The NO-cGMP-PKG Signaling Pathway Coordinately Regulates ERK and ERK-Driven Gene Expression at Pre- and Postsynaptic Sites Following LTP-Inducing Stimulation of Thalamo-Amygdala Synapses

Figure 5

Pharmacological blockade of NMDAR-driven synaptic plasticity or NOS activation in the LA impairs ERK activation in both the LA and MGm/PIN following HFS, while blockade of extracellular NO impairs ERK activation in the MGm/PIN but not LA. (a) Placement of stimulation electrode and infusion cannula. (b) Schematic representation of the experimental protocol. Rats were given intra-LA infusion of the vehicle or drug (1 μg/side) followed 30 min later by HFS of the MGm/PIN. Rats were sacrificed at 5 min (for the LA group) or 30 min (for the MGm/PIN group) following stimulation. (c) Images of Western blots for phospho-ERK1/2 and associated GAPDH controls from LA (top) and MGm/PIN (bottom) samples. (d) Mean (±SEM) percent phospho-ERK1/2 immunoreactivity from LA punches taken from rats given intra-LA infusions of 50% DMSO (vehicle; 𝑛=5), 1 μg/side ifenprodil (𝑛=5), 7-Ni (𝑛=6) or c-PTIO (𝑛=5). (e) Mean (±SEM) percent phospho-ERK1/2 immunoreactivity from MGm/PIN punches taken from rats given intra-LA infusions of 50% DMSO (vehicle; 𝑛=5), 1 μg/side ifenprodil (𝑛=6), 7-Ni (𝑛=6) or c-PTIO (𝑛=5). For each figure, phospho-ERK1/2 levels have been normalized to total-ERK1/2 levels for each sample and counts on the ipsilateral side have been expressed as a percentage of those on the contralateral side.*𝑃<.05 relative to the ipsilateral side N.S. = not significant