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. Author manuscript; available in PMC: 2012 Oct 1.
Published in final edited form as: Trends Neurosci. 2011 Aug 17;34(10):536–547. doi: 10.1016/j.tins.2011.07.006

Fig. 1.

Fig. 1

Dopamine is required for late LTP in the CA1 region of the hippocampus in rodents. A. Under control conditions (closed black circles), robust LTP was induced after high frequency stimulation at time 0 min (as indicated by arrows) [14]. A significant reduction in LTP was observed in the presence of a D1 antagonist SCH23390 (open circles), and a complete absence of LTP induction in the presence of the NMDAR antagonist, APV (grey circles) [14]. Experiments were done in the acute slice preparation. B. Effect of SCH23390 on LTP measured in vivo [17]. C. Experiments in acute slice from D1 receptor knockout mouse (circles) and wild type controls (squares)[15]. LTP in the CA1 region of the hippocampus in D1-deficient mutant mice (circles) and wild-type (squares). Asterisks indicate statistically significant deviations (*, p< 0.05; ** p< 0.01) between the two groups at late stages of LTP. D. Block of late LTP by in vivo dopamine/noradrenaline depletion with 6-hyroxydopamine (open circles) is reversed by the addition of the D1 agonist, dihydrexidine (DHX) (black circles) [18]. The duration of potentiation in depleted animals is quite short, but consistent with the short potentiation after protein synthesis inhibition seen in some experiments [84]. Reproduced with permission from [14, 15, 17, 18], respectively.