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. Author manuscript; available in PMC: 2009 Sep 17.
Published in final edited form as: J Neurophysiol. 2005 Jul 20;94(4):2867–2877. doi: 10.1152/jn.00465.2005

Fig. 5.

Fig. 5

Ionotropic glutamate receptors are not required for the induction of LLFR and N-methyl-D-aspartate (NMDA) or α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA)/kainate receptor activity alone is sufficient for the expression of LLFR. A1: scatterplot of reflex strength demonstrating that, in the presence of D-2-amino-5-phosphonovaleric acid (AP5), DOI is still capable of inducing LLFR (compare boxed regions). A2: graph showing mean reflex strength after DOI washout but still in the presence of AP5 (n = 3) expressed as a percentage of AP5 control (LLFR in 3/3, P < 0.05). B1: scatterplot of MK212-induced LLFR in the presence of bicuculline and AP5. B2: effect of MK212 or DOI on mean reflex strength (n = 12) after agonist washout but still in the presence of bicuculline/AP5, expressed as a percentage of bicuculline/AP5 control (LLFR in 7/12, P < 0.05). C1: scatterplot of DOI-induced LLFR in the presence of 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX). C2: effect of DOI on mean reflex strength after DOI washout but still in the presence of CNQX (n = 3) normalized to that observed in CNQX before DOI application (LLFR in 3/3, P < 0.05). D1: scatterplot showing actions of DOI in the in the presence of kynurenate. Note that the DOI-induced LLFR is only observed once kynurenate is removed from the bath (compare white boxes). D2: effect of DOI on reflex strength normalized to control, after washout of both DOI and kynurenate (LLFR in 4/4, P < 0.05).