In this review, we will discuss the current knowledge of AMPAR subunit-specific trafficking, with a particular emphasis on the involvement of GluA1-homomeric receptor trafficking in synaptic plasticity and brain disorders.The incidence of chronic pain is high in the general population and it is closely related to anxiety disorders, which promote negative effects on the quality of life. see more The cannabinoid system has essential participation in the pain sensitivity circuit. In this perspective, cannabidiol (CBD) is considered a promising strategy for treating neuropathic pain. Our study aimed to evaluate the effects of sub-chronic systemic treatment with CBD (0.3, 3, 10, or 30 mg/kg, i.p.) in male in rats submitted to chronic constriction injury of the sciatic nerve (CCI) or not (SHAM) and assessed in nociceptive tests (von Frey, acetone, and hot plate, three days CBD’s treatment) and in the open field test (OFT, two days CBD’s treatment). We performed a screening immunoreactivity of CB1 and TRPV1 receptors in cortical and limbic regions tissues, which were collected after 1.5 h of behavioral tests on the 24th experimental day. This study presents a dose-response curve to understand better the effects of low doses (3 mg/kg) on CBD’s antiallodynic and anxiolytic effects. Also, low doses of CBD were able to (1) reverse mechanical and thermal allodynia (cold) and hyperalgesia, (2) reverse anxious behaviors (reduction of the % of grooming and freezing time, and increase of the % of center time in the OFT) induced by chronic pain. The peripheral neuropathy promoted the increase in the expression of CB1 and TRPV1 receptors in the anterior cingulate cortex (ACC), anterior insular cortex (AIC), basolateral amygdala (BLA), dorsal hippocampus (DH), and ventral hippocampus (VH). CBD potentiated this effect in the ACC, AIC, BLA, DH, and VH regions. These results provide substantial evidence of the role of the ACC-AIC-BLA corticolimbic circuit, and BLA-VH for pain regulation. These results can be clinically relevant since they contribute to the evidence of CBD’s beneficial effects on treating chronic pain and associated comorbidities such as anxiety.For the last 20 years, researchers have focused their intention on the impact of gut microbiota in healthy and pathological conditions. This year (2021), more than 25,000 articles can be retrieved from PubMed with the keywords “gut microbiota and physiology”, showing the constant progress and impact of gut microbes in scientific life. As a result, numerous therapeutic perspectives have been proposed to modulate the gut microbiota composition and/or bioactive factors released from microbes to restore our body functions. Currently, the gut is considered a primary site for the development of pathologies that modify brain functions such as neurodegenerative (Parkinson’s, Alzheimer’s, etc.) and metabolic (type 2 diabetes, obesity, etc.) disorders. Deciphering the mode of interaction between microbiota and the brain is a real original option to prevent (and maybe treat in the future) the establishment of gut-brain pathologies. The objective of this review is to describe recent scientific elements that explore the communication between gut microbiota and the brain by focusing our interest on the enteric nervous system (ENS) as an intermediate partner. The ENS, which is known as the “second brain”, could be under the direct or indirect influence of the gut microbiota and its released factors (short-chain fatty acids, neurotransmitters, gaseous factors, etc.). Thus, in addition to their actions on tissue (adipose tissue, liver, brain, etc.), microbes can have an impact on local ENS activity. This potential modification of ENS function has global repercussions in the whole body via the gut-brain axis and represents a new therapeutic strategy.AMPA receptors (AMPARs) are the major excitatory neurotransmitter receptor in the brain, and their expression at synapses is a critical determinant of synaptic transmission and therefore brain function. Synaptic plasticity involves increases or decreases in synaptic strength, caused by changes in the number or subunit-specific subtype of AMPARs expressed at synapses, and resulting in modifications of functional connectivity of neuronal circuits, a process which is thought to underpin learning and the formation or loss of memories. Furthermore, numerous neurological disorders involve dysregulation of excitatory synaptic transmission or aberrant recruitment of plasticity processes. MicroRNAs (miRNAs) repress the translation of target genes by partial complementary base pairing with mRNAs, and are the core component of a mechanism widely used in a range of cell processes for regulating protein translation. MiRNA-dependent translational repression can occur locally in neuronal dendrites, close to synapses, and can also result in relatively rapid changes in protein expression. MiRNAs are therefore well-placed to regulate synaptic plasticity via the local control of AMPAR subunit synthesis, and can also result in synaptic dysfunction in the event of dysregulation in disease. Here, I will review the miRNAs that have been identified as playing a role in physiological or pathological changes in AMPAR subunit expression at synapses, focussing on miRNAs that target mRNAs encoding AMPAR subunits, and on miRNAs that target AMPAR accessory proteins involved in AMPAR trafficking and hence the regulation of AMPAR synaptic localisation.Dupuytren’s disease (DD) is a common, progressive fibroproliferative disease affecting the palmar fascia of the hands, causing fingers to irreversibly flex towards the palm with significant loss of function. Surgical treatments are limited, therefore effective new therapies for DD are urgently required. To identify key cellular and molecular pathways driving DD we employed single-cell RNA sequencing (scRNA-seq), profiling the transcriptomes of 35,250 human single cells from DD, non-pathogenic fascia, and healthy dermis. We identify a DD-specific population of pathogenic PDPN+/FAP+ mesenchymal cells displaying elevated expression of fibrillar collagens and profibrogenic genes. In silico trajectory analysis reveals resident fibroblasts to be the source of this pathogenic population. To resolve the processes governing DD progression, genes differentially expressed during fibroblast differentiation were identified including upregulated TNFRSF12A and transcription factor SCX. Knockdown of SCX and blockade of TNFRSF12A inhibited proliferation and altered pro-fibrotic gene expression of cultured human FAP+ mesenchymal cells, demonstrating a functional role for these genes in DD.