Biology subjects

Ferre, S.

Publications and source records attributed to Ferre, S..

3 recordsLinked to original sources

bioRxiv2025

Press Releases Shape Online Attention for Neuroscience Articles

Alternative indexes (altmetrics), such as the number of social media posts or news mentions, assess the relevance of a publication beyond academia. At the same time, composite metrics, like Altmetric Attention Score (AAS), gather these indicators to provide an overall measure of the online attention of an article. Communication departments at research institutions aim to help publications reach the general public and, therefore, play a key role in improving the altmetrics performance of scientific articles. However, the most effective strategies to achieve this remain unclear. No standardized protocols exist to guide communication professionals in maximizing the impact of their outreach efforts. Thus, in the present research, carried out by the communication department of a neuroscience research center, we conducted three complementary analyses to help to fill this gap. First, a study involving more than 3,000 neuroscience publications from 8 similar research centers revealed correlations between altmetrics and citations. Second, a retrospective analysis of 201 in-house articles found that active communication campaigns were associated with better altmetric performance, with notable differences between publications that included a press release (PR) and those that did not. Finally, a prospective experiment involving 25 articles examined changes in altmetrics before and after the dissemination of a PR or posting on X. Results showed that PRs significantly increased the number of news mentions and X posts, leading to an average rise of approximately 70 points in the AAS. These findings highlight the importance of PRs in maximizing the societal visibility and impact of scientific publications.

scientific communication and education↗

bioRxiv2021

Cell-type specific expression and behavioral impact of galanin and GalR1 in the locus coeruleus during opioid withdrawal

The neuropeptide galanin is reported to attenuate opioid withdrawal symptoms, potentially by reducing neuronal hyperactivity in the noradrenergic locus coeruleus (LC) via galanin receptor 1 (GalR1). We evaluated this mechanism by using RNAscope in situ hybridization to characterize GalR1 mRNA distribution in the dorsal pons and to compare galanin and GalR1 mRNA expression in tyrosine hydroxylase-positive (TH+) LC cells at baseline and following chronic morphine or precipitated withdrawal. We then used genetically altered mouse lines and pharmacology to test whether noradrenergic galanin (NE-Gal) modulates withdrawal symptoms. RNAscope revealed that, while GalR1 signal was abundant in the dorsal pons, 80.7% of the signal was attributable to TH-neurons outside the LC. Galanin and TH mRNA were abundant in LC cells at baseline and were further increased by withdrawal, whereas low basal GalR1 mRNA expression was unaltered by chronic morphine or withdrawal. Naloxone-precipitated withdrawal symptoms in mice lacking NE-Gal (GalcKO-Dbh) were largely similar to WT littermates, indicating that loss of NE-Gal does not exacerbate withdrawal. Complimentary experiments using NE-Gal overexpressor mice (NE-Gal OX) and systemic administration of the galanin receptor agonist galnon revealed that increasing galanin signaling also failed to alter behavioral withdrawal, while suppressing noradrenergic transmission with the alpha-2 adrenergic receptor agonist clonidine attenuated multiple symptoms. These results indicate that galanin does not acutely attenuate precipitated opioid withdrawal via an LC-specific mechanism, which has important implications for the general role of galanin in regulation of somatic and affective opioid responses and LC activity.

neuroscience↗

bioRxiv2019

Modulation of dopamine D1 receptors via histamine H3 receptors is a novel therapeutic target for Huntington’s disease

Early Huntingtons disease (HD) include over-activation of dopamine D1 receptors (D1R), producing an imbalance in dopaminergic neurotransmission and cell death. To reduce D1R over-activation, we present a strategy based on targeting complexes of D1R and histamine H3 receptors (H3R). Using an HD striatal cell model and HD organotypic brain slices we found that D1R-induced cell death signaling and neuronal degeneration, are mitigated by an H3R antagonist. We demonstrate that the D1R-H3R heteromer is expressed in HD animal models at early but not late stages of HD, correlating with HD progression. In accordance, we found this target expressed in human control subjects and low-grade HD patients. Finally, treatment of HD mice with an H3R antagonist prevented cognitive and motor learning deficits, as well as the loss of heteromer expression. Taken together, our results indicate that D1R - H3R heteromers play a pivotal role in dopamine signaling and represent novel targets for treating HD.\n\nImpact StatementProgression of Huntingtons disease can be slowed by altering dopamine signalling through the Dopamine 1 receptor - Histamine 3 receptor heteromer.

neuroscience↗