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Spatial regulation of coordinated excitatory and inhibitory synaptic plasticity at dendritic synapses.

Cell reports (2022-02-10)
Tiziana Ravasenga, Massimo Ruben, Vincenzo Regio, Alice Polenghi, Enrica Maria Petrini, Andrea Barberis
RESUMEN

The induction of synaptic plasticity at an individual dendritic glutamatergic spine can affect neighboring spines. This local modulation generates dendritic plasticity microdomains believed to expand the neuronal computational capacity. Here, we investigate whether local modulation of plasticity can also occur between glutamatergic synapses and adjacent GABAergic synapses. We find that the induction of long-term potentiation at an individual glutamatergic spine causes the depression of nearby GABAergic inhibitory synapses (within 3 μm), whereas more distant ones are potentiated. Notably, L-type calcium channels and calpain are required for this plasticity spreading. Overall, our data support a model whereby input-specific glutamatergic postsynaptic potentiation induces a spatially regulated rearrangement of inhibitory synaptic strength in the surrounding area through short-range heterosynaptic interactions. Such local coordination of excitatory and inhibitory synaptic plasticity is expected to influence dendritic information processing and integration.

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Nω-Nitro-L-arginine methyl ester hydrochloride, ≥97% (TLC), powder
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1(S),9(R)-(−)-Bicuculline methiodide, ≥95.0% (HPCE)
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KN-93, A cell-permeable, reversible and competitive inhibitor of rat brain CaM kinase II (Ki = 370 nM).
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KN-92, KN-92, CAS 1135280-28-2, is useful as a negative control for KN-93 (Cat. No. 422708), a Ca2+/CaM Kinase II inhibitor.