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. Author manuscript; available in PMC: 2010 Jun 25.
Published in final edited form as: Neuron. 2009 Jun 25;62(6):826–838. doi: 10.1016/j.neuron.2009.05.011

Figure 2. PI-Coupled Receptor Activation and Release of Ca2+ from Internal Stores Is Necessary for NMDAR LTP Induction.

Figure 2

(A) Time graph of a representative experiment conducted in the presence of CPA (10 μM). Sample traces to the right show average NMDAR EPSCs before (1) and after (2) synaptic stimulation-burst pairing (top traces) and IK(Ca) with (black) and without (gray) synaptic stimulation (bottom traces). Note the lack of facilitation of IK(Ca) by synaptic stimulation.

(B) Summary time graph of experiments conducted in the presence of CPA (n = 6) and experiments where PI-coupled receptors were blocked during the induction, as indicated by the gray bar, with a cocktail containing the mGluR1 antagonist CPCCOEt (50–75 μM), the muscarinic acetylcholine receptor antagonist scopolamine (100 nM), and the α1-adrenergic receptor antagonist prazosin (1 μM) (n = 6).

(C) Summary graph depicting lack of significant facilitation of IK(Ca) by synaptic stimulation in CPA or during PI-coupled receptor blockade. Gray open circles indicate individual experiments; black squares represent mean.

Error bars indicate SEM.