Mechanisms underlying induction of LTP-associated changes in short-term dynamics of transmission at immature synapses.

Abstract:

:While the activity-dependent mechanisms guiding functional maturation of synaptic transmission postsynaptically are well characterized, less is known about the corresponding presynaptic mechanisms. Here we show that during the first postnatal week, a subset of CA3-CA1 synapses express postsynaptically induced LTP that is tightly associated with a robust decrease in synaptic facilitation, consistent with an increase in release probability (P(r)). The loss of facilitation is readily induced by physiologically relevant pairing protocols at immature synapses and is dependent on activation of NMDA-receptors but not L-type calcium channels. The putative pre- and postsynaptic components of neonatal LTP were distinguished in their downstream signaling requirements, PKC activity being selectively needed for the decrease in facilitation but not for synaptic potentiation per se. These data suggest that maturation of glutamatergic synapses involves a critical period during which presynaptic function is highly susceptible to activity-dependent regulation via a PKC-dependent mechanism.

journal_name

Neuropharmacology

journal_title

Neuropharmacology

authors

Luchkina NV,Sallert M,Clarke VR,Taira T,Lauri SE

doi

10.1016/j.neuropharm.2012.11.019

subject

Has Abstract

pub_date

2013-04-01 00:00:00

pages

494-502

eissn

0028-3908

issn

1873-7064

pii

S0028-3908(12)00566-7

journal_volume

67

pub_type

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