bioRxiv Science⌕ Search

Biology subjects

BECKER, J. A. J.

Publications and source records attributed to BECKER, J. A. J..

2 recordsLinked to original sources

Neurobiological alterations and autism-like phenotype in mice following regulatory-limit exposure to fungicides in drinking water

Neurodevelopmental conditions, including attention deficit hyperactivity disorder (ADHD) and autism spectrum disorders (ASD), have increased markedly over recent decades. This rise parallels the widespread use of agrochemicals, suggesting a contribution of environmental exposures. We hypothesize that pesticide residues may disrupt brain development and promote neurodevelopmental disorders. Here, we test whether concentrations permitted in drinking water affect brain development using a maternal exposure model in wild-type mice. Exposure to a fungicide mixture at 0.3 g/L, below the current European regulatory limit of 0.5 g/L, impairs corticogenesis and is associated with alterations in synaptic function and glutamatergic signaling. Offspring exhibit delays in sensory development, reduced social interactions, and increased stereotyped behaviors. We identify the adenosine A2A receptor as a molecular target of anilinopyrimidine fungicides. Together, these findings indicate that low-dose exposure to this fungicide mixture can induce an autism spectrum-like phenotype in the offspring.

neuroscience↗

Acute, chronic and conditioned effects of intranasal oxytocin in the mu opioid receptor knockout mouse model of autism: social context matters

Autism Spectrum Disorders (ASD) are neurodevelopmental disorders whose diagnosis relies on deficient social interaction and communication together with repetitive behaviours. Multiple studies have highlighted the potential of oxytocin (OT) to ameliorate behavioural abnormalities in animal models and subjects with ASD. Clinical trials, however, yielded disappointing results. Our study aimed at challenging hypotheses accounting for such negative results by assessing the behavioural effects of different regimens of OT administration in the Oprm1 null mouse model of ASD. We assessed the effects of intranasal OT injected once at different doses and time points following administration, or chronically, on ASD-related behaviours in Oprm1+/+and Oprm1-/- mice. We then tested whether pairing intranasal OT injection with social experience would influence its outcome on ASD-like core symptoms, and measured gene expression in several regions of the reward/social circuit. Acute intranasal OT improved social behaviour in Oprm1-/- mice at a moderate dose (0.3 IU) shortly after administration (5 min). Effects on non-social behaviours were limited. Chronic OT at this dose maintained beneficial effects in Oprm1 null mice but was deleterious in wild-type mice. Finally, improvements in the social behaviour of Oprm1-/- mice were greater and longer lasting when OT was administered in a social context, while the expression of OT and vasopressin receptor genes, as well as marker genes of striatal projection neurons, was suppressed. Our results highlight the importance of considering dosage and social context when evaluating the effects of OT treatment in ASD. HighlightsO_LIAcute intranasal oxytocin improved social behaviour shortly after administration C_LIO_LIEffects of oxytocin on non-social behaviours were limited C_LIO_LIChronic oxytocin maintained beneficial effects in mutant mice but was deleterious in wild-type mice C_LIO_LIOxytocin triggers greater and longer-lasting improvements in social behaviour when administered within a social context C_LIO_LIChronic oxytocin suppresses the expression of its own receptor gene and key striatal neuron gene markers C_LI

animal behavior and cognition↗