Neuroanatomy of basic cognitive function
Mark J. Ashley, David A. Hovda in Traumatic Brain Injury, 2017
Dopaminergic projections travel via the tuberoinfundibular, mesostriatal, mesocortical, and mesolimbic dopaminergic pathways. The tuberoinfundibular pathway projects from the hypothalamus to the pituitary. The mesostriatal pathway arises from the substantia nigra and serves the striatum, specifically the caudate and putamen. Lesions of the mesostriatal pathway result in movement disorders, such as Parkinsonism, and are often treated with dopaminergic agonists.177 The mesolimbic pathway serves the medial temporal cortex, amygdala, cingulate gyrus, and the nucleus accumbens. As such, lesions of this pathway may result in difficulty encoding and retrieving information (medial temporal cortex), information conflict resolution (cingulate gyrus), and “positive” symptoms of schizophrenia, such as hallucination. Dopaminergic antagonists are used to treat symptoms of schizophrenia. The mesocortical pathway arises largely from the ventral tegmental area and projects to the PFC. Lesions of this pathway may result in deficits of working memory, attention, abulia, hypokinesis, and the “negative” symptoms of schizophrenia.
Pharmaceutical interventions
Jane Hanley, Mark Williams in 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).
Biological Basis of Behavior
Mohamed Ahmed Abd El-Hay in 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.
Amantadine and memantine: a comprehensive review for acquired brain injury
Published in Brain Injury, 2020
Heather M. Ma, Ross D. Zafonte
A third proposed mechanism for increasing the level of severely injured patients’ clinical arousal and awareness is through targeted dopamine enhancement. The theoretical basis of this concept involved pharmacologically targeting three of the four major dopaminergic pathways in the brain (15): The mesolimbic pathway, associated with motivation, learning, and memory.The nigrostriatal pathway, involved in initiation and velocity of movement.The mesocortical pathway, involved in motivation or activation, planning, and temporal organization, as well as associated with cortical tone and attention.
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.
Related Knowledge Centers
- Dopaminergic Pathways
- Dorsolateral Prefrontal Cortex
- Emotion
- Motivation
- Psychosis
- Prefrontal Cortex
- Dopamine
- Brain
- Ventral Tegmental Area
- Executive Functions