98%
921
2 minutes
20
Increasing evidence shows changes in gut microbiota composition in association with psychiatric disorders, including anxiety and depression. Moreover, it has been reported that perturbations in gut microbe diversity and richness influence serotonergic, GABAergic, noradrenergic, and dopaminergic neurotransmission. Among these, dopamine is regarded as a main regulator of cognitive functions such as decision making, attention, memory, motivation, and reward. In this work, we will highlight findings that link alterations in intestinal microbiota and dopaminergic neurotransmission, with a particular emphasis on the mesocorticolimbic circuit, which is involved in reward to natural reinforcers, as well as abuse substances. For this, we reviewed evidence from studies carried out on germ-free animals, or in rodents subjected to intestinal dysbiosis using antibiotics, and also through the use of probiotics. All this evidence strongly supports that the microbiota-gut-brain axis is key to the physiopathology of several neuropsychiatric disorders involving those where dopaminergic neurotransmission is compromised. In addition, the gut microbiota appears as a key player when it comes to proposing novel strategies to the treatment of these psychiatric conditions.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1007/s00213-019-05265-5 | DOI Listing |
Mol Ther Nucleic Acids
September 2025
Center of Emphasis in Neuroscience, Department of Molecular and Translational Medicine, Paul L. Foster School of Medicine, Texas Tech University Health Sciences Center El Paso, El Paso, TX 79905, USA.
Parkinson's disease (PD) is a debilitating neurodegenerative condition. Synaptic dysfunctions are associated with the onset and progressive neurodegeneration exhibited in PD. Healthy, active synapses are a prerequisite for non-pathological neurotransmission.
View Article and Find Full Text PDFFront Biosci (Landmark Ed)
August 2025
Department of Biomedical Sciences, University of Missouri-Kansas City, School of Medicine, Kansas City, MO 64108, USA.
Glutamate is an important neurotransmitter in the mammalian brain. Among the receptors that glutamate interacts with is metabotropic glutamate (mGlu) receptor 2, a Gα-coupled receptor. These receptors are primarily located on glutamatergic nerve terminals and act as presynaptic autoreceptors to produce feedback inhibition of glutamate release.
View Article and Find Full Text PDFMol Psychiatry
September 2025
Department of Psychological Medicine, Institute of Psychiatry, Psychology & Neuroscience, King's College London, 16 De Crespigny Park, London, SE5 8AB, UK.
Disrupted gamma-aminobutyric acid (GABA) neurotransmission may contribute to the pathophysiology of schizophrenia. Reductions in hippocampal GABAergic neurons have been found in schizophrenia, and increased hippocampal perfusion has been described in schizophrenia and in people at clinical high-risk for psychosis (CHRp). We have also found decreases in hippocampal GABA receptors containing the α5 subunit (GABARα5) in a well-validated neurodevelopmental rat model of relevance for schizophrenia.
View Article and Find Full Text PDFActa Neuropsychiatr
September 2025
Kent and Medway NHS Partnership Trust, Maidstone, UK.
Progress in the development of new and improved medications for psychosis has been notably slow and disappointing. The first treatment for schizophrenia was introduced in early 1950s and the majority of medications available today exclusively function through dopamine antagonism. The search for a new drug treatment with a different mechanism of action was extremely slow-paced mainly due to the limited understanding of the aetiology, pathophysiology and genetics of schizophrenia.
View Article and Find Full Text PDFClin Drug Investig
September 2025
Department of Psychology, University of Cambridge, Cambridge, UK.
Attention-deficit hyperactivity disorder (ADHD) is characterized by core symptoms of inattention, hyperactivity, and impulsivity. Aberrant dopaminergic and noradrenergic neurotransmission are often implicated in the pathogenesis of these symptoms because ADHD treatments increase synaptic levels of these neurotransmitters in brain regions associated with attention and impulse control. However, some ADHD treatments also enhance serotonergic neurotransmission in these regions, which could contribute to their efficacy.
View Article and Find Full Text PDF