Postsynaptic inositol 1,4,5-triphosphate signaling maintains presynaptic function of parallel fiber-Purkinje cell synapses via BDNF

Kazuharu Furutani, Yohei Okubo, Sho Kakizawa, Masamitsu Iino

Research output: Contribution to journalArticle

32 Scopus citations


The maintenance of synaptic functions is essential for neuronal information processing, but cellular mechanisms that maintain synapses in the adult brain are not well understood. Here, we report an activity-dependent maintenance mechanism of parallel fiber (PF)-Purkinje cell (PC) synapses in the cerebellum. When postsynaptic metabotropic glutamate receptor (mGluR) or inositol 1,4,5-trisphosphate (IP3) signaling was chronically inhibited in vivo, PF-PC synaptic strength decreased because of a decreased transmitter release probability. The same effects were observed when PF activity was inhibited in vivo by the suppression of NMDA receptor-mediated inputs to granule cells. PF-PC synaptic strength similarly decreased after the in vivo application of an antibody against brain-derived neurotrophic factor (BDNF). Furthermore, the weakening of synaptic connection caused by the blockade of mGluR-IP3 signaling was reversed by the in vivo application of BDNF. These results indicate that a signaling cascade comprising PF activity, postsynaptic mGluR-IP3 signaling and subsequent BDNF signaling maintains presynaptic functions in the mature cerebellum.

Original languageEnglish (US)
Pages (from-to)8528-8533
Number of pages6
JournalProceedings of the National Academy of Sciences of the United States of America
Issue number22
StatePublished - May 30 2006
Externally publishedYes



  • Adult mouse
  • Cerebellum
  • Metabotropic glutamate receptor
  • Neuronal activity
  • Retrograde signaling

ASJC Scopus subject areas

  • General

Cite this