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The net effect of interaction between glutamatergic and GABAergic signaling depends on location of glutamatergic input.

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posted on 19.02.2013 by Naomi Lewin, Emre Aksay, Colleen E. Clancy

(A) Schematic indicating location of synaptic inputs in simulations. 10 Hz glutamatergic pulses were applied either to proximal apical dendrites (in B) or basal dendrites (in C). A noisy input current was applied to a somatic compartment so that the probability of spiking in response to a glutamate pulse was less than 50%. For both (B) and (C), HFS of GABA receptors was applied to the soma and apical dendrites (for the duration indicated by the shaded box in B and C). (B) and (C) The probability of action potential firing within 10 ms of a glutamate pulse with GABA (gray circles) and without GABA (black circles) is plotted for 500 trials each, with the error bars representing the 95% confidence interval. During the initial fast hyperpolarization (region outlined by red boxes), HFS and consequent GABA activation completely inhibited action potential firing independently of glutamate input (grey circles). HFS resulting in GABA activation inhibits the response to apical glutamatergic input throughout its course (B), whereas the response to basal glutamatergic input is enhanced (C) (region outlined by green boxes). The slow depolarization following 400 ms of HFS enhanced the response to basal glumatergic input (C) more than apical glutamatergic input (B).

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