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. Author manuscript; available in PMC: 2013 Feb 9.
Published in final edited form as: Neuron. 2012 Feb 9;73(3):497–510. doi: 10.1016/j.neuron.2011.11.023

Figure 3. Adrenergic metaplasticity can be primed and is independent of NMDAR.

Figure 3

(A-D) Priming the adrenergic suppression of LTP and LTD . (A) Experimental temporal scheme: the seal was made and ruptured after the 10 min agonist application (10μM Iso, or 5 μM Metx). The time course of the changes in NMDAR-mediated responses are depicted below (thin line). (B-D) Pairing at 0 and -40 mV induced respectively LTP (filled circles) and LTD (open circles) in control conditions (B), but no LTD when the cells were pretreated with isoproterenol (C), and no LTP after pretreatment with methoxamine (D). (E-F) The priming of the adrenergic suppression does not require co-activation of NMDA. Bath application of APV (50μM) at the time of the agonist application (E) does not affect the induction of LTP and LTD (F), nor it affects the suppression of LTD by isoproterenol (G) or LTP by nethoxamine (H). The number of experiments is indicated in parentheses. (I-K) the duration of the priming depends on agonist exposure. (I) LTD magnitude (measured 60 min after pairing) induced at different times after a 10 min isoproterenol exposure. Open circles: individual experiments; filled circles: averages for the time intervals (in min) 21<t<40, 41<t<60, 60<t100. (J-L) One-hour agonist exposure causes a long-lasting suppression of LTD and LTD. (J) Experimental diagram. (K, L) Individual experiments showing the magnitude of LTP (open triangles) and LTD (inverted triangles) induced after prolonged wash out of isoproterenol (K) or methoxamine (L). Filled triangles: experiments in which methoxamine or Isopropterenol were respectively applied (10 min) right before induction of LTD (K) or LTD (L).