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Development ; 151(13)2024 Jul 01.
Artigo em Inglês | MEDLINE | ID: mdl-38856043

RESUMO

The function of medial entorhinal cortex layer II (MECII) excitatory neurons has been recently explored. MECII dysfunction underlies deficits in spatial navigation and working memory. MECII neurons comprise two major excitatory neuronal populations, pyramidal island and stellate ocean cells, in addition to the inhibitory interneurons. Ocean cells express reelin and surround clusters of island cells that lack reelin expression. The influence of reelin expression by ocean cells and interneurons on their own morphological differentiation and that of MECII island cells has remained unknown. To address this, we used a conditional reelin knockout (RelncKO) mouse to induce reelin deficiency postnatally in vitro and in vivo. Reelin deficiency caused dendritic hypertrophy of ocean cells, interneurons and only proximal dendritic compartments of island cells. Ca2+ recording showed that both cell types exhibited an elevation of calcium frequencies in RelncKO, indicating that the hypertrophic effect is related to excessive Ca2+ signalling. Moreover, pharmacological receptor blockade in RelncKO mouse revealed malfunctioning of GABAB, NMDA and AMPA receptors. Collectively, this study emphasizes the significance of reelin in neuronal growth, and its absence results in dendrite hypertrophy of MECII neurons.


Assuntos
Moléculas de Adesão Celular Neuronais , Dendritos , Córtex Entorrinal , Proteínas da Matriz Extracelular , Camundongos Knockout , Proteínas do Tecido Nervoso , Proteína Reelina , Serina Endopeptidases , Animais , Córtex Entorrinal/metabolismo , Dendritos/metabolismo , Moléculas de Adesão Celular Neuronais/metabolismo , Moléculas de Adesão Celular Neuronais/genética , Serina Endopeptidases/metabolismo , Serina Endopeptidases/genética , Proteínas do Tecido Nervoso/metabolismo , Proteínas do Tecido Nervoso/genética , Proteínas da Matriz Extracelular/metabolismo , Proteínas da Matriz Extracelular/genética , Camundongos , Interneurônios/metabolismo , Neurônios/metabolismo , Sinalização do Cálcio
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