Remodeling of Neuronal Circuits After Reach Training in Chronic Capsular Stroke

Cho, Jongwook; Kwon, Dae‐Hyuk; Kim, Ra Gyung; Song, Hanlim; Rosa‐Neto, Pedro; Lee, Min-Cheol; Kim, Hyoung-Ihl

doi:10.1177/1545968316650282

Cited by 13 publications

(22 citation statements)

References 33 publications

(37 reference statements)

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“…The mechanisms underlying this spontaneous behavioural recovery are not well understood, but such recovery is frequently attributed to spontaneous repair and restoration at the CNS level. For example, it may involve the resolution of acute dysfunction in neural activity and cellular metabolism in regions connected to the injury site 182,183 , the return of more-normal blood flow in peri-infarct tissue 184 and the reorganization of the connectivity patterns of surviving neurons 106 .…”

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confidence: 99%

Motor compensation and its effects on neural reorganization after stroke

2017

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Stroke instigates a dynamic process of repair and remodelling of remaining neural circuits, and this process is shaped by behavioural experiences. The onset of motor disability simultaneously creates a powerful incentive to develop new, compensatory ways of performing daily activities. Compensatory movement strategies that are developed in response to motor impairments can be a dominant force in shaping post-stroke neural remodelling responses and can have mixed effects on functional outcome. The possibility of selectively harnessing the effects of compensatory behaviour on neural reorganization is still an insufficiently explored route for optimizing functional outcome after stroke.

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Section: Figure 1 |mentioning

confidence: 99%

Motor compensation and its effects on neural reorganization after stroke

2017

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“…Using an established microPET protocol, animals were injected with CLZ and F 18-FDG (100 mCi/100 g) through the tail vein during brief isoflurane anesthesia, followed by a 30-minute uptake period. Then, static PET scans (25 minutes) and attenuation-correction computerized tomography (5 minutes) were performed with an Inveon PET/CT scanner 24 (Siemens Medical Solutions, TN, USA) ( Fig. 1b).…”

Section: Clz-induced Metabolic and Behavioral Changes In Naive Ratsmentioning

confidence: 99%

“…After a 30-minute uptake period, rats were anesthetized with 2% isoflurane and placed in the microPET scanner under head fixation. We then performed a 25-minute static PET scan and a 5-minute attenuation-correction computed tomography (CT) scan 24 . After completing the microPET/CT scans, the acquired images were reconstructed with a 3-D OSEM/MAP iterative algorithm.…”

Section: Viral Vector Injectionmentioning

confidence: 99%

“…Recently invasive and noninvasive neuromodulatory techniques, including transcranial magnetic stimulation (TMS), transcranial direct current stimulation (tDCS), and epidural cortical stimulation (ECS), have been used to modulate cortical excitability and induce neuronal plasticity in motor or sensory cortex [20][21][22][23] . In particular, neuromodulation of somatosensory cortex may rescue post-stroke deficits in a rodent model of subcortical capsular infarct 24,25 . However, DREADD-driven chemogenetic neuromodulation has not yet been attempted in the cortex.…”

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Optimizing clozapine for chemogenetic neuromodulation of somatosensory cortex

Cho

Ryu

Lee

et al. 2020

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clozapine (cLZ) has been proposed as an agonist for Designer Receptors exclusively Activated by Designer Drugs (DREADDs), to replace Clozapine-N-oxide (CNO); however, there are no reliable guidelines for the use of cLZ for chemogenetic neuromodulation. We titrated the optimal dose of cLZ required to evoke changes in neural activity whilst avoiding off-target effects. We also performed [ 18 f] fluoro-deoxy-glucose micro positron emission tomography (fDG-micropet) scans to determine the global effect of CLZ-induced hM3D(Gq) DREADD activation in the rat brain. Our results show that low doses of CLZ (0.1 and 0.01 mg/kg) successfully induced neural responses without off-target effects. CLZ at 1 mg/kg evoked a stronger and longer-lasting neural response but produced off-target effects, observed as changes in locomotor behavior and FDG-microPET imaging. Unexpectedly, FDG-microPET imaging failed to demonstrate an increase in regional glucose metabolism in the stimulated cortex during CLZ chemogenetic neuromodulation. Therefore, caution should be used when interpreting FDGpet images in the context of cortical chemogenetic activation.

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“…Medullary pyramidotomy (pyramidotomy) has been used to study the role of the CST in skilled movements[2], axonal remodeling and brain plasticity in unlesioned sections of the CST[3, 4], and recovery mechanisms from white-matter stroke[5, 6]. Considering the paucity of white matter stroke models and the different pathogenesis and recovery mechanisms involved in cortical grey-matter and subcortical white-matter stroke, a pyramidotomy model has the potential to expand stroke research beyond grey-matter stroke[7–9].…”

Section: Introductionmentioning

confidence: 99%

Transcortical photothrombotic pyramidotomy model with persistent motor deficits

et al. 2018

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Traditional pyramidotomy models have a high mortality rate from breathing difficulties and show early recovery from the induced motor deficits. This study establishes a novel pyramidotomy technique in Sprague Dawley rats that generates persistent motor deficits and has a reduced mortality rate. We used viral neural tracing to identify the course and relative distribution of forelimb and hindlimb motor fibers (n = 9). On basis of the neural tracing data, the medullary pyramid was targeted dorsally from the cerebellar cortex for photothrombotic infarct lesioning (n = 18). The photothrombotic technique selectively destroyed the corticospinal fibers in the medullary pyramid with relative preservation of neighboring grey-matter tissue. MicroPET imaging using 2-deoxy-2-[18F]-fluoro-D-glucose (FDG-microPET) showed a decrease in regional cerebral glucose metabolism (rCGM) in the bilateral pyramid and ipsilateral sensory cortex (p < 0.001, FDR q < 0.05). In addition, the trapezoid bodies and superior olivary nuclei showed a decrease in rCGM, compatible with damage caused during the introduction of the optical fiber. Connected structures such as the inferior colliculi and auditory cortices also showed decreases in rCGM in both hemispheres (p < 0.001, FDR q < 0.05). There was a significant and persistent decrease in motor and sensory function in the contralateral limb following pyramidotomy, as demonstrated by performance in the single pellet reaching task and the foot-fault test. There was no operative mortality or loss of respiratory function in this study. These results indicate that photothrombotic pyramidotomy with a dorsal transcortical approach is a safe and reliable technique for generating a pyramidotomy model with persistent motor deficits.

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Remodeling of Neuronal Circuits After Reach Training in Chronic Capsular Stroke

Cited by 13 publications

References 33 publications

Motor compensation and its effects on neural reorganization after stroke

Motor compensation and its effects on neural reorganization after stroke

Optimizing clozapine for chemogenetic neuromodulation of somatosensory cortex

Transcortical photothrombotic pyramidotomy model with persistent motor deficits

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