Purinergic receptor- and gap junction-mediated intercellular signalling as a mechanism of heterosynaptic metaplasticity.

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 Mem

authors

Jones OD,Hulme SR,Abraham WC

doi

10.1016/j.nlm.2013.05.010

subject

Has Abstract

pub_date

2013-10-01 00:00:00

pages

31-9

eissn

1074-7427

issn

1095-9564

pii

S1074-7427(13)00091-9

journal_volume

105

pub_type

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