Figure - PMC

Skip to main content

An official website of the United States government

Here's how you know

Here's how you know

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

View full-text article in PMC

. 2015 Mar;145(3):225–251. doi: 10.1085/jgp.201411330

Search in PMC
Search in PubMed
View in NLM Catalog
Add to search

© 2015 Mlinar et al.

This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 3.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/3.0/).

PMC Copyright notice

Figure 9. — Extracellular Ca²⁺ is not required for autoinhibition. (A–D) Experiments in Ca²⁺-free extracellular solution. (A) Time course of a representative experiment (n = 6) illustrating the effect of 1 µM citalopram and its antagonism after the addition of 20 nM Way-100635 (+Way) in Ca²⁺-free extracellular solution, containing the cocktail of synaptic blockers: 5.5 mM [K⁺]_o, 0.5 µM TTX, 10 µM Tbz, and 10 µM Trp. (B) The current–voltage plot of the same experiment. Traces are averages of the last nine individual ramps recorded before citalopram application (Bsl), in citalopram (Cita), and after the addition of Way-100635 (Way; red trace). Downward shift of the trace in Way in respect to the Bsl was caused by the gradual increase in leak, typical for recordings in Ca²⁺-free extracellular solution. (C) Time course of a representative experiment (n = 3) in which 1 µM citalopram was applied 30 min before obtaining whole-cell recording configuration, permitting the completion of the experiment under leak-free conditions. (D) Scatter plot summarizing the magnitude of 5-HT_1A autoreceptor-mediated activation of GIRK conductance by 1 µM citalopram in Ca²⁺-free extracellular solution. Error bars correspond to mean ± SD. The addition of Way-100635 in the continuous presence of citalopram decreased inwardly rectifying K⁺ conductance by 2.86 ± 1.93 nS (mean ± SD; n = 9; P = 0.0011; one-tailed paired t test; normal distribution; P = 0.07; D’Agostino and Pearson omnibus test). (E–H) Experiments in the presence of the nonselective VGCC blocker Cd²⁺. (E) Time course of a representative experiment in extracellular solution containing the cocktail of synaptic blockers: 5.5 mM [K⁺]_o, 0.5 µM TTX, 10 µM Tbz, 10 µM Trp, and 100 µM CdCl₂. (F) The current–voltage plot of the same experiment. Traces are averages of 13 individual ramps recorded under the indicated conditions. (G) Current–voltage plot of net 5-HT1A autoreceptor-activated GIRK current (I_5-HT1A) of the same experiment. The trace in Way-100635 is shown in red. (H) Scatter plot summarizing the magnitude of 5-HT_1A autoreceptor-mediated activation of GIRK conductance by 1 µM citalopram in Cd²⁺-containing extracellular solution. Bars correspond to mean ± SD. The addition of 20 µM Way-100635 decreased inwardly rectifying K⁺ conductance by 2.66 ± 1.35 nS (mean ± SD; n = 8; P = 0.0004; one-tailed paired t test; normal distribution; P = 0.77; D’Agostino and Pearson omnibus test).