choline acetyltransferase cre dependent Search Results


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BFCN axon stimulation evokes nAChR- and mAChR-mediated postsynaptic responses in L6-PNs neurons within primary ACtx. A) Schematic of the experimental strategy. Cre-dependent ChR2 was injected into the caudal tail of the cholinergic basal forebrain in <t>ChAT-IRES-Cre(∆neo):Cdh23</t> mice ( n = 6 mice). BFCN axons in ACtx were optically stimulated (470 nm LED, 14 mW/mm 2 , 5 ms) and whole-cell current clamp recordings were obtained from L1-INs and L6-PNs. B) Pie chart summarizing BFCN-evoked PSPs. All L1-INs exhibited monosynaptic depolarizing PSPs, whereas L6-PNs displayed monosynaptic depolarizing, hyperpolarizing and biphasic PSPs. C) Top: example recordings in L1-INs and L6-PNs characterized by spiking patterns in response to intrinsic current pulses. Scale bar: 50 mV, 250 ms. Middle : BFCN-evoked PSPs (mean ± SD of 10 trials) recorded in the presence of AMPA and NMDA receptor blockers (DNQX, 20 μM; AP5, 50 μM). Bottom: PSPs were abolished by nAChR antagonists DHβE (10 μM) and MLA (10 μM) and by the mAChR antagonist atropine (10 μM). Scale bar: 5 mV, 500 ms. D) Depolarizing PSPs in L6-PNs (3.25 ± 0.45 mV) were significantly larger than those in L1-INs from the same slices (1.66 ± 0.28 mV) and were eliminated by nAChR antagonists DHβE and MLA (0.09 ± 0.03 mV). Wilcoxon test L1 vs L6: P = 0.012; Wilcoxon test L6 vs L6 DHβE + MLA: P = 0.0005. E) Hyperpolarizing PSPs in L6-PNs (−2.05 ± 0.21 mV) were abolished by atropine (Atr, 0.18 ± 0.09 mV). Paired t -test L6 vs Atr: P = 0.001. F) Biphasic PSPs in L6-PNs (2.15 ± 0.20 mV) were sequentially eliminated by DHβE + MLA (−2.27 ± 0.23 mV) and atropine (Atr, 0.12 ± 0.03 mV). RM-ANOVA with post-hoc Fisher’s comparison (F 2,8 = 139.60, P < 0.0001): L6 vs L6 DHβE + MLA ( P = 0.0002); L6 vs L6 DHβE + MLA + Atr ( P = 0.0004); L6 DHβE + MLA vs L6 DHβE + MLA + Atr ( P = 0.0005).
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endogenous choline acetyltransferase promoter  (Jackson Laboratory)
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BFCN axon stimulation evokes nAChR- and mAChR-mediated postsynaptic responses in L6-PNs neurons within primary ACtx. A) Schematic of the experimental strategy. Cre-dependent ChR2 was injected into the caudal tail of the cholinergic basal forebrain in <t>ChAT-IRES-Cre(∆neo):Cdh23</t> mice ( n = 6 mice). BFCN axons in ACtx were optically stimulated (470 nm LED, 14 mW/mm 2 , 5 ms) and whole-cell current clamp recordings were obtained from L1-INs and L6-PNs. B) Pie chart summarizing BFCN-evoked PSPs. All L1-INs exhibited monosynaptic depolarizing PSPs, whereas L6-PNs displayed monosynaptic depolarizing, hyperpolarizing and biphasic PSPs. C) Top: example recordings in L1-INs and L6-PNs characterized by spiking patterns in response to intrinsic current pulses. Scale bar: 50 mV, 250 ms. Middle : BFCN-evoked PSPs (mean ± SD of 10 trials) recorded in the presence of AMPA and NMDA receptor blockers (DNQX, 20 μM; AP5, 50 μM). Bottom: PSPs were abolished by nAChR antagonists DHβE (10 μM) and MLA (10 μM) and by the mAChR antagonist atropine (10 μM). Scale bar: 5 mV, 500 ms. D) Depolarizing PSPs in L6-PNs (3.25 ± 0.45 mV) were significantly larger than those in L1-INs from the same slices (1.66 ± 0.28 mV) and were eliminated by nAChR antagonists DHβE and MLA (0.09 ± 0.03 mV). Wilcoxon test L1 vs L6: P = 0.012; Wilcoxon test L6 vs L6 DHβE + MLA: P = 0.0005. E) Hyperpolarizing PSPs in L6-PNs (−2.05 ± 0.21 mV) were abolished by atropine (Atr, 0.18 ± 0.09 mV). Paired t -test L6 vs Atr: P = 0.001. F) Biphasic PSPs in L6-PNs (2.15 ± 0.20 mV) were sequentially eliminated by DHβE + MLA (−2.27 ± 0.23 mV) and atropine (Atr, 0.12 ± 0.03 mV). RM-ANOVA with post-hoc Fisher’s comparison (F 2,8 = 139.60, P < 0.0001): L6 vs L6 DHβE + MLA ( P = 0.0002); L6 vs L6 DHβE + MLA + Atr ( P = 0.0004); L6 DHβE + MLA vs L6 DHβE + MLA + Atr ( P = 0.0005).
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BFCN axon stimulation evokes nAChR- and mAChR-mediated postsynaptic responses in L6-PNs neurons within primary ACtx. A) Schematic of the experimental strategy. Cre-dependent ChR2 was injected into the caudal tail of the cholinergic basal forebrain in <t>ChAT-IRES-Cre(∆neo):Cdh23</t> mice ( n = 6 mice). BFCN axons in ACtx were optically stimulated (470 nm LED, 14 mW/mm 2 , 5 ms) and whole-cell current clamp recordings were obtained from L1-INs and L6-PNs. B) Pie chart summarizing BFCN-evoked PSPs. All L1-INs exhibited monosynaptic depolarizing PSPs, whereas L6-PNs displayed monosynaptic depolarizing, hyperpolarizing and biphasic PSPs. C) Top: example recordings in L1-INs and L6-PNs characterized by spiking patterns in response to intrinsic current pulses. Scale bar: 50 mV, 250 ms. Middle : BFCN-evoked PSPs (mean ± SD of 10 trials) recorded in the presence of AMPA and NMDA receptor blockers (DNQX, 20 μM; AP5, 50 μM). Bottom: PSPs were abolished by nAChR antagonists DHβE (10 μM) and MLA (10 μM) and by the mAChR antagonist atropine (10 μM). Scale bar: 5 mV, 500 ms. D) Depolarizing PSPs in L6-PNs (3.25 ± 0.45 mV) were significantly larger than those in L1-INs from the same slices (1.66 ± 0.28 mV) and were eliminated by nAChR antagonists DHβE and MLA (0.09 ± 0.03 mV). Wilcoxon test L1 vs L6: P = 0.012; Wilcoxon test L6 vs L6 DHβE + MLA: P = 0.0005. E) Hyperpolarizing PSPs in L6-PNs (−2.05 ± 0.21 mV) were abolished by atropine (Atr, 0.18 ± 0.09 mV). Paired t -test L6 vs Atr: P = 0.001. F) Biphasic PSPs in L6-PNs (2.15 ± 0.20 mV) were sequentially eliminated by DHβE + MLA (−2.27 ± 0.23 mV) and atropine (Atr, 0.12 ± 0.03 mV). RM-ANOVA with post-hoc Fisher’s comparison (F 2,8 = 139.60, P < 0.0001): L6 vs L6 DHβE + MLA ( P = 0.0002); L6 vs L6 DHβE + MLA + Atr ( P = 0.0004); L6 DHβE + MLA vs L6 DHβE + MLA + Atr ( P = 0.0005).
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BFCN axon stimulation evokes nAChR- and mAChR-mediated postsynaptic responses in L6-PNs neurons within primary ACtx. A) Schematic of the experimental strategy. Cre-dependent ChR2 was injected into the caudal tail of the cholinergic basal forebrain in <t>ChAT-IRES-Cre(∆neo):Cdh23</t> mice ( n = 6 mice). BFCN axons in ACtx were optically stimulated (470 nm LED, 14 mW/mm 2 , 5 ms) and whole-cell current clamp recordings were obtained from L1-INs and L6-PNs. B) Pie chart summarizing BFCN-evoked PSPs. All L1-INs exhibited monosynaptic depolarizing PSPs, whereas L6-PNs displayed monosynaptic depolarizing, hyperpolarizing and biphasic PSPs. C) Top: example recordings in L1-INs and L6-PNs characterized by spiking patterns in response to intrinsic current pulses. Scale bar: 50 mV, 250 ms. Middle : BFCN-evoked PSPs (mean ± SD of 10 trials) recorded in the presence of AMPA and NMDA receptor blockers (DNQX, 20 μM; AP5, 50 μM). Bottom: PSPs were abolished by nAChR antagonists DHβE (10 μM) and MLA (10 μM) and by the mAChR antagonist atropine (10 μM). Scale bar: 5 mV, 500 ms. D) Depolarizing PSPs in L6-PNs (3.25 ± 0.45 mV) were significantly larger than those in L1-INs from the same slices (1.66 ± 0.28 mV) and were eliminated by nAChR antagonists DHβE and MLA (0.09 ± 0.03 mV). Wilcoxon test L1 vs L6: P = 0.012; Wilcoxon test L6 vs L6 DHβE + MLA: P = 0.0005. E) Hyperpolarizing PSPs in L6-PNs (−2.05 ± 0.21 mV) were abolished by atropine (Atr, 0.18 ± 0.09 mV). Paired t -test L6 vs Atr: P = 0.001. F) Biphasic PSPs in L6-PNs (2.15 ± 0.20 mV) were sequentially eliminated by DHβE + MLA (−2.27 ± 0.23 mV) and atropine (Atr, 0.12 ± 0.03 mV). RM-ANOVA with post-hoc Fisher’s comparison (F 2,8 = 139.60, P < 0.0001): L6 vs L6 DHβE + MLA ( P = 0.0002); L6 vs L6 DHβE + MLA + Atr ( P = 0.0004); L6 DHβE + MLA vs L6 DHβE + MLA + Atr ( P = 0.0005).
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BFCN axon stimulation evokes nAChR- and mAChR-mediated postsynaptic responses in L6-PNs neurons within primary ACtx. A) Schematic of the experimental strategy. Cre-dependent ChR2 was injected into the caudal tail of the cholinergic basal forebrain in <t>ChAT-IRES-Cre(∆neo):Cdh23</t> mice ( n = 6 mice). BFCN axons in ACtx were optically stimulated (470 nm LED, 14 mW/mm 2 , 5 ms) and whole-cell current clamp recordings were obtained from L1-INs and L6-PNs. B) Pie chart summarizing BFCN-evoked PSPs. All L1-INs exhibited monosynaptic depolarizing PSPs, whereas L6-PNs displayed monosynaptic depolarizing, hyperpolarizing and biphasic PSPs. C) Top: example recordings in L1-INs and L6-PNs characterized by spiking patterns in response to intrinsic current pulses. Scale bar: 50 mV, 250 ms. Middle : BFCN-evoked PSPs (mean ± SD of 10 trials) recorded in the presence of AMPA and NMDA receptor blockers (DNQX, 20 μM; AP5, 50 μM). Bottom: PSPs were abolished by nAChR antagonists DHβE (10 μM) and MLA (10 μM) and by the mAChR antagonist atropine (10 μM). Scale bar: 5 mV, 500 ms. D) Depolarizing PSPs in L6-PNs (3.25 ± 0.45 mV) were significantly larger than those in L1-INs from the same slices (1.66 ± 0.28 mV) and were eliminated by nAChR antagonists DHβE and MLA (0.09 ± 0.03 mV). Wilcoxon test L1 vs L6: P = 0.012; Wilcoxon test L6 vs L6 DHβE + MLA: P = 0.0005. E) Hyperpolarizing PSPs in L6-PNs (−2.05 ± 0.21 mV) were abolished by atropine (Atr, 0.18 ± 0.09 mV). Paired t -test L6 vs Atr: P = 0.001. F) Biphasic PSPs in L6-PNs (2.15 ± 0.20 mV) were sequentially eliminated by DHβE + MLA (−2.27 ± 0.23 mV) and atropine (Atr, 0.12 ± 0.03 mV). RM-ANOVA with post-hoc Fisher’s comparison (F 2,8 = 139.60, P < 0.0001): L6 vs L6 DHβE + MLA ( P = 0.0002); L6 vs L6 DHβE + MLA + Atr ( P = 0.0004); L6 DHβE + MLA vs L6 DHβE + MLA + Atr ( P = 0.0005).
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Image Search Results


BFCN axon stimulation evokes nAChR- and mAChR-mediated postsynaptic responses in L6-PNs neurons within primary ACtx. A) Schematic of the experimental strategy. Cre-dependent ChR2 was injected into the caudal tail of the cholinergic basal forebrain in ChAT-IRES-Cre(∆neo):Cdh23 mice ( n = 6 mice). BFCN axons in ACtx were optically stimulated (470 nm LED, 14 mW/mm 2 , 5 ms) and whole-cell current clamp recordings were obtained from L1-INs and L6-PNs. B) Pie chart summarizing BFCN-evoked PSPs. All L1-INs exhibited monosynaptic depolarizing PSPs, whereas L6-PNs displayed monosynaptic depolarizing, hyperpolarizing and biphasic PSPs. C) Top: example recordings in L1-INs and L6-PNs characterized by spiking patterns in response to intrinsic current pulses. Scale bar: 50 mV, 250 ms. Middle : BFCN-evoked PSPs (mean ± SD of 10 trials) recorded in the presence of AMPA and NMDA receptor blockers (DNQX, 20 μM; AP5, 50 μM). Bottom: PSPs were abolished by nAChR antagonists DHβE (10 μM) and MLA (10 μM) and by the mAChR antagonist atropine (10 μM). Scale bar: 5 mV, 500 ms. D) Depolarizing PSPs in L6-PNs (3.25 ± 0.45 mV) were significantly larger than those in L1-INs from the same slices (1.66 ± 0.28 mV) and were eliminated by nAChR antagonists DHβE and MLA (0.09 ± 0.03 mV). Wilcoxon test L1 vs L6: P = 0.012; Wilcoxon test L6 vs L6 DHβE + MLA: P = 0.0005. E) Hyperpolarizing PSPs in L6-PNs (−2.05 ± 0.21 mV) were abolished by atropine (Atr, 0.18 ± 0.09 mV). Paired t -test L6 vs Atr: P = 0.001. F) Biphasic PSPs in L6-PNs (2.15 ± 0.20 mV) were sequentially eliminated by DHβE + MLA (−2.27 ± 0.23 mV) and atropine (Atr, 0.12 ± 0.03 mV). RM-ANOVA with post-hoc Fisher’s comparison (F 2,8 = 139.60, P < 0.0001): L6 vs L6 DHβE + MLA ( P = 0.0002); L6 vs L6 DHβE + MLA + Atr ( P = 0.0004); L6 DHβE + MLA vs L6 DHβE + MLA + Atr ( P = 0.0005).

Journal: Cerebral Cortex (New York, NY)

Article Title: Layer 6 is a hub for cholinergic modulation in the mouse auditory cortex

doi: 10.1093/cercor/bhaf338

Figure Lengend Snippet: BFCN axon stimulation evokes nAChR- and mAChR-mediated postsynaptic responses in L6-PNs neurons within primary ACtx. A) Schematic of the experimental strategy. Cre-dependent ChR2 was injected into the caudal tail of the cholinergic basal forebrain in ChAT-IRES-Cre(∆neo):Cdh23 mice ( n = 6 mice). BFCN axons in ACtx were optically stimulated (470 nm LED, 14 mW/mm 2 , 5 ms) and whole-cell current clamp recordings were obtained from L1-INs and L6-PNs. B) Pie chart summarizing BFCN-evoked PSPs. All L1-INs exhibited monosynaptic depolarizing PSPs, whereas L6-PNs displayed monosynaptic depolarizing, hyperpolarizing and biphasic PSPs. C) Top: example recordings in L1-INs and L6-PNs characterized by spiking patterns in response to intrinsic current pulses. Scale bar: 50 mV, 250 ms. Middle : BFCN-evoked PSPs (mean ± SD of 10 trials) recorded in the presence of AMPA and NMDA receptor blockers (DNQX, 20 μM; AP5, 50 μM). Bottom: PSPs were abolished by nAChR antagonists DHβE (10 μM) and MLA (10 μM) and by the mAChR antagonist atropine (10 μM). Scale bar: 5 mV, 500 ms. D) Depolarizing PSPs in L6-PNs (3.25 ± 0.45 mV) were significantly larger than those in L1-INs from the same slices (1.66 ± 0.28 mV) and were eliminated by nAChR antagonists DHβE and MLA (0.09 ± 0.03 mV). Wilcoxon test L1 vs L6: P = 0.012; Wilcoxon test L6 vs L6 DHβE + MLA: P = 0.0005. E) Hyperpolarizing PSPs in L6-PNs (−2.05 ± 0.21 mV) were abolished by atropine (Atr, 0.18 ± 0.09 mV). Paired t -test L6 vs Atr: P = 0.001. F) Biphasic PSPs in L6-PNs (2.15 ± 0.20 mV) were sequentially eliminated by DHβE + MLA (−2.27 ± 0.23 mV) and atropine (Atr, 0.12 ± 0.03 mV). RM-ANOVA with post-hoc Fisher’s comparison (F 2,8 = 139.60, P < 0.0001): L6 vs L6 DHβE + MLA ( P = 0.0002); L6 vs L6 DHβE + MLA + Atr ( P = 0.0004); L6 DHβE + MLA vs L6 DHβE + MLA + Atr ( P = 0.0005).

Article Snippet: Experimental model. All experiments were carried out in mice generated by crossing ChAT-IRES-Cre(∆neo) males (RRID: IMSR_JAX:031661 ) with Cdh23 females (RRID: IMSR_JAX:018399 ), both obtained from the Jackson Laboratory.

Techniques: Injection, Comparison