Presynaptic CaMKII is necessary for synaptic plasticity in cultured hippocampal neurons.

Abstract:

:Calcium/calmodulin-dependent protein kinase II (CaMKII) is a multifunctional enzyme that is very critical for synaptic plasticity and memory formation. Although significant progress has been made in understanding the role of postsynaptic CaMKII in synaptic plasticity, very little is known about its presynaptic function during plasticity changes. Here we report that KN-93, a membrane-permeable CaMKII inhibitor, blocked glutamate-induced increases in the frequency of miniature excitatory postsynaptic currents (mEPSCs) and the number of presynaptic functional boutons in cultured hippocampal pyramidal neurons. In addition, presynaptic injection of the membrane-impermeable CaMKII inhibitor peptide 281-309 blocked synaptic plasticity induced by tetanus, glutamate, or NO/cGMP pathway activation as expressed by long-lasting increases in EPSC amplitude and functional presynaptic boutons. Presynaptic injection of CaMKII itself coupled with weak tetanus produced an immediate and long-lasting enhancement of EPSC amplitude. Thus, the present results conclusively prove that presynaptic CaMKII is essential for synaptic plasticity in cultured hippocampal neurons.

journal_name

Neuron

journal_title

Neuron

authors

Ninan I,Arancio O

doi

10.1016/s0896-6273(04)00143-6

subject

Has Abstract

pub_date

2004-04-08 00:00:00

pages

129-41

issue

1

eissn

0896-6273

issn

1097-4199

pii

S0896627304001436

journal_volume

42

pub_type

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