Abstract:
:Synaptic plasticity is subject to activity-dependent long-term modification (metaplasticity). We have recently described a novel form of heterosynaptic metaplasticity in hippocampal CA1, whereby 'priming' activity at one set of synapses confers a metaplastic state that inhibits subsequent LTP both within and between dendritic compartments. Here, we investigated the roles of purinergic signalling and gap junctions in mediating this long-distance communication between synapses. We found that the heterosynaptic metaplasticity requires the hydrolysis of extracellular ATP to adenosine, and activation of adenosine A2, but not A1 receptors. The metaplasticity was also blocked by the non-selective gap junction blockers carbenoxolone and meclofenamic acid, and by a connexin43-specific mimetic peptide. These results indicate that an intercellular signalling cascade underlies the long-distance communication required for this form of metaplasticity.
journal_name
Neurobiol Learn Memjournal_title
Neurobiology of learning and memoryauthors
Jones OD,Hulme SR,Abraham WCdoi
10.1016/j.nlm.2013.05.010subject
Has Abstractpub_date
2013-10-01 00:00:00pages
31-9eissn
1074-7427issn
1095-9564pii
S1074-7427(13)00091-9journal_volume
105pub_type
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