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Lanuza, E.

Publications and source records attributed to Lanuza, E..

2 recordsLinked to original sources

The maternal hormone in the male brain: sexually dimorphic distribution of prolactin signalling in the mouse brain

Research of the central actions of prolactin is virtually restricted to females, but this hormone has also documented roles in male physiology and behaviour. Here, we provide the first description of the pattern of prolactin-derived signalling in the male mouse brain, employing the immunostaining of phosphorylated signal transducer and activator of transcription 5 (pSTAT5) after exogenous prolactin administration. Next, we explore possible sexually dimorphic differences by comparing pSTAT5 immunoreactivity in prolactin-supplemented males and females. We also assess the role of testosterone in the regulation of central prolactin signalling in males by comparing intact with castrated prolactin-supplemented males.\n\nProlactin-supplemented males displayed a widespread pattern of pSTAT5 immunoreactivity, restricted to brain centres showing expression of the prolactin receptor. Immunoreactivity for pSTAT5 was present in several nuclei of the preoptic, anterior and tuberal hypothalamus, as well as in the septofimbrial nucleus or posterodorsal medial amygdala of the telencephalon. Conversely, non-supplemented control males were virtually devoid of pSTAT5-immunoreactivity, suggesting that central prolactin actions in males are limited to situations concurrent with substantial hypophyseal prolactin release (e.g. stress or mating). Furthermore, comparison of prolactin-supplemented males and females revealed a significant, female-biased sexual dimorphism, supporting the view that prolactin has a preeminent role in female physiology and behaviour. Finally, in males, castration significantly reduced pSTAT5 immunoreactivity in some structures, including the paraventricular and ventromedial hypothalamic nuclei and the septofimbrial region, thus indicating a region-specific regulatory role of testosterone over central prolactin signalling.

neuroscience

TIMELINE OF BRAIN ALTERATIONS IN ALZHEIMER’S DISEASE ACROSS THE ENTIRE LIFESPAN

Brain imaging studies have shown that progressive cerebral atrophy characterized the development of Alzheimers Disease (AD). The key question is how long before the diagnosis of AD the neurodegenerative process started leading to these structural alterations. To answer this question, we proposed an innovative way by inferring brain structure volume trajectories across the entire lifespan using massive number of MRI (N=4714). Our study provides evidences of early divergence of the AD model from the control model for the hippocampus before 40 years, followed by the lateral ventricles and the amygdala around 40 years for the AD model. Moreover, our lifespan investigation reveals the dynamic of the evolution of these biomarkers and suggest close abnormality trajectories for the hippocampus and the amygdala. Finally, our results highlight that the temporal lobe atrophy, a key biomarker in AD, is a very early pathophysiological event potentially associated to early life exposures to risk factors.

neuroscience