Deficits in decoding rewarding (and aversive) signals are present in several neuropsychiatric conditions such as depression and addiction, emphasising the importance of studying the underlying neural circuits in detail. One of the key regions of the reward circuit is the nucleus accumbens (NAc). The classical view on the field postulates that NAc dopamine receptor D1expressing medium spiny neurons (D1-MSNs) convey reward signals, while dopamine receptor D2-expressing MSNs (D2-MSNs) encode aversion. Here, we show that both MSN subpopulations can drive reward and aversion, depending on their neuronal stimulation pattern. Brief D1-or D2-MSN optogenetic stimulation elicited positive reinforcement and enhanced cocaine conditioning. Conversely, prolonged activation induced aversion, and in the case of D2-MSNs, decreased cocaine conditioning. Brief stimulation was associated with increased ventral tegmenta area (VTA) dopaminergic tone either directly (for D1-MSNs) or indirectly via ventral pallidum (VP) (for D1-and D2-MSNs). Importantly, prolonged stimulation of either MSN subpopulation induced remarkably distinct electrophysiological effects in these target regions. We further show that blocking κ-opioid receptors in the VTA (but not in VP) abolishes the behavioral effects induced by D1-MSN prolonged stimulation. In turn, blocking δ-opioid receptors in the VP (but not in VTA) blocks the behavioral effects elicited by D2-MSN prolonged stimulation. Our findings demonstrate that D1-and D2-MSNs can bidirectionally control reward and aversion, explaining the existence of controversial studies in the field, and highlights that the proposed striatal functional opposition needs to be reconsidered.

Epidemiologic studies have provided compelling evidence that prenatal stress, through excessive maternal glucocorticoids exposure, is associated with psychiatric disorders later in life. We have recently reported that anxiety associated with prenatal exposure to dexamethasone (DEX, a synthetic glucocorticoid) correlates with a gender‐specific remodeling of microglia in the medial prefrontal cortex (mPFC), a core brain region in anxiety‐related disorders. Gender differences in microglia morphology, the higher prevalence of anxiety in women and the negative impact of anxiety in cognition, led us to specifically evaluate cognitive behavior and associated circuits (namely mPFC‐dorsal hippocampus, dHIP), as well as microglia morphology in female rats prenatally exposed to dexamethasone (in utero DEX, iuDEX). We report that iuDEX impaired recognition memory and deteriorated neuronal synchronization between mPFC and dHIP. These functional deficits are paralleled by microglia hyper‐ramification in the dHIP and decreased ramification in the mPFC, showing a heterogeneous remodeling of microglia morphology, both postnatally and at adulthood in different brain regions, that differently affect mood and cognition. The chronic blockade of adenosine A2A receptors (A2AR), which are core regulators of microglia morphology and physiology, ameliorated the cognitive deficits, but not the anxiety‐like behavior. Notably, A2AR blockade rectified both microglia morphology in the dHIP and the lack of mPFC‐dHIP synchronization, further heralding their role in cognitive function.

John Cunningham virus (JCV) infects chronically human populations worldwide and probably might confer a higher risk for colorectal cancer (CRC). The prevalence of JCV DNA has been determined in normal colon mucosa and compared it with different degrees of colorectal lesions, as well as viral presence in the urine of the individuals in the study. JCV DNA was detected by a nested-PCR approach targeting the JCV small-t antigen in 100 healthy controls, and 100 patients undergoing biopsy for diagnosis of colorectal disorders. JCV DNA was detected in 40% of normal mucosa from controls and patients. JCV DNA presence in urine was also similar in controls and patients (37-41% range). JCV DNA detection in normal mucosa and urine reflects the infected population in Portugal. However, in cases with colorectal tumor lesions, JCV DNA was detected in 90% cases, independently of histological type or grade, and this increase was significantly higher with respect to its normal surrounding mucosa. This higher detection of JCV DNA in tumor lesions with respect to its own normal mucosa suggested that a selection for virus containing cells has occurred at some early stage in tumor initiation or progression. JCV may have a specific tropism for colon epithelial cells with some inherent predisposition that makes them more prone to oncogenic transformation, with selection of infected cells. Several p53 polymorphisms in intron 2, common to both groups, were more frequently detected in colorectal pathology cases. A novel p53 mutation in the 3' untranslated region (exon 11) was identified in 10 patients.

The introduction of exotic organisms in marine ecosystems can lead to economic and ecological losses. Globally, seaweeds represent a significant part of these non-indigenous species (NIS), with 407 introduced algal species. Furthermore, the presence of NIS seaweeds has been reported as a major concern worldwide since the patterns of their potential invasion mechanisms and vectors are not yet fully understood. Currently, in the Iberian Peninsula, around 50 NIS seaweeds have been recorded. Some of these are also considered invasive due to their overgrowth characteristic and competition with other species. However, invasive seaweeds are suitable for industrial applications due to their high feedstock. Hence, seaweeds’ historical use in daily food diet, allied to research findings, showed that macroalgae are a source of nutrients and bioactive compounds with nutraceutical properties. The main goal of this review is to evaluate the records of NIS seaweeds in the Iberian Peninsula and critically analyze the potential of invasive seaweeds application in the food industry.