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N-type voltage gated calcium channels mediate excitatory synaptic transmission in the anterior cingulate cortex of adult mice.

Kang SJ, Liu MG, Shi TY, Zhao MG, Kaang BK, Zhuo M - Mol Pain (2013)

Bottom Line: We also tested the effects of several neuromodulators with or without ω-Ctx-GVIA.We found that N-type VGCC contributed partially to (1S,3R)-1-aminocyclopentane-1,3-dicarboxylic acid- and (R)-Baclofen-induced synaptic inhibition.By contrast, the inhibitory effects of 2-Chloroadenosine and carbamoylcholine chloride did not differ with or without ω-Ctx-GVIA, indicating that they may act through other mechanisms.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Brain and Cognitive Sciences, College of Natural Sciences, Seoul National University, Seoul 151-746, South Korea. min.zhuo@utoronto.ca.

ABSTRACT
Voltage gated calcium channels (VGCCs) are well known for its importance in synaptic transmission in the peripheral and central nervous system. However, the role of different VGCCs in the anterior cingulate cortex (ACC) has not been studied. Here, we use a multi-electrode array recording system (MED64) to study the contribution of different types of calcium channels in glutamatergic excitatory synaptic transmission in the ACC. We found that only the N-type calcium channel blocker ω-conotoxin-GVIA (ω-Ctx-GVIA) produced a great inhibition of basal synaptic transmission, especially in the superficial layer. Other calcium channel blockers that act on L-, P/Q-, R-, and T-type had no effect. We also tested the effects of several neuromodulators with or without ω-Ctx-GVIA. We found that N-type VGCC contributed partially to (1S,3R)-1-aminocyclopentane-1,3-dicarboxylic acid- and (R)-Baclofen-induced synaptic inhibition. By contrast, the inhibitory effects of 2-Chloroadenosine and carbamoylcholine chloride did not differ with or without ω-Ctx-GVIA, indicating that they may act through other mechanisms. Our results provide strong evidence that N-type VGCCs mediate fast synaptic transmission in the ACC.

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Comparison of the effects of the N-type VGCC blocker in the superficial layer and deep layer of the ACC. A, The same slice as Figure 1A. Two channels (Ch. 30 from LII/III and Ch. 28 from LV/VI) are selected for further comparison. B, ω-Ctx GVIA (1 μM) was bath applied for 15 min (filled circle: Ch. 30; open circle: Ch. 28) in a single slice. Sample fEPSP recordings taken at the times indicated by the corresponding numbers are shown above the plot. Calibration: 500 μV, 20 ms. C, Averaged data of 5–7 activated channels in the superficial layer (filled circle: LII/III) and deep layer (open circle: LV/VI) in one slice. D, Pooled data of 7 mice (LII/III: 45.8 ± 4.4% of baseline, LV/VI: 59.6 ± 2.8% of baseline, n = 7 slices/7 mice, t(12) = −2.663, P = 0.021). ω-Ctx GVIA produced a stronger inhibition of superficial layer responses than those of the deep layer in the ACC. The horizontal bars indicate the period of drug application. Asterisk indicates the statistical significance between superficial layer and deep layer of the ACC slice. Error bars represent SEM.
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Figure 2: Comparison of the effects of the N-type VGCC blocker in the superficial layer and deep layer of the ACC. A, The same slice as Figure 1A. Two channels (Ch. 30 from LII/III and Ch. 28 from LV/VI) are selected for further comparison. B, ω-Ctx GVIA (1 μM) was bath applied for 15 min (filled circle: Ch. 30; open circle: Ch. 28) in a single slice. Sample fEPSP recordings taken at the times indicated by the corresponding numbers are shown above the plot. Calibration: 500 μV, 20 ms. C, Averaged data of 5–7 activated channels in the superficial layer (filled circle: LII/III) and deep layer (open circle: LV/VI) in one slice. D, Pooled data of 7 mice (LII/III: 45.8 ± 4.4% of baseline, LV/VI: 59.6 ± 2.8% of baseline, n = 7 slices/7 mice, t(12) = −2.663, P = 0.021). ω-Ctx GVIA produced a stronger inhibition of superficial layer responses than those of the deep layer in the ACC. The horizontal bars indicate the period of drug application. Asterisk indicates the statistical significance between superficial layer and deep layer of the ACC slice. Error bars represent SEM.

Mentions: To determine if the contribution of the N-type calcium channel to synaptic transmission varies according to the cortical layers, we compared the effect of ω-Ctx GVIA in different layers in the same slice. We selected two channels (Ch. 30 and 28) that had similar response size and shape in superficial and deep layer (layer V/VI) of the ACC, respectively (Figure 2A). Significant difference was detected in the reduction process and the inhibited level between the two channels after drug treatment (Ch. 30: 37.2% of baseline; Ch. 28: 51.2% of baseline; Figure 2B). The averaged data of 5–7 channels for one single slice (Figure 2C) and the pooled data of several mice demonstrate the same layer-related difference (superficial layer: 45.8 ± 4.4% of baseline, deep layer: 59.6 ± 2.8% of baseline, n = 7 slices/7 mice, t(12) = −2.663, P = 0.021; Figure 2D). These results suggest that N-type VGCCs mediate excitatory synaptic transmission in the ACC and there were differences between layers.


N-type voltage gated calcium channels mediate excitatory synaptic transmission in the anterior cingulate cortex of adult mice.

Kang SJ, Liu MG, Shi TY, Zhao MG, Kaang BK, Zhuo M - Mol Pain (2013)

Comparison of the effects of the N-type VGCC blocker in the superficial layer and deep layer of the ACC. A, The same slice as Figure 1A. Two channels (Ch. 30 from LII/III and Ch. 28 from LV/VI) are selected for further comparison. B, ω-Ctx GVIA (1 μM) was bath applied for 15 min (filled circle: Ch. 30; open circle: Ch. 28) in a single slice. Sample fEPSP recordings taken at the times indicated by the corresponding numbers are shown above the plot. Calibration: 500 μV, 20 ms. C, Averaged data of 5–7 activated channels in the superficial layer (filled circle: LII/III) and deep layer (open circle: LV/VI) in one slice. D, Pooled data of 7 mice (LII/III: 45.8 ± 4.4% of baseline, LV/VI: 59.6 ± 2.8% of baseline, n = 7 slices/7 mice, t(12) = −2.663, P = 0.021). ω-Ctx GVIA produced a stronger inhibition of superficial layer responses than those of the deep layer in the ACC. The horizontal bars indicate the period of drug application. Asterisk indicates the statistical significance between superficial layer and deep layer of the ACC slice. Error bars represent SEM.
© Copyright Policy - open-access
Related In: Results  -  Collection

License 1 - License 2
Show All Figures
getmorefigures.php?uid=PMC3842823&req=5

Figure 2: Comparison of the effects of the N-type VGCC blocker in the superficial layer and deep layer of the ACC. A, The same slice as Figure 1A. Two channels (Ch. 30 from LII/III and Ch. 28 from LV/VI) are selected for further comparison. B, ω-Ctx GVIA (1 μM) was bath applied for 15 min (filled circle: Ch. 30; open circle: Ch. 28) in a single slice. Sample fEPSP recordings taken at the times indicated by the corresponding numbers are shown above the plot. Calibration: 500 μV, 20 ms. C, Averaged data of 5–7 activated channels in the superficial layer (filled circle: LII/III) and deep layer (open circle: LV/VI) in one slice. D, Pooled data of 7 mice (LII/III: 45.8 ± 4.4% of baseline, LV/VI: 59.6 ± 2.8% of baseline, n = 7 slices/7 mice, t(12) = −2.663, P = 0.021). ω-Ctx GVIA produced a stronger inhibition of superficial layer responses than those of the deep layer in the ACC. The horizontal bars indicate the period of drug application. Asterisk indicates the statistical significance between superficial layer and deep layer of the ACC slice. Error bars represent SEM.
Mentions: To determine if the contribution of the N-type calcium channel to synaptic transmission varies according to the cortical layers, we compared the effect of ω-Ctx GVIA in different layers in the same slice. We selected two channels (Ch. 30 and 28) that had similar response size and shape in superficial and deep layer (layer V/VI) of the ACC, respectively (Figure 2A). Significant difference was detected in the reduction process and the inhibited level between the two channels after drug treatment (Ch. 30: 37.2% of baseline; Ch. 28: 51.2% of baseline; Figure 2B). The averaged data of 5–7 channels for one single slice (Figure 2C) and the pooled data of several mice demonstrate the same layer-related difference (superficial layer: 45.8 ± 4.4% of baseline, deep layer: 59.6 ± 2.8% of baseline, n = 7 slices/7 mice, t(12) = −2.663, P = 0.021; Figure 2D). These results suggest that N-type VGCCs mediate excitatory synaptic transmission in the ACC and there were differences between layers.

Bottom Line: We also tested the effects of several neuromodulators with or without ω-Ctx-GVIA.We found that N-type VGCC contributed partially to (1S,3R)-1-aminocyclopentane-1,3-dicarboxylic acid- and (R)-Baclofen-induced synaptic inhibition.By contrast, the inhibitory effects of 2-Chloroadenosine and carbamoylcholine chloride did not differ with or without ω-Ctx-GVIA, indicating that they may act through other mechanisms.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Brain and Cognitive Sciences, College of Natural Sciences, Seoul National University, Seoul 151-746, South Korea. min.zhuo@utoronto.ca.

ABSTRACT
Voltage gated calcium channels (VGCCs) are well known for its importance in synaptic transmission in the peripheral and central nervous system. However, the role of different VGCCs in the anterior cingulate cortex (ACC) has not been studied. Here, we use a multi-electrode array recording system (MED64) to study the contribution of different types of calcium channels in glutamatergic excitatory synaptic transmission in the ACC. We found that only the N-type calcium channel blocker ω-conotoxin-GVIA (ω-Ctx-GVIA) produced a great inhibition of basal synaptic transmission, especially in the superficial layer. Other calcium channel blockers that act on L-, P/Q-, R-, and T-type had no effect. We also tested the effects of several neuromodulators with or without ω-Ctx-GVIA. We found that N-type VGCC contributed partially to (1S,3R)-1-aminocyclopentane-1,3-dicarboxylic acid- and (R)-Baclofen-induced synaptic inhibition. By contrast, the inhibitory effects of 2-Chloroadenosine and carbamoylcholine chloride did not differ with or without ω-Ctx-GVIA, indicating that they may act through other mechanisms. Our results provide strong evidence that N-type VGCCs mediate fast synaptic transmission in the ACC.

Show MeSH
Related in: MedlinePlus