期刊
JOURNAL OF NEUROSCIENCE
卷 27, 期 46, 页码 12464-12474出版社
SOC NEUROSCIENCE
DOI: 10.1523/JNEUROSCI.0178-07.2007
关键词
metabotropic glutamate receptor; synaptic inhibition; GABA(A) receptor; dendritic release; DSI; endocannabinoids
资金
- BBSRC [BB/D01817X/1] Funding Source: UKRI
- MRC [G0601529] Funding Source: UKRI
- Biotechnology and Biological Sciences Research Council [BB/D01817X/1] Funding Source: Medline
- Medical Research Council [G0601529] Funding Source: Medline
- Wellcome Trust Funding Source: Medline
- Biotechnology and Biological Sciences Research Council [BB/D01817X/1] Funding Source: researchfish
- Medical Research Council [G0601529] Funding Source: researchfish
In the cerebellum, the process of retrograde signaling via presynaptic receptors is important for the induction of short-and long-term changes in inhibitory synaptic transmission at interneuron-Purkinje cell (PC) synapses. Endocannabinoids, by activating presynaptic CB1 receptors, mediate a short-term decrease in inhibitory synaptic efficacy, whereas glutamate, acting on presynaptic NMDA receptors, induces a longer-latency sustained increase in GABA release. We now demonstrate that either low-frequency climbing fiber stimulation or direct somatic depolarization of Purkinje cells results in SNARE-dependent vesicular release of glutamate from the soma and dendrites of PCs. The activity-dependent release of glutamate caused the activation of postsynaptic metabotropic glutamate receptor 1 (mGluR1) on PCsomatodendritic membranes, resulting in the cooperative release of endocannabinoids and an mGluR1-mediated slow membrane conductance. The activity of excitatory amino acid transporters regulated the spatial spread of glutamate and thus the extent of PC mGluR1 activation. We propose that activity-dependent somatodendritic glutamate release and autocrine activation of mGluR1 on PCs provides a powerful homeostatic mechanism to dynamically regulate inhibitory synaptic transmission in the cerebellar cortex.
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