Biology subjects

Ezan, P.

Publications and source records attributed to Ezan, P..

3 recordsLinked to original sources

bioRxiv2026

Astrocytes control oxytocin-based maternal behavior via connexin 30

Prosocial and affiliative behaviors rely on complex neuroendocrine neuronal circuits. Dynamic neuroglial interactions play prominent roles in shaping synaptic networks, whose alterations contribute to psychiatric disorders associated with social deficits. However, a role for astrocytes in regulating maternal behavior remains elusive. Here we show that female mice exhibiting increased oxytocin levels in the hypothalamic supraoptic nucleus upon social interactions with pups display neuroglial structural plasticity and downregulation of astroglial connexin 30, a protein involved in morphological remodeling. We found that impairing astroglial connexin 30 expression alters the structural properties of astrocytes by decreasing their volume and coverage of oxytocinergic synapses in the supraoptic nucleus of female mice. This functionally sets levels of plasma oxytocin and maternal behavior, exacerbating maternal care in virgin pup-naive female mice deficient for astroglial Cx30. Hypothalamic astrocytes, via connexin 30, are thus key determinants of oxytocin-based maternal behavior, whose alteration is known to impair social skills development in offspring.

neuroscience↗

bioRxiv2025

Astroglial deficiency for oligophrenin-1 contributes to intellectual disability

Neurodevelopmental disorders, including X-linked intellectual disability, autism spectrum disorder or schizophrenia, can result from the mutation of oligophrenin-1 (Ophn1), encoding a Rho-GTPase-activating protein. Ophn1 regulates synaptic development and function, in part via cytoskeleton reorganization, and is expressed in both neurons and astrocytes. Despite the crucial role of astrocytes in synapse function, altered in neurodevelopmental disorders, and their Ophn1 expression, the specific impact of astroglial Ophn1 deficiency on synaptic transmission and behavior remains unknown. Here, we show that Ophn1 deficiency postnatally in hippocampal astrocytes impairs synaptic transmission, short-term plasticity and spatial working memory in adults. This involves an adenosine A1 receptor-dependent presynaptic mechanism associated with astroglial morphological rearrangements resulting in increased astroglial synapse coverage. The structural, functional and behavioral alterations induced by astroglial Ophn1 deficiency are rescued in adults by pharmacological inhibition of the RhoA/ROCK pathway. Our findings uncover an important role for astroglial Ophn1 deficiency in synaptic and behavioral dysfunctions, pointing to a novel cellular therapeutic target for neurodevelopmental disorders.

neuroscience↗

bioRxiv2020

Astrocytes close the critical period for visual plasticity

Summary paragraphBrain postnatal development is characterized by critical periods of experience-dependent remodeling1,2. Termination of these periods of intense plasticity is associated with settling of neuronal circuits, allowing for efficient information processing3. Failure to end critical periods thus results in neurodevelopmental disorders4,5. Yet, the cellular processes defining the timing of these developmental periods remain unclear. Here we show in the mouse visual cortex that astrocytes control the closure of the critical period. We uncover a novel underlying pathway involving regulation of the extracellular matrix that allows interneurons maturation via an unconventional astroglial connexin signaling. We find that timing of the critical period closure is controlled by a marked developmental upregulation of the astroglial protein connexin 30 that inhibits expression of the matrix degrading enzyme MMP9 through the RhoA-GTPase signaling pathway. Our results thus demonstrate that astrocytes not only influence activity and plasticity of single synapses, but are also key elements in the experience-dependent wiring of brain developing circuits. This work, by revealing that astrocytes promote the maturation of inhibitory circuits, hence provide a new cellular target to alleviate malfunctions associated to impaired closure of critical periods.

neuroscience↗