The Journal of Neuroscience, May 17, 2006, ():
GABAergic Network Activation of Glial Cells Underlies Hippocampal Heterosynaptic Depression
J. Neurosci. Serrano et al.
26: 5370
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Supplemental figure 1. Model of interactions between GABAergic cells and glial cells in heterosynaptic depression. High frequency stimulation of Schaffer collaterals in the tetanized pathway (bottom, LTP) activates GABAergic cells through NMDA receptors (1). GABA released locally activates GABAB receptors on glial cells (2). Activation of GABAB receptors elicits a Ca2+ rise in glial cells (3). This GABAB-induced Ca2+-mediated activation of glial cells induces the release of ATP (4) which is degraded into adenosine, giving rise to A1 receptor-mediated presynaptic inhibition of Schaffer collaterals in the test pathway (5), and heterosynaptic depression (HSD). This glial-mediated phenomenon occurs in parallel, but with a slower time course, with the direct presynaptic GABAB modulation of glutamatergic synapses by GABAergic cells (dotted line).
