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Broisin, L.

Publications and source records attributed to Broisin, L..

2 recordsLinked to original sources

Melatonin modulates habituation learning via the convergent action of two MT1-type receptors.

Melatonin is a hormone produced by the pineal gland and retina, with roles in sleep and circadian rhythms as well as other neuronal processes, including the regulation of learning and memory. Using larval zebrafish, we previously identified Melatonin as a potent modulator of habituation learning: the progressive suppression of responses to a repeated stimulus. Here we have extended these analyses and have found that Melatonin has strong effects on separate aspects of habituation learning: it potentiates habituation of response probability and latency, while simultaneously inhibiting habituation of movement amplitude and duration. We performed a systematic CRISPR mutagenesis of all six zebrafish Melatonin receptors, and found that only two MT1-type receptors (Mtnr1aa and Mtnr1al) are required for Melatonin's effects on habituation. These receptors showed a cooperative interaction, with each individual mutant showing reduced sensitivity to Melatonin, and mtnr1aa;mtnr1al double mutants showing complete insensitivity. To map where these receptors act, we used whole-brain activity mapping. Despite distinct footprints, both perturbed a shared set of brain areas, including the torus longitudinalis, cerebellum, and preoptic area, with the double mutant producing the most extensive phenotype by combining and expanding the effects seen in each single mutant. Thus, we propose that two MT1-type receptors act at overlapping circuit nodes to reinforce Melatonin's bidirectional control of learning.

neuroscience↗

Quantification of Human DNA from Century-Old Archived FFPE Samples for Retrospective Genomic Studies

BackgroundFormalin-fixed, paraffin-embedded (FFPE) tissue archives are an invaluable resource for genomic research, offering the potential to link genomic data to long-term clinical outcomes. Their utility has however been limited by the degradation caused by fixation and long-term storage, particularly for samples archived for many decades. MethodsThis study evaluates a cohort of 79 FFPE tissue blocks collected and archived in 1973 from the Strasbourg Pathological Tissue Archive (SPTA), and a cohort of 51 FFPE tissue blocks from the Geneva Brain Bank (GBB), collected between 1928 and 1971. DNA was quantified using a forensic-grade quantitative PCR (qPCR) assay (QIAGEN Investigator Quantiplex Pro Kit on a Rotor-Gene Q) to precisely measure human DNA concentration, assess degradation, and detect PCR inhibition. ResultsA high proportion of the samples yielded human DNA fragments of 80bp and 95bp and very few fragments of 205bp. All organ samples treated with Bouin liquid (n=12) gave poor results, but among samples fixed in formalin (n=117), 58.1% showed over 0.25ng/{micro}L of 80bp human DNA fragments and 37.6% over 1ng/{micro}L. We propose a model to describe the decay of these samples and estimate the proportion of samples that should yield at least a 0.25ng/{micro}L concentration of fragments over 100bp to 45.1%. ConclusionsThis work demonstrates that automated extraction methods optimized for FFPE allow for the recovery of usable material even in century-old archived samples with inconsistent conditions of conservation. Our data suggests that the time spent in storage is much less influential on DNA quality than initial fixation time. Crucially, given the fragmented nature of the material recovered (an expected result), future analyses of this material will have to be conducted using next-generation sequencing (NGS) technologies and approaches that rely on short fragments.

genetics↗