Hone AJ , McIntosh JM .

R35 GM136430 NIGMS NIH HHS

	FIGURE 1. Ligand-binding promotes function of human α10 nAChRs expressed in X. laevis oocytes. Oocytes were injected with cRNA encoding human α10 subunits and treated for 3 days with frog saline or saline containing the indicated compounds then assessed by voltage-clamp electrophysiology for functional responses to acetylcholine (ACh; 1 mM). (A) Scatter plots of the data obtained under the indicated treatment conditions. (B) expanded data for oocytes injected with water, untreated (saline incubation only), and treated with saline containing ACh (5 mM) or α-Bgtx (1 μM). The noise amplitude recorded from oocytes injected with water was −1.7 ± 0.5 nA (n = 9). Oocytes injected with water containing cRNA for α10 subunits responded to ACh with current amplitudes that were −3.6 ± 2.8 nA (n = 32). Oocytes treated with STR (20 μM), BRU (20 μM) or MLA (20 μM) responded to ACh with current amplitudes that were significantly larger than those from controls; −735 ± 545 nA with a range of −76 to −2,378 nA (n = 28) for STR, −302 ± 225 nA with a range of −50 to −888 nA (n = 13) for BRU, and −813 ± 641 nA with a range of −146 to −2,443 nA (n = 16) for MLA. Oocytes treated with α-Bgtx, ACh, Cho, or Nic were −39 ± 21 nA (n = 9), −17 ± 11 nA (n = 13), −3.7 ± 1.5 nA (n = 10), and −6.0 ± 6.2 nA (n = 15), respectively. Currents from oocytes treated with α-Bgtx were slightly larger than saline controls, but there were no significant differences in current amplitudes recorded from oocytes treated with ACh, Cho or Nic compared to saline controls. (D) Example of a current trace from a control oocyte injected with water and stimulated with ACh. (D–K) Current traces from oocytes treated with the indicated ligand. The −5 nA scale bar applies to traces in (C,D), and (H–K) and the −150 nA scale bar applies to (E–G). The “±” and error bars indicate. The “n” indicates the number of oocytes obtained from 15 donors.
	FIGURE 2. Human α10 nAChR currents are smaller in the presence of Ba2+ compared to those in Ca2+. Oocytes were injected with cRNA encoding human α10 subunits and treated for 36 h with frog saline containing STR (20 μM) and assessed by voltage-clamp electrophysiology for functional responses to acetylcholine (ACh; 1 mM) in the presence of calcium or barium. (A) Current traces from an oocyte perfused with saline containing calcium (1.8 mM) then with saline where calcium was replaced with equimolar barium. The responses in the presence of barium were smaller than those recorded in the presence of calcium (−373 ± 273 nA vs. −301 ± 225 nA, respectively; n = 11). The experiment was repeated with sibling oocytes that had been incubated with 1 µM actinomycin-D (Actino-D) to inhibit RNA transcription. (B) Current traces from an oocyte treated with Actino-D and perfused with saline containing calcium (1.8 mM) then with saline where calcium was replaced with equimolar barium. (C) No differences in response amplitudes in the presence of calcium compared those recorded in the presence of barium (−186 ± 96 nA vs. −164 ± 96 nA, respectively; n = 14) were found in oocytes treated with Actino-D. The current traces in (A) and (B) are shown with the 30 s the interpulse intervals reduced to 5 s for brevity and the scale bar in (A) also applies to (B). The “±” and error bars indicate SD. The “n” indicates the number of oocytes obtained from two donors.
	FIGURE 3. Strychnine, BRU, and MLA produce differential effects on α10 nAChR functionality. X. laevis oocytes were injected with cRNA encoding human α10 subunits and treated for 3 days in frog saline containing MLA (20 μM), STR (20 μM), or BRU (20 μM) and assessed by voltage-clamp electrophysiology. (A) Current traces from an oocyte treated with MLA and stimulated with acetylcholine (ACh; 1 mM) immediately after being placed in the recording chamber. (B) Current traces from an oocyte treated with STR and stimulated with ACh immediately after being placed in the recording chamber. (C) The calculated plateau values indicated that currents from oocytes treated with MLA would decay to 12 (11–13) % (n = 8) of initial current amplitudes. (D) Similarly, currents from oocytes treated with BRU would decay to 15 (13–17) % (n = 8) of initial values. By contrast, oocytes treated with STR decayed to only 74 (72–76) % (n = 13) of initial values. Representative current traces for MLA and STR are shown with the 30 s interpulse intervals reduced to 5 s for brevity. The error bars in (C) and (D) indicate SD and values in parenthesis indicate 95% CI. The “n” indicates the number of oocytes obtained from five donors.
	FIGURE 4. Currents evoked by ACh are enhanced by acute exposure to STR, BRU, or MLA. X. laevis oocytes were injected with cRNA encoding human α10 subunits and incubated for 3–4 days with frog saline then assessed by voltage-clamp electrophysiology. (A) Oocytes incubated in saline were stimulated with acetylcholine (ACh; 1 mM) and acutely perfused with STR (20 μM) for 30 min. The responses to ACh before and after perfusion with STR were −6.0 ± 2.9 nA and −294 ± 149 nA (n = 7), respectively. The traces in red indicate control responses obtained prior to perfusion with STR. Current traces are shown with the 30 s interpulse intervals reduced to 5 s for brevity. (B) Methyllycaconitine enhanced responses to ACh in a concentration-dependent manner. Oocytes were stimulated with ACh and the current amplitudes monitored for changes in amplitude during continuous perfusion with MLA at the indicated concentrations. The responses in the presence of MLA (10 nM through 100 μM) were 108 ± 6%, 286 ± 68%, 431 ± 235%, 173 ± 119%, and 90 ± 33% (n = 5), respectively, of control values; responses in the presence of 1 μM were significantly larger than those in the presence of 10 nM MLA. (C) Brucine enhanced responses to ACh in a concentration-dependent manner. Oocytes were stimulated with ACh and the current amplitudes monitored for changes in amplitude during continuous perfusion with BRU at the indicated concentrations. The responses in the presence of BRU (100 nM through 300 μM) were 87 ± 16%, 246 ± 74%, 371 ± 101%, 260 ± 102%, and 168 ± 73% (n = 5), respectively, of control values; responses in the presence of 10 μM were significantly larger than those in the presence of 100 nM BRU. (D) Acetylcholine responses in oocytes treated with MLA were enhanced by acute perfusion with STR. Oocytes were stimulated with ACh and the current amplitudes monitored for changes in amplitude during continuous perfusion with STR at the indicated concentrations. The responses in the presence of STR (10 nM through 100 μM) were 92 ± 14%, 157 ± 31%, 278 ± 72%, 186 ± 51%, and 51 ± 17% (n = 4), respectively, of control values; responses in the presence of 1 μM were significantly larger than those in the presence of 10 nM STR. (E) Acetylcholine responses in oocytes treated with STR were inhibited by acute perfusion of STR. The responses in the presence of STR (10 nM through 100 μM) were 97 ± 2%, 91 ± 8%, 92 ± 12%, 71 ± 18%, and 12 ± 8% (n = 5), respectively, of control values; responses in the presence of 1 μM were no different than those in the presence of 10 nM STR. The estimated IC50 for STR was determined to be 20.2 (13.8–29.5) μM. The error bars and the “±” and indicate SD and values in parentheses indicate the 95% CI; “n” indicates the number of oocytes obtained from four donors; ns is not significant. Oocytes in (B,D) were incubated with saline containing MLA (20 μM), those in (C) with BRU (20 μM), and in (E) with STR (20 μM).
	FIGURE 5. Strychnine is an antagonist of human α9, α10, and α9α10 nAChRs expressed in X. laevis oocytes. Oocytes were injected with cRNA encoding either human α9 subunits or α10 subunits to form homomeric subtypes or with cRNA for α9 subunits and α10 subunits together (1:1) to form heteromeric α9α10 nAChRs. Oocytes were then incubated for 3–4 days prior to voltage-clamp electrophysiology. (A) Current traces from an oocyte, preincubated with saline containing 5 mM choline, expressing α9 nAChRs. The ACh-evoked currents after acute application of STR (20 μM) were 3 ± 3% (n = 5) of control values. (B) Current traces from an oocyte, preincubated with STR (20 μM), expressing α10 nAChRs; the ACh-evoked currents after acute application of STR (20 μM) were 52 ± 13% (n = 5) of control values. (C) Current traces from an oocyte, preincubated in saline, injected with cRNA for α9 and α10 nAChRs; the ACh-evoked currents after acute application of STR (20 μM) were 1.0 ± 0.5% (n = 5) of control values. Current traces are shown with the 30 s interpulse intervals reduced to 5 s for brevity, and the horizontal bars above the traces indicate a 5 min perfusion with saline containing STR. The “±” indicates the SD and “n” indicates the number of oocytes obtained from three donors.
	FIGURE 6. Choline enhances whereas STR inhibits functionality of human α9 nAChRs expressed in X. laevis oocytes. Oocytes were injected with cRNA encoding human α9 subunits and incubated for 3 days in frog saline or saline containing choline (5 mM) or STR (20 μM) and assessed by voltage-clamp electrophysiology for functional responses to acetylcholine (ACh; 100 μM). (A) A single 30 s current trace from a control oocyte incubated in frog saline. The oocytes responded to ACh with current amplitudes that were −9 ± 19 nA (n = 22). (B) Current amplitudes recorded from oocytes incubated with choline were −44 ± 47 nA (n = 25); a subset of this group of oocytes was incubated in frog saline containing STR (20 μM) for 24 h and reassessed for functional responses. The current amplitudes after exposure to STR were reduced to −2.1 ± 1.2 nA compared to −78 ± 44 nA (n = 5). (C) Similarly, oocytes incubated with STR for 3 days had ACh responses of −1.8 ± 1.2 nA (n = 17). (D) Scatter plot of the data for the experiments shown in (A–C). Current amplitudes from oocytes incubated with choline were significantly larger compared to saline controls. The current amplitude and duration scale-bars apply to all traces. The “±” and the error bars in (D) indicate SD. The “n” indicates the number of oocytes obtained from three donors.
	FIGURE 7. Currents evoked by acetylcholine (ACh; 1 mM) from oocytes expressing human α10 nAChRs are potently inhibited by α-Bgtx and α-Cbtx. X. laevis oocytes were injected with cRNA encoding human α10 subunits and incubated for 3–5 days in frog saline containing MLA (20 μM) or STR (20 μM) and assessed by voltage-clamp electrophysiology. (A) α-Bungarotoxin inhibited ACh-evoked responses with an IC50 of 21 (19–24) nM and the Hill slope was −1.0 (−1.1 to −0.9) (n = 5). (B) Current traces showing inhibition of ACh-evoked currents by α-Bgtx; the trace in red indicates a control response to ACh in the absence of α-Bgtx. (C) Graph showing the activities of select α-Ctxs, α-Cbtx, atropine, nicotine, MLA, and STR on human α10 nAChRs. The ACh responses in the presence of α-Ctx RgIA were 97 ± 8% (n = 5), 92 ± 9% (n = 9) for α-Ctx Vc1.1, and 97 ± 7% (n = 5) for α-Ctx PeIA. The responses in the presence of α-Cbtx were 3 ± 1% (n = 5). Responses in the presence of atropine, nicotine, MLA, and STR were 106 ± 7% (n = 7), 99 ± 8% (n = 5), 171 ± 71% (n = 8), and 203 ± 52% (n = 8), respectively. All ligands were tested at 10 μM. The parentheses indicate the 95% CI and the error bars in (A) and (C) indicate SD. The “n” indicates the number of oocytes obtained from nine donors. Oocytes in (A–B) were incubated with saline containing MLA (20 μM). In (C), all experiments were conducted on oocytes incubated with STR (20 μM) except those used for testing MLA and STR which were incubated in MLA (20 μM).
	FIGURE 8. Currents evoked by acetylcholine (ACh) from oocytes expressing human α9 or α9α10 nAChRs are inhibited by α-Ctx RgIA-5474, but those from oocytes expressing α10 nAChRs are not. (A) Traces showing inhibition of ACh-evoked (100 μM) currents by RgIA-5474 from an oocyte expressing α9 nAChRs. The responses in the presence of the peptide were 1.0 ± 0.4% (n = 5) of control values. (B) Traces from an oocyte expressing α10 nAChRs showing lack of inhibition by RgIA-5474 on ACh-evoked (1 mM) currents. The responses in the presence of the peptide were 100 ± 3% (n = 5) of control values. (C) Traces showing inhibition of ACh-evoked (100 μM) currents by RgIA-5474 from an oocyte expressing α9α10 nAChRs. The responses in the presence of the peptide were 3 ± 2% (n = 5) of control values. The horizontal bars above the current traces in (A–C) indicate perfusion with saline containing RgIA-5474 (50 nM). Current traces are shown with the 30 s interpulse intervals reduced to 5 s for brevity. The “±” indicates SD and “n” indicates the number of oocytes obtained from three donors. Oocytes in (A) were preincubated in saline containing choline (5 mM) and those in (B) with STR (20 μM) for 3 days.
	FIGURE 9. Acetylcholine (ACh) and choline, but not nicotine, evoke currents from oocytes expressing α10 nAChRs. X. laevis oocytes were injected with cRNA encoding human α10 subunits and incubated for 3–4 days in frog saline containing STR (20 μM) then assessed by voltage-clamp electrophysiology. (A) Concentration-response curve for acetylcholine, choline, and nicotine. The EC50 for activation of α10 nAChRs by ACh was 1.35 (1.15–1.58) mM and the Hill Slope was 1.1 (0.9–1.3) (n = 5). Choline was a partial agonist but evoked detectable currents only at 10 mM; the maximal response was 4 ± 2% (n = 5) of the calculated maximal response to ACh. Nicotine failed to induce detectable currents at concentrations up to 1 mM (n = 5). (B) Current traces evoked by 10 μM, 30 μM, 100 μM, 300 μM, 1 mM, 3 mM, and 10 mM ACh. (C) Current traces evoked by 100 μM, 1 mM, and 10 mM choline. (D) Current traces from an oocyte stimulated with 100 μM and 1 mM nicotine. All current traces in (B–D) were obtained from the same oocyte and are shown with the 35 s interpulse intervals reduced to 5 s for brevity. The current amplitude and time-scale bars apply to all traces in B-D. Values in parentheses indicate the 95% CI and the “±” indicates SD; “n” indicates the number of oocytes obtained from one donor.
	FIGURE 10. Acetylcholine-evoked currents from human homomeric α10 nAChRs desensitize faster relative to those from human α9α10 nAChRs. X. laevis oocytes were injected with cRNA encoding human α10 subunits and incubated in frog saline containing STR (20 μM) or with cRNAs for α9 plus α10 subunits, incubated in saline only, and subjected to voltage-clamp electrophysiology after 3 days. (A) Current traces from α10 nAChRs showing the response to a 15 s pulse of ACh in the presence of calcium (red) compared to barium (black). (B) The peak current amplitudes in response to ACh were −1,818 ± 1,329 nA (n = 5) in the presence of calcium and −1,430 ± 1,424 nA (n = 5) in the presence of barium. The responses decayed to −553 ± 396 nA or 31 ± 6% (n = 5) of peak amplitude at the end of the 15 s pulse of ACh in the presence of calcium. The responses decayed to −459 ± 375 nA or 35 ± 11% (n = 5) of peak amplitude at the end of the 15 s pulse of ACh in the presence of barium. (C) Current traces from α9α10 nAChRs showing the response to a 15 s pulse of ACh in the presence of calcium (red) compared to barium (black). (D) The peak current amplitudes in response to ACh were −484 ± 270 nA (n = 5) in the presence of calcium and −31 ± 40 nA (n = 5) in the presence of barium. The responses decayed to −154 ± 74 nA or 33 ± 4% (n = 5) of peak amplitude at the end of the 15 s pulse of ACh in the presence of calcium. The responses decayed to −23 ± 30 nA or 73 ± 8% (n = 5) of peak amplitude at the end of the 15 s pulse of ACh in the presence of barium. The inset shows expanded data for ACh-evoked currents obtained in the presence of barium. The “±” indicates SD and “n” indicates the number of oocytes obtained from two donors.

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