scholarly journals Meditation reduces pain-related neural activity in the anterior cingulate cortex, insula, secondary somatosensory cortex, and thalamus

2014 ◽  
Vol 5 ◽  
Author(s):  
Hiroki Nakata ◽  
Kiwako Sakamoto ◽  
Ryusuke Kakigi
2019 ◽  
Vol 316 (5) ◽  
pp. G615-G622
Author(s):  
Patrick Sanvanson ◽  
Zhixin Li ◽  
Ling Mei ◽  
Venelin Kounev ◽  
Mark Kern ◽  
...  

Esophageal acid sensory signals are transmitted by both vagal and spinal pathways to the cerebral cortex. The influence and interplay of these pathways on esophageal acid-related functional connectivity has been elusive. Our aim was to evaluate the esophageal acid exposure-related effect on the anterior cingulate cortex (ACC) functional connectivity networks using functional MRI-guided functional connectivity MRI (fcMRI) analysis. We studied six Sprague-Dawley rats for fcMRI experiments under dexmedetomidine hydrochloride anesthesia. Each rat was scanned for 6 min before and after esophageal hydrochloric acid infusion (0.1 N, 0.2 ml/min). The protocol was repeated before and after bilateral cervical vagotomy on the same rat. Seed-based fcMRI analysis was used to examine ACC networks and acid-induced network alterations. Three-factor repeated-measures ANOVA analysis among all four subgroups revealed that the interaction of acid infusion and bilateral vagotomy was mainly detected in the hypothalamus, insula, left secondary somatosensory cortex, left parietal cortex, and right thalamus in the left ACC network. In the right ACC network, this interaction effect was detected in the caudate putamen, insula, motor, primary somatosensory cortex, secondary somatosensory cortex, and thalamic regions. These regions in the ACC networks showed decreased intranetwork connectivity due to acid infusion. However, after bilateral vagotomy, intranetwork connectivity strength inversed and became stronger following postvagotomy acid infusion. Signals transmitted through both the vagal nerve and spinal nerves play a role in esophageal acid-related functional connectivity of the ACC. The vagal signals appear to dampen the acid sensation-related functional connectivity of the ACC networks. NEW & NOTEWORTHY These studies show that esophageal acid-induced brain functional connectivity changes are vagally mediated and suggest that signals transmitted through both the vagal nerve and spinal nerves play a role in esophageal acid-related functional connectivity of the anterior cingulate cortex. This paper focuses on the development of a novel rat functional MRI model fostering improved understanding of acid-related esophageal disorders.


2009 ◽  
Vol 65 ◽  
pp. S190-S191
Author(s):  
Koji Toda ◽  
Takashi Mizuhiki ◽  
Yasuko Sugase-Miyamoto ◽  
Kiyonori Inaba ◽  
Shigeru Ozaki ◽  
...  

2020 ◽  
Author(s):  
Han Lu ◽  
Júlia V. Gallinaro ◽  
Claus Normann ◽  
Stefan Rotter ◽  
Ipek Yalcin

AbstractSynapse formation and network rewiring is key to build neural circuits during development and has been widely observed in adult brains. Maintaining neural activity with the help of synaptic plasticity is essential to enable normal brain function. The model of homeostatic structural plasticity (HSP) was proposed to reflect the homeostatic regulation of neural activity and explain structural changes seen after perturbations. However, the specific temporal profile of such plastic responses has not yet been elucidated in experiments. To address this issue, we combined computational modeling and mouse optogenetic stimulation experiments. Our model predicted that within 48 h post-stimulation, neural activity returns to baseline, while the connectivity among stimulated neurons follows a very specific transient increase and decrease. To capture such dynamics experimentally in vivo, we activated the pyramidal neurons in the anterior cingulate cortex of mice and harvested their brains at 1.5 h, 24 h, and 48 h post-stimulation. Cortical hyperactivity as demonstrated by robust c-Fos expression persisted up to 1.5 h and decayed to baseline after 24 h. However, spine density and spine head volume were increased at 24 h and decreased at 48 h. Synaptic proteins VGLUT1 and PSD-95 were also upregulated and downregulated at 24 h and 48 h, respectively, while the calmodulin-binding protein neurogranin was translocated from the soma to the dendrite. Additionally, lasting astrocyte reactivation and microglia proliferation were observed, suggesting a role of neuron-glia interaction. All this corroborates the interpretation of our experimental results in terms of homeostatic structural plasticity. Our results bring important insights of how external stimulation modulates synaptic plasticity and behaviors.Significance StatementWe combined both computational modeling and mouse experiments to clarify the temporal dynamics of structural and functional homeostatic plasticity in response to external stimulation. We observed the biphasic regulation of spine density, spine head volume, and synaptic proteins at 24 h and 48 h after the optogenetic stimulation of the anterior cingulate cortex, when the neural activity was restored to the homeostatic level. The orchestrated regulation of presynaptic VGLUT1 and postsynaptic PSD-95, as well as the soma-dendrites translocation of neurogranin, suggested an elaborate molecular mechanism underlying homeostatic structural plasticity. Our experimental results thus corroborated the theoretical concept of homeostatic structural plasticity and revealed the temporal evolution of structural and functional plasticity.


Neurosurgery ◽  
2017 ◽  
Vol 64 (CN_suppl_1) ◽  
pp. 230-230 ◽  
Author(s):  
Shaheen Ahmed ◽  
Sven Vanneste

Abstract INTRODUCTION Minimally invasive neuromodulation such as spinal cord stimulation (SCS) and occipital nerve stimulation (ONS) have shown to be successful for treatment of different types of pain such as chronic back or leg pain, complex regional pain syndrome (CRPS), and fibromyalgia. Recently, novel stimulation paradigm called burst stimulation was developed that suppresses pain to better extent than classical tonic stimulation. From clinical point of view, burst stimulation is very promising; however, little is known about its underlying mechanism. Hence, in this work we investigate mechanism of action for burst stimulation in different patient groups and controls using different neuroimaging multimodalities such as EEG, fMRI and PET. METHODS Control subjects and patients with chronic back or leg pain, CRPS, or fibromyalgia enrolled for study. Both controls and patients received SCS or ONS and sham, tonic, and burst stimulation in fMRI, PET, and EEG. RESULTS >EEG shows significant changes for burst stimulation compared to tonic and sham stimulation; evident by increased activity at dorsal anterior cingulate cortex (dACC), dorsolateral prefrontal cortex (dPFC), primary somatosensory cortex, and posterior cingulate cortex (PSC) in alpha frequency band. PET further confirmed by showing increased tracer capitation for burst in dACC, pregenual anterior cingulate cortex (pgACC), parahippocampus, and fusiform gyrus. Furthermore, fMRI showed burst changes in dACC, dPFC, pgACC, cerebellum, hypothalamus, and premotor cortex. A conjunction analysis between tonic and burst stimulation demonstrated theta activity is commonly modulated in somatosensory cortex and PSC. CONCLUSION Our data suggest that burst and tonic stimulation modulate ascending lateral and descending pain inhibitory pathways. Burst stimulation adds by modulating the medial pain pathway, possibly by direct modulation of spinothalamic pathway, as suggested by animal research. Burst normalizes an imbalance between ascending pain via medial system and descending pain inhibitory activity, which could be a plausible reason it's better than to tonic stimulation.


eLife ◽  
2022 ◽  
Vol 11 ◽  
Author(s):  
Siddhartha Joshi ◽  
Joshua I Gold

Ascending neuromodulatory projections from the locus coeruleus (LC) affect cortical neural networks via the release of norepinephrine (NE). However, the exact nature of these neuromodulatory effects on neural activity patterns in vivo is not well understood. Here we show that in awake monkeys, LC activation is associated with changes in coordinated activity patterns in the anterior cingulate cortex (ACC). These relationships, which are largely independent of changes in firing rates of individual ACC neurons, depend on the type of LC activation: ACC pairwise correlations tend to be reduced when ongoing (baseline) LC activity increases but enhanced when external events evoke transient LC responses. Both relationships covary with pupil changes that reflect LC activation and arousal. These results suggest that modulations of information processing that reflect changes in coordinated activity patterns in cortical networks can result partly from ongoing, context-dependent, arousal-related changes in activation of the LC-NE system.


Sign in / Sign up

Export Citation Format

Share Document