Figure 7.

NMDA increases nociceptive spiking in meningeal trigeminal afferents: (A) Sample traces of spontaneous multiple unit activity (MUA) in control (top) and in the presence of NMDA (100 μM with 30 µM glycine) in magnesium free solution (bottom); (B) The time-course of frequency of nociceptive spikes (2 min binning) during 4 min recording in control (before agonist) and during application of NMDA (100 µM, 10 min); (C) Cluster analysis of nociceptive spikes in control and in the presence of NMDA. Spike’s positive phase amplitudes (abscissa) are plotted vs. negative phase amplitudes in arbitrary units (a.u.) (ordinate) to confirm clusters compactness. Color contours outline spike clusters separated by KlustaKwik method. Notice that green MUA increased in numbers whereas black dots (initially the silent cluster) appeared during NMDA application. Insets show average shapes; (D) Example of the time-course of spike frequency for the responder and non-responder clusters before and after NMDA application; (E) Sample traces of spontaneous MUA in control (top) and in the presence of NMDA (100 μM with 30 µM glycine) in basic ACSF solution (bottom); (F) The time-course of frequency of nociceptive spikes (2 min binning) during 4 min recording in control (before agonist) and during application of NMDA (100 µM, 10 min) in basic ACSF solution. * p < 0.05.