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        Electroconvulsive Seizure Normalizes Motor Deficits and Induces Autophagy Signaling in the MPTP-Induced Parkinson Disease Mouse Model

        Seonghoo Huh(Seonghoo Huh),Hyun Sook Yu(Hyun Sook Yu),Nuree Kang(Nuree Kang),Yong Min Ahn(Yong Min Ahn),Yong Sik Kim(Yong Sik Kim),Se Hyun Kim(Se Hyun Kim) 대한신경정신의학회 2023 PSYCHIATRY INVESTIGATION Vol.20 No.3

        Objective Electroconvulsive seizure (ECS) is a potent treatment modality for various neuropsychiatric diseases, including Parkinson disease (PD). Recent animal studies showed that repeated ECS activates autophagy signaling, the impairment of which is known to be involved in PD. However, the effectiveness of ECS on PD and its therapeutic mechanisms have not yet been investigated in detail. Methods Systemic injection of a neurotoxin 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine hydrochloride (MPTP), which destroys dopaminergic neurons in the substantia nigra compacta (SNc), in mice was utilized to induce an animal model of PD. Mice were treated with ECS 3 times per week for 2 weeks. Behavioral changes were measured with a rotarod test. Molecular changes related to autophagy signaling in midbrain including SNc, striatum, and prefrontal cortex were analyzed with immunohistochemistry and immunoblot analyses. Results Repeated ECS treatments normalized the motor deficits and the loss of dopamiergic neurons in SNc of the MPTP PD mouse model. In the mouse model, LC3-II, an autophagy marker, was increased in midbrain while decreased in prefrontal cortex, both of which were reversed by repeated ECS treatments. In the prefrontal cortex, ECS-induced LC3-II increase was accompanied with AMP-activated protein kinase (AMPK)-Unc-51-like kinase 1-Beclin1 pathway activation and inhibition of mamalian target of rapamycin signaling which promotes autophagy initiation. Conclusion The findings revealed the therapeutic effects of repeated ECS treatments on PD, which could be attributed to the neuroprotective effect of ECS mediated by AMPK-autophagy signaling.

      • KCI등재

        Electroconvulsive Seizure Normalizes Motor Deficits and Induces Autophagy Signaling in the MPTP-Induced Parkinson Disease Mouse Model

        Huh Seonghoo,Yu Hyun Sook,Kang Nuree,Ahn Yong Min,Kim Yong Sik,Kim Se Hyun 대한신경정신의학회 2023 PSYCHIATRY INVESTIGATION Vol.20 No.4

        Objective Electroconvulsive seizure (ECS) is a potent treatment modality for various neuropsychiatric diseases, including Parkinson disease (PD). Recent animal studies showed that repeated ECS activates autophagy signaling, the impairment of which is known to be involved in PD. However, the effectiveness of ECS on PD and its therapeutic mechanisms have not yet been investigated in detail.Methods Systemic injection of a neurotoxin 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine hydrochloride (MPTP), which destroys dopaminergic neurons in the substantia nigra compacta (SNc), in mice was utilized to induce an animal model of PD. Mice were treated with ECS 3 times per week for 2 weeks. Behavioral changes were measured with a rotarod test. Molecular changes related to autophagy signaling in midbrain including SNc, striatum, and prefrontal cortex were analyzed with immunohistochemistry and immunoblot analyses.Results Repeated ECS treatments normalized the motor deficits and the loss of dopamiergic neurons in SNc of the MPTP PD mouse model. In the mouse model, LC3-II, an autophagy marker, was increased in midbrain while decreased in prefrontal cortex, both of which were reversed by repeated ECS treatments. In the prefrontal cortex, ECS-induced LC3-II increase was accompanied with AMP-activated protein kinase (AMPK)-Unc-51-like kinase 1-Beclin1 pathway activation and inhibition of mamalian target of rapamycin signaling which promotes autophagy initiation.Conclusion The findings revealed the therapeutic effects of repeated ECS treatments on PD, which could be attributed to the neuroprotective effect of ECS mediated by AMPK-autophagy signaling.

      • KCI등재

        Pilot Study About the Effects of the Soma Experiencing Motion (Soma e-Motion) Program on Interoceptive Awareness and Self-Compassion

        Huh Seonghoo,Kim Sun Je,Chae Jeong-Ho,Bhang Soo-Young,Lee Mimi,Kim Hyeong Beom,Huh Hyu Jung 대한신경정신의학회 2023 PSYCHIATRY INVESTIGATION Vol.20 No.4

        Objective The purpose of this study was to examine the effects of the Soma experiencing motion (Soma e-motion) program on interoceptive awareness and self-compassion among novices.Methods A total of 19 adults (clinical group=9, non-clinical group=10) participated in the intervention. Psychological and physical changes after program were qualitatively analyzed using in-depth interviews. The Korean Multidimensional Assessment of Interoceptive Awareness (K-MAIA) and the Korean version of the Self-Compassion Scale (K-SCS) were used as quantitative measures.Results The non-clinical group showed statistically significant differences in the K-MAIA scores (z=-2.805, p<0.01) and K-SCS scores (z=-2.191, p<0.05); however, the clinical group showed no significant differences (K-MAIA: z=-0.652, p>0.05; K-SCS: z=-0.178, p>0.05). According to the in-depth interviews, the results of the qualitative analysis were categorized into five dimensions (psychological and emotional, physical, cognitive, behavioral, and aspects participants found challenging and needs improvement).Conclusion The Soma e-motion program was feasible for improving interoceptive awareness and self-compassion in the non-clinical group. However, further research is needed to investigate the clinical efficacy of the Soma e-motion program for clinical group.

      • Tau Phosphorylation at Serine 396 Residue Is Required for Hippocampal LTD

        Regan, Philip,Piers, Thomas,Yi, Jee-Hyun,Kim, Dong-Hyun,Huh, Seonghoo,Park, Se Jin,Ryu, Jong Hoon,Whitcomb, Daniel J.,Cho, Kwangwook Society for Neuroscience 2015 The Journal of neuroscience Vol.35 No.12

        <P>Tau is required for the induction of long-term depression (LTD) of synaptic transmission in the hippocampus. Here we probe the role of tau in LTD, finding that an AMPA receptor internalization mechanism is impaired in tau KO mice, and that LTD causes specific phosphorylation at the serine 396 and 404 residues of tau. Surprisingly, we find that phosphorylation at serine 396, specifically, is critical for LTD but has no role in LTP. Finally, we show that tau KO mice exhibit deficits in spatial reversal learning. These findings underscore the physiological role for tau at the synapse and identify a behavioral correlate of its role in LTD.</P>

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