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Transcriptional changes in the rat brain induced by repetitive transcranial magnetic stimulation (rTMS).

ABSTRACT: Transcriptional changes in the rat brain induced by repetitive transcranial magnetic stimulation (rTMS).

PROVIDER: PRJNA957738 | ENA |

REPOSITORIES: ENA

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Transcriptional changes in the rat brain induced by repetitive transcranial magnetic stimulation (rTMS)_EX_VIVO

Project description:Transcranial Magnetic Stimulation (TMS) is a noninvasive technique that uses pulsed magnetic fields to affect the physiology of the brain and central nervous system. Repetitive TMS (rTMS) has been used in the study and treatment of neurological conditions including major depression, stroke, epilepsy, schizophrenia, multiple sclerosis, Parkinson’s, and Alzheimer’s disease, as well as other, non-neurological disorders. Among the effects of rTMS, low-frequency protocols (≤ 1Hz) are generally understood to result in cortical inhibition, whereas high-frequency protocols (≥ 3Hz) increase cortical excitability. However, the complex molecular basis of rTMS is largely unexplored. Using three complementary rat models, in vitro, ex vivo, and in vivo, we show complex patterns of hippocampal and neocortical transcriptional response to stimulation in glutamatergic and GABAergic signaling pathways, as well as multiple inflammatory pathways, among others. This broad-based molecular survey helps provide a foundation to tease out the complex molecular mechanisms of the effects of rTMS.

2023-05-30 | GSE230148 | GEO

Transcriptional changes in the rat brain induced by repetitive transcranial magnetic stimulation (rTMS)_IN_VITRO

2023-05-30 | GSE230147 | GEO

Transcriptional changes in the rat brain induced by repetitive transcranial magnetic stimulation (rTMS)_IN_VIVO

2023-05-30 | GSE230149 | GEO

Transcriptional changes in PC12 cells induced by repetitive transcranial magnetic stimulation (rTMS) in MSCs-inhibited inflammatory conditions

Project description:Neuronal death is the primary cause of poor outcomes in cerebral ischemia. The Inflammatory infiltration in the early phase of ischemic stroke plays a vital role in triggering neuronal death. Either transplantation of mesenchymal stem cells (MSCs) derived from humans or repetitive transcranial magnetic stimulation (rTMS) have respectively proved to be neuroprotective and anti-inflammatory in cerebral ischemia. However, either treatment above has its limitations. Whether these two therapies have synergistic effects on improving neurological function and the underlying mechanisms remains unclear.Using an in vitro model of PC12 nerve cell co-culture with MSCs, we demonstrated a transcriptional response pattern, including REST, in which rTMS inhibited PANoptosis of PC12 cells in a low-inflammation environment induced by MSCs. This molecular investigation is helpful in providing a basis for sorting out the complex molecular mechanism of combination of rTMS and MSCs in treating ischemic stroke.

2024-12-06 | GSE282396 | GEO

Transcriptional changes in the rat brain induced by repetitive transcranial magnetic stimulation (rTMS)_EX_VIVO

Project description:Transcriptional changes in the rat brain induced by repetitive transcranial magnetic stimulation (rTMS)_EX_VIVO

| PRJNA957740 | ENA

Transcriptional changes in the rat brain induced by repetitive transcranial magnetic stimulation (rTMS)_IN_VITRO

Project description:Transcriptional changes in the rat brain induced by repetitive transcranial magnetic stimulation (rTMS)_IN_VITRO

| PRJNA957741 | ENA

Transcriptional changes in the rat brain induced by repetitive transcranial magnetic stimulation (rTMS)_IN_VIVO

Project description:Transcriptional changes in the rat brain induced by repetitive transcranial magnetic stimulation (rTMS)_IN_VIVO

| PRJNA957742 | ENA

High-Frequency Repetitive Transcranial Magnetic Stimulation (rTMS) Protects Against Ischemic Stroke by Inhibiting M1 Microglia Polarization through Let-7b-5p/HMGA2/NF-κB Signaling Pathway

Project description:Modulating M1/M2 polarization is a potential therapy for treating ischemic stroke. Repetitive transcranial magnetic stimulation (rTMS) held the capacity to regulate astrocytic polarization, but little is known about rTMS effects on microglia. Therefore, the present study aimed to investigate whether and how rTMS influence microglia polarization in ischemic stroke models. The 10-Hz rTMS was applied to transient middle cerebral artery occlusion (MCAO) rats and oxygen and glucose deprivation/ reoxygenation injured BV2 cells. Western blot, immunofluorescence and ELISA were used to detect M1/M2 markers. High-throughput sequencing, RT-PCR and FISH staining were adopted to test microRNA changes. The 10-Hz rTMS inhibited ischemia/reperfusion induced M1 microglia and significantly increased let-7b-5p. HMGA2 was proved to be the target protein of let-7b-5p and its downstream NF-κB signaling pathway were inhibited by rTMS. Microglia culture medium (MCM) collected from rTMS treated microglia had low TNF-α but high IL-10 concentration, leading to reduced neural death, minor ischemic volumes and improved functional recovery of MCAO animals. However, knockdown of let-7b-5p by antagomir reversed rTMS effects on microglia. In conclusion, high-frequency rTMS could improve functional recovery through inhibiting M1 microglia polarization via regulating let-7b-5p/HMGA2/NF-κB signaling pathway in cerebral ischemic stroke models.

2022-08-10 | GSE192910 | GEO

Transcriptional changes in PC12 cells induced by repetitive transcranial magnetic stimulation (rTMS) in MSCs-inhibited inflammatory conditions

Project description:Transcriptional changes in PC12 cells induced by repetitive transcranial magnetic stimulation (rTMS) in MSCs-inhibited inflammatory conditions

| PRJNA1188501 | ENA

High-Frequency Repetitive Transcranial Magnetic Stimulation (rTMS) Protects Against Ischemic Stroke by Inhibiting M1 Microglia Polarization through Let-7b-5p/HMGA2/NF-κB Signaling Pathway

Project description:High-Frequency Repetitive Transcranial Magnetic Stimulation (rTMS) Protects Against Ischemic Stroke by Inhibiting M1 Microglia Polarization through Let-7b-5p/HMGA2/NF-κB Signaling Pathway

| PRJNA793778 | ENA

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