Brain activity changes in a monkey model of central post-stroke pain

Nagasaka, Kazuaki; Takashima, Ichiro; Matsuda, Keiji; Higo, Noriyuki

doi:10.1016/j.expneurol.2019.113096

Cited by 18 publications

(54 citation statements)

References 52 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…In order to functionally identify SI D2 as the target of focal chemogenetic silencing, we measured BOLD signal in response to sensory stimulation using 7T-MRI under light sedation with propofol (Figures 1A and S1A-S1C; STAR Methods). Consistent with previous studies (Arcaro et al, 2019;Chen et al, 2007;Cle ´ry et al, 2020;Dutta et al, 2014;Hayashi et al, 1999;Lipton et al, 2006;Nagasaka et al, 2020;Sharma et al, 2018;Wang et al, 2013), cutaneous tactile stimulation of hand D2 evoked a significant BOLD response at the contralateral SI (p < 0.05, FWE-corrected) (Figure 1B; STAR Methods). We then injected an AAV vector for the neuron-specific expression of inhibitory DREADD (hM4Di) with GFP as a marker protein into the identified SI D2 (Figure 1A).…”

Section: Resultssupporting

confidence: 91%

Section: Articlementioning

confidence: 99%

“…The upregulated foot sole representation raised the possibility that the same manipulation might also increase behavioral sensitivity to sensory stimulation of the contralateral foot (Nagasaka et al, 2017(Nagasaka et al, , 2020. To test this prediction, we applied a cold (10 C) stimulation, which is known to activate SI in both humans and macaques (Egan et al, 2005;Nagasaka et al, 2017), to the foot sole contralateral to the DREADD-expressing hemisphere, and examined whether focal silencing of the SI hand region behaviorally affects the withdrawal latency of the foot sole from the cold stimulation (Nagasaka et al, 2017(Nagasaka et al, , 2020. We found that the withdrawal latency of the contralateral foot sole from the cold stimulation was significantly shortened following DCZ administration (p < 0.001, paired t test) (Figure 5C, middle, magenta), suggesting that the inhibitory DREADD-induced upregulation of a distant body part representation indeed was accompanied by a corresponding behavioral hypersensitivity.…”

Section: Articlementioning

confidence: 99%

See 2 more Smart Citations

Chemogenetic sensory fMRI reveals behaviorally relevant bidirectional changes in primate somatosensory network

Hirabayashi¹,

Nagai²,

Hori³

et al. 2021

Neuron

View full text Add to dashboard Cite

show abstract

Section: Resultssupporting

confidence: 91%

Section: Articlementioning

confidence: 99%

Section: Articlementioning

confidence: 99%

See 1 more Smart Citation

Chemogenetic sensory fMRI reveals behaviorally relevant bidirectional changes in primate somatosensory network

Hirabayashi¹,

Nagai²,

Hori³

et al. 2021

Neuron

View full text Add to dashboard Cite

show abstract

“…A previous study using the same CPSP model monkeys reported that painful stimulation induced changes in the blood oxygenation level-dependent response in pain-related brain areas, including the posterior insular cortex, S2, anterior cingulate cortex (ACC), and amygdala 32 . Similar results were also reported in studies comparing pain response in healthy individuals and individuals with chronic pain 33 .…”

Section: Discussionmentioning

confidence: 99%

“…However, these drugs influence the activity of brain regions associated with pain. In this study, we used propofol as the anaesthetic, as in a recent fMRI study using primate CPSP models 32 . Propofol is considered to have few analgesic effects 39 ; however, we cannot ignore the effects of anaesthetics on the brain function.…”

Section: Discussionmentioning

confidence: 99%

Repetitive transcranial magnetic stimulation restores altered functional connectivity of central poststroke pain model monkeys

Kadono

Koguchi

Okada

et al. 2021

Sci Rep

View full text Add to dashboard Cite

Central poststroke pain (CPSP) develops after a stroke around the somatosensory pathway. CPSP is hypothesized to be caused by maladaptive reorganization between various brain regions. The treatment for CPSP has not been established; however, repetitive transcranial magnetic stimulation (rTMS) to the primary motor cortex has a clinical effect. To verify the functional reorganization hypothesis for CPSP development and rTMS therapeutic mechanism, we longitudinally pursued the structural and functional changes of the brain by using two male CPSP model monkeys (Macaca fuscata) developed by unilateral hemorrhage in the ventral posterolateral nucleus of the thalamus. Application of rTMS to the ipsilesional primary motor cortex relieved the induced pain of the model monkeys. A tractography analysis revealed a decrease in the structural connectivity in the ipsilesional thalamocortical tract, and rTMS had no effect on the structural connectivity. A region of interest analysis using resting-state functional magnetic resonance imaging revealed inappropriately strengthened functional connectivity between the ipsilesional mediodorsal nucleus of the thalamus and the amygdala, which are regions associated with emotion and memory, suggesting that this may be the cause of CPSP development. Moreover, rTMS normalizes this strengthened connectivity, which may be a possible therapeutic mechanism of rTMS for CPSP.

show abstract

Pharmacological inactivation of the primate posterior insular/secondary somatosensory cortices attenuates thermal hyperalgesia

Nagasaka

Takashima

Matsuda

et al. 2022

European Journal of Pain

Self Cite

View full text Add to dashboard Cite

Background: We previously established a macaque model of central post-stroke pain (CPSP) and confirmed the involvement of increased activity of the posterior insular cortex (PIC) and secondary somatosensory cortex (SII) to somatosensory stimuli in mechanical allodynia by a combination of imaging techniques with local pharmacological inactivation. However, it is unclear whether the same intervention would be effective for thermal hyperalgesia. Therefore, using the macaque model, we examined behavioural responses to thermal stimuli following pharmacological inactivation of the PIC/SII. Methods: Two CPSP model macaques were established based on collagenaseinduced unilateral hemorrhagic lesions in the ventral posterolateral nucleus of the thalamus. To evaluate pain perception, withdrawal latencies to thermal stimuli of 37, 45, 50, 52, and 55 °C to hands were measured. Several weeks after the lesion induction, pharmacological inactivation of the PIC/SII by microinjection of muscimol was performed. The effect of inactivation on withdrawal latency was assessed by comparison with withdrawal latency after vehicle injection. How to cite this article: Nagasaka, K., Takashima, I., Matsuda, K., & Higo, N. (2022). Pharmacological inactivation of the primate posterior insular/ secondary somatosensory cortices attenuates thermal hyperalgesia.

show abstract

Brain activity changes in a monkey model of central post-stroke pain

Cited by 18 publications

References 52 publications

Chemogenetic sensory fMRI reveals behaviorally relevant bidirectional changes in primate somatosensory network

Chemogenetic sensory fMRI reveals behaviorally relevant bidirectional changes in primate somatosensory network

Repetitive transcranial magnetic stimulation restores altered functional connectivity of central poststroke pain model monkeys

Pharmacological inactivation of the primate posterior insular/secondary somatosensory cortices attenuates thermal hyperalgesia

Contact Info

Product

Resources

About