the study of Patti et al., 2005, which demonstrated that morphine decreased locomotion at a dose of 10 mg/kg (50). It has been suggested that dopaminergic activity in the mesocortical pathway inhibits locomotion (51). Hence, the reduction in locomotor activity induced by morphine may be attributed to the release of mesocortical dopamine. In the current research, when quetiapine was administered with morphine, locomotion scores were significantly improved. Regarding the antagonist activity of quetiapine on the dopaminergic system (25,48), it can be concluded that the effects of quetiapine on locomotor activity may be, in part, mediated through the influence of dopamine receptors.