In:
The Journal of Neuroscience, Society for Neuroscience, Vol. 32, No. 40 ( 2012-10-03), p. 13796-13804
Abstract:
Depolarization of presynaptic terminals that arises from activation of presynaptic ionotropic receptors, or somatic depolarization, can enhance neurotransmitter release; however, the molecular mechanisms mediating this plasticity are not known. Here we investigate the mechanism of this enhancement at the calyx of Held synapse, in which presynaptic glycine receptors depolarize presynaptic terminals, elevate resting calcium levels, and potentiate release. Using knock-out mice of the calcium-sensitive PKC isoforms (PKC Ca ), we find that enhancement of evoked but not spontaneous synaptic transmission by glycine is mediated primarily by PKC Ca . Measurements of calcium at the calyx of Held indicate that deficits in synaptic modulation in PKC Ca knock-out mice occur downstream of presynaptic calcium increases. Glycine enhances synaptic transmission primarily by increasing the effective size of the pool of readily releasable vesicles. Our results reveal that PKC Ca can enhance evoked neurotransmitter release in response to calcium increases caused by small presynaptic depolarizations.
Type of Medium:
Online Resource
ISSN:
0270-6474
,
1529-2401
DOI:
10.1523/JNEUROSCI.2158-12.2012
Language:
English
Publisher:
Society for Neuroscience
Publication Date:
2012
detail.hit.zdb_id:
1475274-8
SSG:
12
