Article Figures & Data
Figures
- Fig. 1.
Long-term potentiation of EPSP induced by forskolin in BLA neurons. A, The amplitude of EPSP was plotted as a function of time. Bar denotes period of application of forskolin (25 μm). Insetshows superimposed records taken at different times as indicated. The EPSP was preceded by a transient hyperpolarizing current pulse (0.2 nA, 50 msec) passed through the recording electrode to monitor input resistance. B, Extracellular recordings of a typical biphasic potential, demonstrating that the latter event was sensitive to CNQX (10 μm). C, LTP of extracellularly recorded potentials induced by forskolin (25 μm).
- Fig. 2.
Effect of Sp-cAMPS on the EPSP. A, Application of Sp-cAMPS (25 μm) caused a depression of EPSP that returned to control level after washout of the drug without initiating LTP. B, The depression caused by Sp-cAMPS was prevented by IBMX (50 μm) and, in the presence of IBMX, Sp-cAMPS induced LTP.
- Fig. 3.
Blockade of Iso-induced potentiation by PKA inhibitors. Slices were incubated for at least 1 hr in 25 μm Rp-cAMPS or 1 μm KT 5720 before being transferred to the recording chamber where the same concentration of drugs was maintained. Iso-induced potentiation normally observed in control slices was blocked in the Rp-cAMPS- or KT 5720-treated slices.
- Fig. 4.
Antagonism of Iso- and forskolin-induced potentiation by 5-HT. Application of 5-HT (10 μm) reduced synaptic responses. Subsequent addition of Iso (15 μm) (A) or forskolin (25 μm) (B) in the presence of 5-HT failed to potentiate the EPSP.
- Fig. 5.
The effect of 5-HT is blocked by the selective 5-HT1A receptor antagonist and is mimicked by the selective 5-HT1A agonist. A, In the presence of NAN-190 (2 μm), 5-HT did not affect the EPSP significantly. Subsequent application of forskolin (25 μm) induced potentiation. Inset shows superimposed traces taken at the time points indicated.B, Application of 8-OH-DPAT (10 μm) mimicked 5-HT in reducing synaptic responses. Subsequent addition of forskolin (25 μm) in the presence of 8-OH-DPAT failed to potentiate the EPSP.
- Fig. 6.
Antagonism of Sp-cAMPS-induced LTP by 5-HT. Application of 5-HT (10 μm) depressed the EPSP. Subsequent application of Sp-cAMPS (25 μm) + IBMX (50 μm) failed to potentiate the EPSP.
- Fig. 7.
A rise in intraterminal Ca2+ is required for the Iso-induced potentiation. A, Superfusion of BAPTA-AM concentration-dependently depressed the EPSP and abolished Iso-induced potentiation. The amplitude of EPSP was plotted against time. Bars denote the periods of delivery of BAPTA-AM and 15 μm Iso. B, The effect of Iso was not affected by intracellular BAPTA. Electrodes were filled with BAPTA (50 mm) as described in Materials and Methods.
- Fig. 8.
Forskolin pretreatment did not affect the action of 5-HT. As forskolin (50 μm) was perfused into the bath, the amplitude of field potential gradually increased. Thirty minutes after application of forskolin, 5-HT (30 μm) was added, which still exerted an average of 61 ± 2% inhibition.
- Fig. 9.
Antagonistic effect of 5-HT on the forskolin-induced LTP is mimicked by adenosine A1 or GABAB receptor agonists. Application of CPA (0.5 μm) or baclofen (5 μm) depressed the EPSP. Subsequent addition of forskolin (25 μm) in the presence of these agonists failed to potentiate the EPSP.
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