Limits...
Facilitation of synaptic transmission in the anterior cingulate cortex in viscerally hypersensitive rats.

Wang J, Zhang X, Cao B, Liu J, Li Y - Cereb. Cortex (2013)

Bottom Line: However, only a few reports have indicated the synaptic plasticity of ACC in vivo.In conclusion, we demonstrated for the first time that visceral hypersensitivity is associated with alterations of synaptic plasticity in the ACC.The ACC synaptic strengthening in chronic visceral pain may engage signal transduction pathways that are in common with those activated by electrical stimulation, and serves as an attractive cellular model of functional visceral pain.

View Article: PubMed Central - PubMed

Affiliation: Neuroscience Laboratory, Department of Biology and Chemistry, Centre for Biosystems, Neuroscience, and Nanotechnology, City University of Hong Kong, Hong Kong, China Key Laboratory of Biochip Technology, Shenzhen Biotech and Health Centre, City University of Hong Kong, Shenzhen 518057, PR China.

Show MeSH

Related in: MedlinePlus

Effect of CaMKII inhibitor and NR2B antagonist on ACC-LFP in control and VH rats. (A) Typical recordings of LFP in the ACC to different intensities of MT stimuli (200, 400, and 800 µA) in control and VH rats after application of vehicle (dotted line) and CaMKII inhibitor Antennapedia-CaMKIINtide (solid line). (B) Typical recordings of LFP in the ACC to different intensities of MT stimuli (200, 400, and 800 µA) after application of vehicle and NR2B receptor antagonist Ro25-6981 (solid line). (C) Application of Antennapedia-CaMKIINtide had no effect on ACC-LFP in control rats, whereas it significantly decreased ACC-LFP in VH rats compared with vehicle. (D) Application of Ro25-6981 significantly decreased ACC-LFP in VH rats compared with vehicle. No effects were observed in control rats. Results are presented as mean ± SEM. Statistical significance was determined by 2-way ANOVA, followed by multiple comparisons adjusted by the Bonferroni's test, *P < 0.05, **P < 0.01, ***P < 0.001.
© Copyright Policy - creative-commons
Related In: Results  -  Collection

License
getmorefigures.php?uid=PMC4379994&req=5

BHT273F3: Effect of CaMKII inhibitor and NR2B antagonist on ACC-LFP in control and VH rats. (A) Typical recordings of LFP in the ACC to different intensities of MT stimuli (200, 400, and 800 µA) in control and VH rats after application of vehicle (dotted line) and CaMKII inhibitor Antennapedia-CaMKIINtide (solid line). (B) Typical recordings of LFP in the ACC to different intensities of MT stimuli (200, 400, and 800 µA) after application of vehicle and NR2B receptor antagonist Ro25-6981 (solid line). (C) Application of Antennapedia-CaMKIINtide had no effect on ACC-LFP in control rats, whereas it significantly decreased ACC-LFP in VH rats compared with vehicle. (D) Application of Ro25-6981 significantly decreased ACC-LFP in VH rats compared with vehicle. No effects were observed in control rats. Results are presented as mean ± SEM. Statistical significance was determined by 2-way ANOVA, followed by multiple comparisons adjusted by the Bonferroni's test, *P < 0.05, **P < 0.01, ***P < 0.001.

Mentions: Previous studies have suggested that calcium/calmodulin-dependent protein kinase (CaMKII) binding to the NR2B receptor plays an important role in synaptic plasticity and memory formation (Lisman et al. 2002; Li et al. 2012). Here we showed that, in the control group, application of CaMKII inhibitor Ant-CaMK II Ntide (50 µM, n = 6, Fig. 3C) or NR2B receptor antagonist Ro25-6981(500 µM, n = 6, Fig. 3D) did not change the LFP amplitude in the ACC compared with vehicle in response to different intensities of MT stimuli. In contrast, in VH rats, microdialysis of Ant-CaMK II Ntide (50 µM, n = 6, Fig 3C) or NR2B receptor antagonist Ro25-6981(500 µM, n = 6, Fig 3D) both significantly reduced the LFP amplitude in the ACC compared with vehicle. Representative recording curves in response to different intensities of MT stimuli in control and VH rats with Ant-CaMK II Ntide or Ro25-6981 administration are shown in Figure 3A,B. This result demonstrated that both CaMKII and NR2B receptor activity participate in modulating the MT-ACC basal synaptic transmission in VH rats.Figure 3.


Facilitation of synaptic transmission in the anterior cingulate cortex in viscerally hypersensitive rats.

Wang J, Zhang X, Cao B, Liu J, Li Y - Cereb. Cortex (2013)

Effect of CaMKII inhibitor and NR2B antagonist on ACC-LFP in control and VH rats. (A) Typical recordings of LFP in the ACC to different intensities of MT stimuli (200, 400, and 800 µA) in control and VH rats after application of vehicle (dotted line) and CaMKII inhibitor Antennapedia-CaMKIINtide (solid line). (B) Typical recordings of LFP in the ACC to different intensities of MT stimuli (200, 400, and 800 µA) after application of vehicle and NR2B receptor antagonist Ro25-6981 (solid line). (C) Application of Antennapedia-CaMKIINtide had no effect on ACC-LFP in control rats, whereas it significantly decreased ACC-LFP in VH rats compared with vehicle. (D) Application of Ro25-6981 significantly decreased ACC-LFP in VH rats compared with vehicle. No effects were observed in control rats. Results are presented as mean ± SEM. Statistical significance was determined by 2-way ANOVA, followed by multiple comparisons adjusted by the Bonferroni's test, *P < 0.05, **P < 0.01, ***P < 0.001.
© Copyright Policy - creative-commons
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4379994&req=5

BHT273F3: Effect of CaMKII inhibitor and NR2B antagonist on ACC-LFP in control and VH rats. (A) Typical recordings of LFP in the ACC to different intensities of MT stimuli (200, 400, and 800 µA) in control and VH rats after application of vehicle (dotted line) and CaMKII inhibitor Antennapedia-CaMKIINtide (solid line). (B) Typical recordings of LFP in the ACC to different intensities of MT stimuli (200, 400, and 800 µA) after application of vehicle and NR2B receptor antagonist Ro25-6981 (solid line). (C) Application of Antennapedia-CaMKIINtide had no effect on ACC-LFP in control rats, whereas it significantly decreased ACC-LFP in VH rats compared with vehicle. (D) Application of Ro25-6981 significantly decreased ACC-LFP in VH rats compared with vehicle. No effects were observed in control rats. Results are presented as mean ± SEM. Statistical significance was determined by 2-way ANOVA, followed by multiple comparisons adjusted by the Bonferroni's test, *P < 0.05, **P < 0.01, ***P < 0.001.
Mentions: Previous studies have suggested that calcium/calmodulin-dependent protein kinase (CaMKII) binding to the NR2B receptor plays an important role in synaptic plasticity and memory formation (Lisman et al. 2002; Li et al. 2012). Here we showed that, in the control group, application of CaMKII inhibitor Ant-CaMK II Ntide (50 µM, n = 6, Fig. 3C) or NR2B receptor antagonist Ro25-6981(500 µM, n = 6, Fig. 3D) did not change the LFP amplitude in the ACC compared with vehicle in response to different intensities of MT stimuli. In contrast, in VH rats, microdialysis of Ant-CaMK II Ntide (50 µM, n = 6, Fig 3C) or NR2B receptor antagonist Ro25-6981(500 µM, n = 6, Fig 3D) both significantly reduced the LFP amplitude in the ACC compared with vehicle. Representative recording curves in response to different intensities of MT stimuli in control and VH rats with Ant-CaMK II Ntide or Ro25-6981 administration are shown in Figure 3A,B. This result demonstrated that both CaMKII and NR2B receptor activity participate in modulating the MT-ACC basal synaptic transmission in VH rats.Figure 3.

Bottom Line: However, only a few reports have indicated the synaptic plasticity of ACC in vivo.In conclusion, we demonstrated for the first time that visceral hypersensitivity is associated with alterations of synaptic plasticity in the ACC.The ACC synaptic strengthening in chronic visceral pain may engage signal transduction pathways that are in common with those activated by electrical stimulation, and serves as an attractive cellular model of functional visceral pain.

View Article: PubMed Central - PubMed

Affiliation: Neuroscience Laboratory, Department of Biology and Chemistry, Centre for Biosystems, Neuroscience, and Nanotechnology, City University of Hong Kong, Hong Kong, China Key Laboratory of Biochip Technology, Shenzhen Biotech and Health Centre, City University of Hong Kong, Shenzhen 518057, PR China.

Show MeSH
Related in: MedlinePlus