Introduction: Multiple sclerosis (MS) is a chronic inflammatory neurodegenerative disease mediated by autoimmune reactions against myelin proteins and gangliosides in the grey and white matter of the brain and spinal cord. It is considered one of the most common neurological diseases of non-traumatic origin in young people, especially in women. Recent studies point to a possible association between MS and gut microbiota. Intestinal dysbiosis has been observed, as well as an alteration of short-chain fatty acid-producing bacteria, although clinical data remain scarce and inconclusive. Objective: To conduct a systematic review on the relationship between gut microbiota and multiple sclerosis. Method: The systematic review was conducted in the first quarter of 2022. The articles included were selected and compiled from different electronic databases: PubMed, Scopus, ScienceDirect, Proquest, Cochrane, and CINAHL. The keywords used in the search were: “multiple sclerosis”, “gut microbiota”, and “microbiome”. Results: 12 articles were selected for the systematic review. Among the studies that analysed alpha and beta diversity, only three found significant differences with respect to the control. In terms of taxonomy, the data are contradictory, but confirm an alteration of the microbiota marked by a decrease in Firmicutes, Lachnospiraceae, Bifidobacterium, Roseburia, Coprococcus, Butyricicoccus, Lachnospira, Dorea, Faecalibacterium, and Prevotella and an increase in Bacteroidetes, Akkermansia, Blautia, and Ruminocococcus. As for short-chain fatty acids, in general, a decrease in short-chain fatty acids, in particular butyrate, was observed. Conclusions: Gut microbiota dysbiosis was found in multiple sclerosis patients compared to controls. Most of the altered bacteria are short-chain fatty acid (SCFA)-producing, which could explain the chronic inflammation that characterises this disease. Therefore, future studies should consider the characterisation and manipulation of the multiple sclerosis-associated microbiome as a focus of both diagnostic and therapeutic strategies.

Years before the first two-pore domain potassium channel (K2P) was cloned, certain ion channels had already been demonstrated to be present in the heart with characteristics and properties usually attributed to the TREK channels (a subfamily of K2P channels). K2P channels were later detected in cardiac tissue by RT-PCR, although the distribution of the different K2P subfamilies in the heart seems to depend on the species analyzed. In order to collect relevant information in this regard, we focus here on the TWIK, TASK and TREK cardiac channels, their putative roles in cardiac physiology and their implication in coronary pathologies. Most of the RNA expression data and electrophysiological recordings available to date support the presence of these different K2P subfamilies in distinct cardiac cells. Likewise, we show how these channels may be involved in certain pathologies, such as atrial fibrillation, long QT syndrome and Brugada syndrome.

Among the large number of potassium-channel families implicated in the control of neuronal excitability, G-protein-gated inwardly rectifying potassium channels (GIRK/Kir3) have been found to be a main factor in heart control. These channels are activated following the modulation of G-protein-coupled receptors and, although they have been implicated in different neurological diseases in both human and animal studies of the central nervous system, the therapeutic potential of different subtypes of these channel families in cardiac conditions has remained untapped. As they have emerged as a promising potential tool to treat a variety of conditions that disrupt neuronal homeostasis, many studies have started to focus on these channels as mediators of cardiac dynamics, thus leading to research into their implication in cardiovascular conditions. Our aim is to review the latest advances in GIRK modulation in the heart and their role in the cardiovascular system.

Visceral pain is one of the most common symptoms associated with functional gastrointestinal (GI) disorders. Although the origin of these symptoms has not been clearly defined, the implication of both the central and peripheral nervous systems in visceral hypersensitivity is well established. The role of several pathways in visceral nociception has been explored, as well as the influence of specific receptors on afferent neurons, such as voltage-gated sodium channels (VGSCs). VGSCs initiate action potentials and dysfunction of these channels has recently been associated with painful GI conditions. Current treatments for visceral pain generally involve opioid based drugs, which are associated with important side-effects and a loss of effectiveness or tolerance. Hence, efforts have been intensified to find new, more effective and longer-lasting therapies. The implication of VGSCs in visceral hypersensitivity has drawn attention to tetrodotoxin (TTX), a relatively selective sodium channel blocker, as a possible and promising molecule to treat visceral pain and related diseases. As such, here we will review the latest information regarding this toxin that is relevant to the treatment of visceral pain and the possible advantages that it may offer relative to other treatments, alone or in combination.

Temperature homeostasis is controlled by the vagus nerve. Thermal information is collected by thermoreceptors present in the viscera and driven across sensory neurons of the nodose ganglia (NG), which in turn send it to the hypothalamus. While transient receptor potential channels (TRPs) are traditionally considered for thermal transduction, TREK channels belonging to the two-pore domain K⁺ channels family are emerging as thermosensors, but their role in the NG remains understudied. Patch-clamp recordings revealed that increasing the temperature to physiological levels causes a hyperpolarization of the membrane potential followed by a depolarization and, despite physiological temperature increased the firing rate, we have demonstrated that TREK channels might be taking part in the excitability control by counteracting TRPs’ effects. In fact, single-channel experiments revealed an increase in TREK channel open probability and a subsequent rise in their activity in NG neurons. All this indicates that TREK channels, mainly TREK1, may be responsible along with TRPs for the maintenance of the membrane potential at physiological temperature in NG neurons.