Effects of single and repeated electroconvulsive stimulation on hippocampal cell proliferation and spontaneous behaviors in the rat

Nakamura, Kyoko; Ito, Masanobu; Liu, Yinming; Seki, Tatsunori; Suzuki, Tomohiko; Arai, Heii

doi:10.1016/j.brainres.2012.10.052

Cited by 41 publications

(30 citation statements)

References 46 publications

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“…Similar results have been demonstrated in rodent models of depression (Nakamura et al 2013; Schloesser et al 2015) and non-human primates (Perera et al 2007). …”

Section: Neuroplasticity Changes In Mdd and The Effects Of Antidepressupporting

confidence: 78%

Neurotrophic factors and neuroplasticity pathways in the pathophysiology and treatment of depression

et al. 2018

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Depression is a major health problem with a high prevalence and a heavy socioeconomic burden in western societies. It is associated with atrophy and impaired functioning of cortico-limbic regions involved in mood and emotion regulation. It has been suggested that alterations in neurotrophins underlie impaired neuroplasticity, which may be causally related to the development and course of depression. Accordingly, mounting evidence suggests that antidepressant treatment may exert its beneficial effects by enhancing trophic signaling on neuronal and synaptic plasticity. However, current antidepressants still show a delayed onset of action, as well as lack of efficacy. Hence, a deeper understanding of the molecular and cellular mechanisms involved in the pathophysiology of depression, as well as in the action of antidepressants, might provide further insight to drive the development of novel fast-acting and more effective therapies. Here, we summarize the current literature on the involvement of neurotrophic factors in the pathophysiology and treatment of depression. Further, we advocate that future development of antidepressants should be based on the neurotrophin theory.

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“…Similar results have been demonstrated in rodent models of depression (Nakamura et al 2013; Schloesser et al 2015) and non-human primates (Perera et al 2007). …”

Section: Neuroplasticity Changes In Mdd and The Effects Of Antidepressupporting

confidence: 78%

Neurotrophic factors and neuroplasticity pathways in the pathophysiology and treatment of depression

et al. 2018

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“…Such behavioral amelioration was abolished with X-ray irradiation of the hippocampus, again showing the requirement of neurogenesis for antidepressant effect (Perera et al, 2011). Consequently, it was demonstrated electroconvulsive stimulation (ECS) can increase hippocampal neurogenesis in a dose-dependent manner in rats (Madsen et al, 2000; Nakamura et al, 2013) and proceeds by upregulating β-catenin expression in the dentate gyrus of the rat hippocampus (Madsen et al, 2003). …”

Section: Wnt Signaling In Psychiatric Disordersmentioning

confidence: 99%

Wnt signaling in neuropsychiatric disorders: Ties with adult hippocampal neurogenesis and behavior

Hussaini

Choi

Cho

et al. 2014

Neuroscience & Biobehavioral Reviews

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In an effort to better understand and treat mental disorders, the Wnt pathway and adult hippocampal neurogenesis have received increased attention in recent years. One is a signaling pathway regulating key aspects of embryonic patterning, cell specification, and adult tissue homeostasis. The other is the generation of newborn neurons in adulthood that integrate into the neural circuit and function in learning and memory, and mood behavior. In this review, we discuss the growing relationship between Wnt signaling-mediated regulation of adult hippocampal neurogenesis as it applies to neuropsychiatric disorders. Evidence suggests dysfunctional Wnt signaling may aberrantly regulate new neuron development and cognitive function. Indeed, altered expression of key Wnt pathway components are observed in the hippocampus of patients suffering from neuropsychiatric disorders. Clinically-utilized mood stabilizers also proceed through modulation of Wnt signaling in the hippocampus, while Wnt pathway antagonists can regulate the antidepressant response. Here, we review the role of Wnt signaling in disease etiology and pathogenesis, regulation of adult neurogenesis and behavior, and the therapeutic targeting of disease symptoms.

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“…Moreover, hippocampal cell proliferation and neurogenesis may be key factors in the actions of antidepressant drugs. However, it was also reported that electroconvulsive stimuli affect progenitors that exhibit a limited ability for cell proliferation (18). In a previous report, chronic administration of ACTH (100 g/rat, s.c., 14 days) was found to significantly decrease the number of 5-bromo-2′-deoxyuridine (BrdU)-and Ki-67 (an endogenous marker of cell proliferation)-positive cells compared with the control value in the subgranular zone (SGZ) of the hippocampal dentate gyrus (19,20).…”

Section: The Mechanisms Of Electroconvulsive Stimuli In Brdu-positivementioning

confidence: 99%

The Mechanisms of Electroconvulsive Stimuli in BrdU-Positive Cells of the Dentate Gyrus in ACTH-Treated Rats

et al. 2013

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Abstract. In clinical studies, electroconvulsive stimuli have been associated with improvements in both depression and treatment-resistant depression. In a previous study, treatment with adrenocorticotropic hormone (ACTH) for 14 days decreased adult hippocampal cell proliferation. Furthermore, electroconvulsive stimuli significantly decreased the duration of immobility following repeated administration of ACTH for 14 days in rats. The present study was undertaken to further characterize the mechanism of treatment-resistant antidepressant effects of electroconvulsive stimuli by measuring cell proliferation, brain-derived neurotrophic factor (BDNF) levels, and phosphorylated and total cyclic adenosine monophosphate (cAMP) response elementbinding protein (pCREB/CREB) levels in the hippocampus of ACTH-treated rats. Electroconvulsive stimuli increased cell proliferation in both saline-treated and ACTH-treated rats. Mature-BDNF protein levels showed a tendency to decrease in ACTH-treated rats. Electroconvulsive stimuli treatment increased mature-BDNF protein levels in the hippocampus of both saline-treated and ACTH-treated rats. Furthermore, electroconvulsive stimuli increased phospho-Ser133-CREB (pCREB) levels and the ratio of pCREB/CREB in both saline-treated and ACTH-treated rats. These findings suggest that the treatment-resistant antidepressant effects of electroconvulsive stimuli may be attributed, at least in part, to an enhancement of hippocampal cell proliferation.

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Effects of single and repeated electroconvulsive stimulation on hippocampal cell proliferation and spontaneous behaviors in the rat

Cited by 41 publications

References 46 publications

Neurotrophic factors and neuroplasticity pathways in the pathophysiology and treatment of depression

Neurotrophic factors and neuroplasticity pathways in the pathophysiology and treatment of depression

Wnt signaling in neuropsychiatric disorders: Ties with adult hippocampal neurogenesis and behavior

The Mechanisms of Electroconvulsive Stimuli in BrdU-Positive Cells of the Dentate Gyrus in ACTH-Treated Rats

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