The modulatory role of bone morphogenetic protein signaling in cerebellar synaptic plasticity.

Autor: Hirono M; RIKEN Brain Science Institute, Wako, Saitama, Japan., Kudo M; RIKEN Brain Science Institute, Wako, Saitama, Japan., Yamada M; RIKEN Brain Science Institute, Wako, Saitama, Japan., Yanagawa Y; Department of Genetic and Behavioral Neuroscience, Gunma University Graduate School of Medicine, Maebashi, Japan.
Jazyk: angličtina
Zdroj: Journal of neurochemistry [J Neurochem] 2025 Jan; Vol. 169 (1), pp. e16290.
DOI: 10.1111/jnc.16290
Abstrakt: Bone morphogenetic proteins (BMPs), regulators of bone formation, have been implicated in embryogenesis and morphogenesis of various tissues and organs. BMP signaling plays a role in the formation of appropriate synaptic connections and development of normal neural circuits in the brain. However, physiological roles of BMP signaling in postnatal neural functions, including synaptic plasticity, remain largely unknown. Long-term depression (LTD) of synaptic transmission at parallel fiber (PF)-Purkinje cell (PC) synapses in the cerebellum has been suggested one neuronal mechanism underlying cerebellar functions. Here, we explored the contribution of BMP signaling to the induction of mouse cerebellar LTD. We first demonstrated that BMP2 and/or 4 were expressed in GABAergic neurons in mature networks of the cerebellar cortex. mRNA encoding BMP receptor type 1B (Bmpr1b) was expressed in the PC layer. Exogenous application of noggin, a BMP ligand inhibitor, suppressed the induction of cerebellar LTD by conjunctive stimulation, which caused normal LTD under control condition. Furthermore, mice deficient in BMPR1B exhibited attenuation of the extent of LTD induction, whereas they showed normal excitatory synaptic transmission at PF-PC synapses. These results suggest that after postnatal development, BMP signaling activated by BMPR1B, expressed in the PC layer, plays a crucial role in the facilitation of cerebellar LTD, leading to the modulation of cerebellar functions and behaviors.
(© 2024 International Society for Neurochemistry.)
Databáze: MEDLINE
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