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The Journal of Neuroscience, May 17, 2006, 26(20):5370-5382; doi:10.1523/JNEUROSCI.5255-05.2006

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Cellular/Molecular
GABAergic Network Activation of Glial Cells Underlies Hippocampal Heterosynaptic Depression

Alexandre Serrano, Nasser Haddjeri, Jean-Claude Lacaille, and Richard Robitaille

Centre de Recherche en Sciences Neurologiques et Département de Physiologie, Université de Montréal, Succursale Centre-Ville, Montréal, Québec, Canada H3C 3J7

Correspondence should be addressed to Dr. Richard Robitaille, Département de Physiologie, Faculté de Médecine, Université de Montréal, C.P. 6128 Succursale Centre-ville, Montréal, Québec, Canada H3C 3J7. Email: richard.robitaille{at}umontreal.ca

Tetanus-induced heterosynaptic depression in the hippocampus is a key cellular mechanism in neural networks implicated in learning and memory. A growing body of evidence indicates that glial cells are important modulators of synaptic functions, but very little is known about their role in heterosynaptic plasticity. We examined the role of glial cells in heterosynaptic depression, knowing that tetanization and NMDA application caused depression of synaptic field responses (fEPSPs) and induced Ca²⁺ rise in glial cells. Here we report that chelating Ca²⁺ in a glial syncytium interfered with heterosynaptic depression and NMDA-induced fEPSP depression, suggesting that Ca²⁺ activation of glial cells is necessary for heterosynaptic depression. The NMDA-induced Ca²⁺ rise in glial cells was sensitive to tetrodotoxin and reduced by the GABA_B antagonist CGP55845. Both heterosynaptic depression and simultaneous Ca²⁺ activation of glial cells were prevented by CGP55845, suggesting an involvement of the GABAergic network in glial activation and heterosynaptic depression. Also, the GABA_B agonist baclofen caused both a Ca²⁺ rise in glial cells and fEPSP depression. Heterosynaptic depression, as well as NMDA- and baclofen-induced depression, were attenuated by an A₁ antagonist, cyclopentyl-theophylline, whereas glial cell activation was not, indicating a role of adenosine downstream of glial activation. Finally, heterosynaptic depression requires ATP degradation because ectonucleotidase inhibitors reduced this plasticity. Our work indicates that Ca²⁺ activation of glial cells is necessary for heterosynaptic depression, which involves the sequential interaction of Schaffer collaterals, the GABAergic network, and glia. Thus, glial and neuronal networks are functionally associated during the genesis of heterosynaptic plasticity at mammalian central excitatory synapses.

Key words: neuron–glia interactions; heterosynaptic depression; GABA; GABA_B receptors; NMDA; adenosine

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Received June 30, 2005; revised April 10, 2006; accepted April 11, 2006.

Correspondence should be addressed to Dr. Richard Robitaille, Département de Physiologie, Faculté de Médecine, Université de Montréal, C.P. 6128 Succursale Centre-ville, Montréal, Québec, Canada H3C 3J7. Email: richard.robitaille{at}umontreal.ca

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