Sonic hedgehog maintains cellular and neurochemical homeostasis in the adult nigrostriatal circuit

Non cell-autonomous processes are thought to play critical roles in the cellular maintenance of the healthy and diseased brain but mechanistic details remain unclear. We report that the interruption of a non cell-autonomous mode of sonic hedgehog (Shh) signaling originating from dopaminergic neurons...

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Detalles Bibliográficos
Autores: Gonzalez-Reyes, Luis E., Verbitsky, Miguel, Blesa, Javier, Jackson-Lewis, Vernice, Paredes, Daniel, Tillack, Karsten, Phani, Sudarshan, Kramer, Edgar R., Przedborski, Serge, Kottmann, Andreas H.
Tipo de recurso: artículo
Fecha de publicación:2012
País:España
Institución:Universidad Camilo José Cela (UCJC)
Repositorio:Depósito Digital e-UCJC
OAI Identifier:oai:repositorio.ucjc.edu:20.500.12020/1503
Acceso en línea:https://www.cell.com/neuron/fulltext/S0896-6273(12)00484-9?_returnURL=https%3A%2F%2Flinkinghub.elsevier.com%2Fretrieve%2Fpii%2FS0896627312004849%3Fshowall%3Dtrue
http://hdl.handle.net/20.500.12020/1503
https://doi.org/10.1016/j.neuron.2012.05.018
Access Level:acceso abierto
Palabra clave:Ciencias Biomédicas
Substantia Nigra
Sonic Hedgehog
Parkinson's Disease
Striatum
32 Ciencias Médicas
Descripción
Sumario:Non cell-autonomous processes are thought to play critical roles in the cellular maintenance of the healthy and diseased brain but mechanistic details remain unclear. We report that the interruption of a non cell-autonomous mode of sonic hedgehog (Shh) signaling originating from dopaminergic neurons causes progressive, adult-onset degeneration of dopaminergic, cholinergic, and fast spiking GABAergic neurons of the mesostriatal circuit, imbalance of cholinergic and dopaminergic neurotransmission, and motor deficits reminiscent of Parkinson's disease. Variable Shh signaling results in graded inhibition of muscarinic autoreceptor- and glial cell line-derived neurotrophic factor (GDNF)-expression in the striatum. Reciprocally, graded signals that emanate from striatal cholinergic neurons and engage the canonical GDNF receptor Ret inhibit Shh expression in dopaminergic neurons. Thus, we discovered a mechanism for neuronal subtype specific and reciprocal communication that is essential for neurochemical and structural homeostasis in the nigrostriatal circuit. These results provide integrative insights into non cell-autonomous processes likely at play in neurodegenerative conditions such as Parkinson's disease.