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. 1999:120:275-85.
doi: 10.1016/s0079-6123(08)63562-1.

An adenosine A3 receptor-selective agonist does not modulate calcium-activated potassium currents in hippocampal CA1 pyramidal neurons

T V Dunwiddie  1 , K A Jacobson, L Diao
Affiliations

An adenosine A3 receptor-selective agonist does not modulate calcium-activated potassium currents in hippocampal CA1 pyramidal neurons

T V Dunwiddie et al. Prog Brain Res. 1999.
No abstract available

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Figures

Fig. 1
Fig. 1
Effect of adenosine and Cl-IB-MECA on holding currents. Changes induced in current required to clamp CA1 hippocampal pyramidal neurons to −55 mV are indicated for groups of cells treated with identical drug superfusion protocols. Although not indicated, CPT + DMPX superfusion was maintained for at least 20 min prior to superfusion with adenosine or Cl-IB-MECA. CPT is an A1 selective antagonist with approximately 130X selectivity for A1 vs. A2A receptors and a K1 for A1 receptors of 11 nM (Bruns et al., 1986); DMPX has a K1 of 11 μM at A2A receptors and is 4–11 x selective forA2A vs. A1 (Ukena et al., 1986; Seale et al., 1988). Adenosine induced a highly significant outward change in the holding current (A) and this effect was blocked by CPT + DMPX Neither concentration of Cl-IB-MECA produced any change in the holding current in the presence of the A1/A2 receptor antagonists.
Fig. 2
Fig. 2
Effects of carbachol and isoproterenol on IAHP. Superfusion with 10 μM carbachol (A1) or with 500 nM isoproterenol (ISO; B1) rapidly blocked the currents evoked by a 150 ms depolarizing step to 0 mV. The amplitudes shown at the left correspond to the peak amplitude of the IAHP, or in the case of the inhibited responses, to the holding current at the time corresponding to the peak amplitude of IAHP prior to drug superfusion. The actual currents elicited by the depolarizing step are indicated at right (A2 and A1); the numbers in the figures at the left indicate the times at which the actual waveforms at the right were acquired.
Fig. 3
Fig. 3
Effects of Cl-IB-MECA and adenosine on IAHP amplitude. The time courses of changes in the amplitude of IAHP are shown at the left and averaged responses obtained at the indicated times at the right, as in Fig. 2. Neither concentration of Cl-IB-MECA had any significant effect on the response, but 50 μM adenosine depressed IAHP amplitude in a readily reversible fashion.
Fig. 4
Fig. 4
Average time course of the effects of Cl-IB-MECA and adenosine on IAHP amplitude. Groups of slices were superfused with drugs using identical treatment protocols, and the mean ± SEM response as a percentage of pre-drug response amplitude is illustrated. Adenosine induced a reversible depression of this response that was blocked by CPT + DMPX (A), whereas Cl-IB-MECA had no effect, either in the absence of inhibitors (Fig. 3A and B), or in slices pretreated with the A1/A2 inhibitors (B).
Fig. 5
Fig. 5
Average effects of drug superfusion on holding current and IAHP The mean ± SEM response for changes in the holding current (upper) and IAHP (lower) are shown. All of the effects observed with adenosine were completely antagonized by CPT + DMPX (**P < 0.01; hatched bars), whereas Cl-IB-MECA had no significant effect upon either measure, either alone or in combination with the combined antagonists.
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References

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