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Publication : Age-dependent remodelling of inhibitory synapses onto hippocampal CA1 oriens-lacunosum moleculare interneurons.

First Author  Salesse C Year  2011
Journal  J Physiol Volume  589
Issue  Pt 20 Pages  4885-901
PubMed ID  21825029 Mgi Jnum  J:189386
Mgi Id  MGI:5445462 Doi  10.1113/jphysiol.2011.215244
Citation  Salesse C, et al. (2011) Age-dependent remodelling of inhibitory synapses onto hippocampal CA1 oriens-lacunosum moleculare interneurons. J Physiol 589(Pt 20):4885-901
abstractText  Stratum oriens-lacunosum moleculare interneurons (O-LM INs) represent the major element of the hippocampal feedback inhibitory circuit, which provides inhibition to the distal dendritic sites of CA1 pyramidal neurons. Although the intrinsic conductance profile and the properties of glutamatergic transmission to O-LM INs have become a subject of intense investigation, far less is known about the properties of the inhibitory synapses formed onto these cells. Here, we used whole-cell patch-clamp recordings in acute mouse hippocampal slices to study the properties and plasticity of GABAergic inhibitory synapses onto O-LM INs. Surprisingly, we found that the kinetics of inhibitory postsynaptic currents (IPSCs) were slower in mature synapses (P26-40) due to the synaptic incorporation of the alpha5 subunit of the GABA(A) receptor (a5-GABA(A)R). Moreover, this age-dependent synaptic expression of a5-GABA(A)Rs was directly associated with the emergence of long-term potentiation at IN inhibitory synapses. Finally, the slower time course of IPSCs observed in O-LM INs of mature animals had a profound effect on IN excitability by significantly delaying its spike firing. Our data suggest that GABAergic synapses onto O-LM INs undergo significant modifications during postnatal maturation. The developmental switch in IPSC properties and plasticity is controlled by the synaptic incorporation of the a5-GABA(A)R subunit and may represent a potential mechanism for the age-dependent modifications in the inhibitory control of the hippocampal feedback inhibitory circuit.
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