Publications by authors named "Maya Molinari"
Article Synopsis
- Autism spectrum disorder (ASD) includes a range of neurodevelopmental conditions with core behavioral symptoms critical for diagnosis, linked to altered dopamine (DA) neurotransmission in the striatum.
- Research in a mouse model with elevated eukaryotic initiation factor 4E (eIF4E) expression shows that this increase leads to behavioral inflexibility and impaired DA release in the striatum.
- These impairments stem from defective nicotinic receptor signaling affecting calcium dynamics in dopaminergic axons, highlighting the complex interactions between eIF4E, DA neurotransmission, and ASD symptoms, which could guide future therapies.
The substantia nigra pars reticulata (SNr), a crucial basal ganglia output nucleus, contains a dense expression of dopamine D1 receptors (D1Rs), along with dendrites belonging to dopaminergic neurons of substantia nigra pars compacta. These D1Rs are primarily located on the terminals of striatonigral medium spiny neurons, suggesting their involvement in the regulation of neurotransmitter release from the direct pathway in response to somatodendritic dopamine release. To explore the hypothesis that D1Rs modulate GABA release from striatonigral synapses, we conducted optical recordings of striatonigral activity and postsynaptic patch-clamp recordings from SNr neurons in the presence of dopamine and D1R agonists.
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- Genetic changes affecting a protein called HNRNPU are found in several brain disorders in kids.
- HNRNPU is important for the brain's growth, especially in the part called the cerebellum, but we don’t know how it affects this area yet.
- Researchers found that when HNRNPU is missing, it changes how brain cells develop, which might connect to issues like epilepsy, autism, and learning challenges.
Macroautophagy (hereafter referred to as autophagy) plays a critical role in neuronal function related to development and degeneration. Here, we investigated whether autophagy is developmentally regulated in the striatum, a brain region implicated in neurodevelopmental disease. We demonstrate that autophagic flux is suppressed during striatal postnatal development, reaching adult levels around postnatal day 28 (P28).
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