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. Author manuscript; available in PMC: 2016 May 1.
Published in final edited form as: Trends Neurosci. 2015 Apr 14;38(5):279–294. doi: 10.1016/j.tins.2015.03.003

Figure 4. Serotonin causes a 5-HT1BR-dependent potentiation of TA-CA1 synapses and this potentiation is altered by chronic stress.

Figure 4

A. fEPSPs are recorded in stratum lacunosum moleculare in response to stimulation of the TA pathway during application of the tricyclic antidepressant imipramine in control saline (black) or saline containing the 5-HT1BR antagonist isamoltane. Elevation of endogenous serotonin produces a doubling of synaptic strength. B. Activation of 5-HT1BRs with the selective agonist anpirtoline promotes action potential discharge in CA1 cells. C. Anpirtoline produces a robust and reversible potentiation of TA-CA1 excitatory postsynaptic currents in slices from unstressed control animals, but produces an enhanced and persistent potentiation in slices from rats subjected to chronic unpredictable stress. Modified with permission from Cai et al., 2013 [76].