GABAergic Network Activation of Glial Cells Underlies Hippocampal Heterosynaptic Depression

• DOI: 10.1523/jneurosci.5255-05.2006
• Publication Date: 2006-05-18T00:19:27Z
• Authors: Alexandre Serrano; Nasser Haddjeri; Jean-Claude Lacaille; Richard Robitaille
• Keywords: Long-term depression

Tetanus-induced heterosynaptic depression in the hippocampus is a key cellular mechanism neural networks implicated learning and memory. A growing body of evidence indicates that glial cells are important modulators synaptic functions, but very little known about their role plasticity. We examined depression, knowing tetanization NMDA application caused field responses (fEPSPs) induced Ca 2+ rise cells. Here we report chelating syncytium interfered with NMDA-induced fEPSP suggesting activation necessary for depression. The was sensitive to tetrodotoxin reduced by GABA B antagonist CGP55845 . Both simultaneous were prevented , an involvement GABAergic network Also, agonist baclofen both Heterosynaptic as well NMDA- baclofen-induced attenuated 1 antagonist, cyclopentyl-theophylline, whereas cell not, indicating adenosine downstream activation. Finally, requires ATP degradation because ectonucleotidase inhibitors this Our work which involves sequential interaction Schaffer collaterals, network, glia. Thus, neuronal functionally associated during genesis plasticity at mammalian central excitatory synapses.