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Postnatal alterations in induction threshold and expression magnitude of long‐term potentiation and long‐term depression at hippocampal synapses
Author(s) -
Dumas Theodore C.
Publication year - 2012
Publication title -
hippocampus
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.767
H-Index - 155
eISSN - 1098-1063
pISSN - 1050-9631
DOI - 10.1002/hipo.20881
Subject(s) - long term potentiation , neuroscience , synaptic plasticity , excitatory postsynaptic potential , postsynaptic potential , post tetanic potentiation , metaplasticity , synaptic fatigue , nonsynaptic plasticity , long term depression , ltp induction , synaptic augmentation , hippocampus , inhibitory postsynaptic potential , biology , nmda receptor , ampa receptor , receptor , biochemistry
Abstract Activity‐dependent synaptic plasticity refines neural networks during development and subserves information processing in adulthood. Previous research has revealed postnatal alterations in synaptic plasticity at nearly all forebrain synapses, suggesting different forms of synaptic plasticity may contribute to network development and information processing. To assess possible relationships between modifications in synaptic plasticity and maturation of cognitive ability, we examined excitatory synaptic function in area CA1 of the mouse hippocampus ∼3 weeks of age, when hippocampal‐dependent learning and memory abilities first emerge. Long‐term potentiation (LTP) and depression (LTD) of synaptic efficacy were observed in slices from juvenile animals younger than 3 weeks of age. Both pre‐ and postsynaptic mechanisms supported LTP and LTD in juveniles. After the third postnatal week, the magnitude of LTP was reduced and the threshold for postsynaptic induction was reduced, but the threshold for presynaptic induction was increased. The reduced threshold for postsynaptic LTP appeared to be due, partly, to an increase in baseline excitatory synaptic strength, which likely permitted greater postsynaptic depolarization during induction. Low frequency stimulation did not induce LTD at this more mature stage, but it blocked subsequent induction of LTP, suggesting metaplastic differences across age groups. Late postnatal modifications in activity‐dependent synaptic plasticity might reflect attenuation of mechanisms more closely tied to network formation (presynaptic potentiation and pre‐ and postsynaptic depression) and unmasking of mechanisms underlying information processing and storage (associative postsynaptic potentiation), which likely impact the integrative capacity of the network and regulate the emergence of adult‐like cognitive abilities. © 2010 Wiley Periodicals, Inc.