Dopamine Signaling Pathway in Health and Disease—2nd Edition

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Molecular and Translational Medicine".

Deadline for manuscript submissions: 31 March 2025 | Viewed by 3612

Special Issue Editors


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Guest Editor
Department of Pharmacy, School of Medicine and Surgery, University of Naples Federico II, 80131, Naples, Italy
Interests: synaptic plasticity; synaptic transmission; signaling pathways; regulation of gene expression
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E-Mail Website
Guest Editor
Department of Pharmacy, School of Medicine and Surgery, University of Naples Federico II, 80131, Naples, Italy
Interests: Neuromodulation; synaptic plasticity; learning and memory; neurodegeneration
Special Issues, Collections and Topics in MDPI journals

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Guest Editor
Department of Pharmacy, School of Medicine, University of Naples Federico II, Naples, Italy
Interests: metabotropic glutamate receptor 1 (mGluR1); 5-HT7 receptor (5-HT7R); dendritic spines; neuronal primary cultures; structural plasticity; autophagy; synaptopathies; animal models
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Dopamine plays a pivotal role as a neurotransmitter, regulating numerous essential physiological functions within the central nervous system. These functions encompass motor behavior, affective and emotional states, reward and reinforcement behaviors, as well as various higher cognitive functions. The four primary dopaminergic pathways are the nigrostriatal, mesocortical, mesolimbic, and tuberoinfundibular pathways. Dysfunction in the dopaminergic transmission is recognized as a core alteration in several neurological and psychiatric disorders, including Parkinson’s disease, schizophrenia, bipolar disorder, attention deficit hyperactivity disorder (ADHD), and addiction. 

This Special Issue, titled "Dopamine Signaling Pathway in Health and Disease—2nd Edition", will feature a curated collection of original research papers and reviews. These contributions will explore the cellular and molecular mechanisms that underlie dopaminergic neuromodulation under physiological conditions, as well as in preclinical cellular and animal models of dopaminergic neurodegeneration. Additionally, the issue will examine innovative pharmacological approaches for addressing dopamine-related disorders.

Prof. Dr. Floriana Volpicelli
Prof. Dr. Maria Concetta Miniaci
Dr. Luisa Speranza
Guest Editors

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Keywords

  • differentiation
  • disease modeling 
  • dopamine and drugs
  • gene expression
  • human stem cells
  • neuronal development
  • reprogramming
  • signaling pathways
  • neurodegeneration
  • neuromodulation

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Published Papers (3 papers)

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Research

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18 pages, 3851 KiB  
Article
Possible Potentiating Effects of Combined Administration of Alcohol, Caffeine, and Nicotine on In Vivo Dopamine Release in Addiction-Related Circuits Within the CNS of Rats
by Carmen Costas-Ferreira, Martiño Barreiro-Chapela, Rafael Durán and Lilian R. Ferreira Faro
Biomedicines 2024, 12(11), 2591; https://doi.org/10.3390/biomedicines12112591 - 13 Nov 2024
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Abstract
Background: Studies that assess the effects of the interaction of psychoactive substances on dopamine release, the key neurotransmitter in the neurochemical and behavioral effects related to drug consumption, are crucial to understand both their roles and the dysfunctions they produce in the central [...] Read more.
Background: Studies that assess the effects of the interaction of psychoactive substances on dopamine release, the key neurotransmitter in the neurochemical and behavioral effects related to drug consumption, are crucial to understand both their roles and the dysfunctions they produce in the central nervous system. Objective: We evaluated the effects of individual and combined administration of the three most widely consumed psychoactive substances in the world, ethanol, caffeine, and nicotine, on dopaminergic neurotransmission in three brain regions of rats related to addiction: the prefrontal cortex (PFC), the nucleus accumbens (NAcc), and the dorsal striatum. Methods: The dopamine levels were measured in vivo by cerebral microdialysis associated with HPLC-ED. Results: We observed that local administration of a single concentration of caffeine (5 mM) or nicotine (5 mM) significantly increased the dopamine levels in all three areas studied, while ethanol (300 mM) increased them in the NAcc and striatum. Perfusion of nicotine + caffeine produced a synergistic effect in both the NAcc and striatum, with increases in the in vivo dopamine release greater than the sum of the effects of both substances. When administering the combination of nicotine + caffeine + ethanol, we observed an additive effect in the NAcc, while in the PFC we observed a synergistic effect. Conclusions: Our results support the stimulating effects of caffeine, nicotine, and ethanol on the brain reward system. In addition, we also observed that the administration of different mixtures of these substances produces synergistic and additive effects on the release of dopamine in the mesocortical and nigrostriatal systems. Full article
(This article belongs to the Special Issue Dopamine Signaling Pathway in Health and Disease—2nd Edition)
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Review

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34 pages, 1692 KiB  
Review
Enduring Neurobiological Consequences of Early-Life Stress: Insights from Rodent Behavioral Paradigms
by Luisa Speranza, Kardelen Dalim Filiz, Pellegrino Lippiello, Maria Grazia Ferraro, Silvia Pascarella, Maria Concetta Miniaci and Floriana Volpicelli
Biomedicines 2024, 12(9), 1978; https://doi.org/10.3390/biomedicines12091978 - 2 Sep 2024
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Abstract
Stress profoundly affects physical and mental health, particularly when experienced early in life. Early-life stress (ELS) encompasses adverse childhood experiences such as abuse, neglect, violence, or chronic poverty. These stressors can induce long-lasting changes in brain structure and function, impacting areas involved in [...] Read more.
Stress profoundly affects physical and mental health, particularly when experienced early in life. Early-life stress (ELS) encompasses adverse childhood experiences such as abuse, neglect, violence, or chronic poverty. These stressors can induce long-lasting changes in brain structure and function, impacting areas involved in emotion regulation, cognition, and stress response. Consequently, individuals exposed to high levels of ELS are at an increased risk for mental health disorders like depression, anxiety, and post-traumatic stress disorders, as well as physical health issues, including metabolic disorders, cardiovascular disease, and cancer. This review explores the biological and psychological consequences of early-life adversity paradigms in rodents, such as maternal separation or deprivation and limited bedding or nesting. The study of these experimental models have revealed that the organism’s response to ELS is complex, involving genetic and epigenetic mechanisms, and is associated with the dysregulation of physiological systems like the nervous, neuroendocrine, and immune systems, in a sex-dependent fashion. Understanding the impact of ELS is crucial for developing effective interventions and preventive strategies in humans exposed to stressful or traumatic experiences in childhood. Full article
(This article belongs to the Special Issue Dopamine Signaling Pathway in Health and Disease—2nd Edition)
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28 pages, 6931 KiB  
Review
BDNF-Regulated Modulation of Striatal Circuits and Implications for Parkinson’s Disease and Dystonia
by Daniel Wolf, Maurilyn Ayon-Olivas and Michael Sendtner
Biomedicines 2024, 12(8), 1761; https://doi.org/10.3390/biomedicines12081761 - 5 Aug 2024
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Abstract
Neurotrophins, particularly brain-derived neurotrophic factor (BDNF), act as key regulators of neuronal development, survival, and plasticity. BDNF is necessary for neuronal and functional maintenance in the striatum and the substantia nigra, both structures involved in the pathogenesis of Parkinson’s Disease (PD). Depletion of [...] Read more.
Neurotrophins, particularly brain-derived neurotrophic factor (BDNF), act as key regulators of neuronal development, survival, and plasticity. BDNF is necessary for neuronal and functional maintenance in the striatum and the substantia nigra, both structures involved in the pathogenesis of Parkinson’s Disease (PD). Depletion of BDNF leads to striatal degeneration and defects in the dendritic arborization of striatal neurons. Activation of tropomyosin receptor kinase B (TrkB) by BDNF is necessary for the induction of long-term potentiation (LTP), a form of synaptic plasticity, in the hippocampus and striatum. PD is characterized by the degeneration of nigrostriatal neurons and altered striatal plasticity has been implicated in the pathophysiology of PD motor symptoms, leading to imbalances in the basal ganglia motor pathways. Given its essential role in promoting neuronal survival and meditating synaptic plasticity in the motor system, BDNF might have an important impact on the pathophysiology of neurodegenerative diseases, such as PD. In this review, we focus on the role of BDNF in corticostriatal plasticity in movement disorders, including PD and dystonia. We discuss the mechanisms of how dopaminergic input modulates BDNF/TrkB signaling at corticostriatal synapses and the involvement of these mechanisms in neuronal function and synaptic plasticity. Evidence for alterations of BDNF and TrkB in PD patients and animal models are reviewed, and the potential of BDNF to act as a therapeutic agent is highlighted. Advancing our understanding of these mechanisms could pave the way toward innovative therapeutic strategies aiming at restoring neuroplasticity and enhancing motor function in these diseases. Full article
(This article belongs to the Special Issue Dopamine Signaling Pathway in Health and Disease—2nd Edition)
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