Increased number of new neurons in the olfactory bulb and hippocampus of adult non-human primates after focal ischemia

Koketsu, Daisuke; Furuichi, Yasuhisa; Maeda, Masashi; Matsuoka, Naoki; Miyamoto, Yusei; Hisatsune, Tatsuhiro

doi:10.1016/j.expneurol.2006.03.012

Cited by 56 publications

(44 citation statements)

References 44 publications

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“…This finding is consistent with rodent studies, in which antidepressant drugs and ECS appear to induce precursor cell proliferation (Malberg et al, 2000), whereas cell survival and maturational fate seem to be mediated by other factors such as brain-derived neurotrophic factor (Sairanen et al, 2005) and BCL2 (Kuhn et al, 2005). Approximately 60% of proliferating cells matured into neurons in the bonnet macaques, a proportion that is similar to neuronal differentiation rates at a comparable postmitotic stage in adult rhesus and cynomolgus monkeys (Koketsu et al, 2006).…”

Section: Discussionsupporting

confidence: 78%

Antidepressant-Induced Neurogenesis in the Hippocampus of Adult Nonhuman Primates

Perera¹,

Coplan²,

Lisanby³

et al. 2007

J. Neurosci.

405

266

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New neurons are generated in the adult hippocampus of many species including rodents, monkeys, and humans. Conditions associated with major depression, such as social stress, suppress hippocampal neurogenesis in rodents and primates. In contrast, all classes of antidepressants stimulate neuronal generation, and the behavioral effects of these medications are abolished when neurogenesis is blocked. These findings generated the hypothesis that induction of neurogenesis is a necessary component in the mechanism of action of antidepressant treatments. To date, the effects of antidepressants on newborn neurons have been reported only in rodents and tree shrews. This study examines whether neurogenesis is increased in nonhuman primates after antidepressant treatment. Adult monkeys received repeated electroconvulsive shock (ECS), which is the animal analog of electroconvulsive therapy (ECT), the most effective short-term antidepressant. Compared with control conditions, ECS robustly increased precursor cell proliferation in the subgranular zone (SGZ) of the dentate gyrus in the monkey hippocampus. A majority of these precursors differentiated into neurons or endothelial cells, while a few matured into glial cells. The ECS-mediated induction of cell proliferation and neurogenesis was accompanied by increased immunoreactivity for the neuroprotective gene product BCL2 (B cell chronic lymphocytic lymphoma 2) in the SGZ. The ECS interventions were not accompanied by increased hippocampal cell death or injury. This study demonstrates that ECS is capable of inducing neurogenesis in the nonhuman primate hippocampus and supports the possibility that antidepressant interventions produce similar alterations in the human brain.

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Section: Discussionsupporting

confidence: 78%

Antidepressant-Induced Neurogenesis in the Hippocampus of Adult Nonhuman Primates

Perera¹,

Coplan²,

Lisanby³

et al. 2007

J. Neurosci.

405

266

View full text Add to dashboard Cite

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“…The advantages of this approach complement features offered by other NHP models of stroke, such as the transorbital approach, 44 endovascular approach, 26 and photothrombotic stroke. 45 These data are in agreement with previous reports 12,20,25,26 and suggests that the open surgical model provides less variability in volume and outcome measures and rare mortality in comparison to the endovascular approach, 20,37 including the autologous blood clots model. 33,34,46 The restoration of blood flow and reperfusion post occlusion in the ischemic area are readily achieved and provide a transient model to study reperfusion injury in NHP.…”

Section: Strokesupporting

confidence: 83%

Impaired Arm Function and Finger Dexterity in a Nonhuman Primate Model of Stroke

McEntire

Choudhury

Torres

et al. 2016

Stroke

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The World Health Organization reports that stroke claims 6.2 million lives each year. There are ≈5.4 million stroke survivors with ≈80% requiring hand therapy. 1 The estimated economic burden for stroke exceeds $56.8 billion per year in the United States alone.Acute thrombolysis has a significant impact on the management of stroke, 2,3 with a therapeutic window that may extend ≤6 hours with intra-arterial delivery. 4 Yet only a minority of stroke victims benefit, and the majority experience progression of ischemia associated with neurological disabilities.Animal models that recapitulate human disabilities and disease pathology remain an unmet need in stroke research. There has been a tremendous advance in developing rodent experimental model stroke (reviewed in Durukan and Tatlisumak 5 and Carmichael 6 ). However, the lack of success in developing neuroprotective therapies in small animal models for stroke 7,8 prompted recommendations for additional research and development in large animal models with physiological, structural, and functional traits closer to those of humans before clinical trials.9,10 There has been a concerted effort in developing relevant large animal models. 11,12 Interspecies comparison suggests that cerebral venous angioarchitecture in large animals is closer to that of humans 13 ; nevertheless, such models remain relatively underdeveloped. Nonhuman primate (NHP) models offer an assessment of complex physiological, immunologic, biochemical, and behavioral outcomes most similar to those of humans.14-24 These outcome measures complement those from other animal models by improving our understanding Background and Purpose-Ischemic stroke is the leading cause of upper extremity motor impairments. Although several well-characterized experimental stroke models exist, modeling of upper extremity motor impairments, which are unique to primates, is not well established. Cortical representation of dexterous movements in nonhuman primates is functionally and topographically similar to that in humans. In this study, we characterize the African green monkey model of focal ischemia reperfusion with a defined syndrome, impaired dexterous movements. Methods-Cerebral ischemia was induced by transient occlusion of the M3 segment of the left middle cerebral artery.Motor and cognitive functions after stroke were evaluated using the object retrieval task with barrier-detour. Postmortem magnetic resonance imaging and histopathology were performed to map and characterize the infarct. Results-The middle cerebral artery occlusion consistently produced a necrotic infarct localized in the sensorimotor cortex in the middle cerebral artery territory. The infarction was reproducible and resulted in significant loss of fine motor function characterized by impaired dexterity. No significant cognitive impairment was detected. Magnetic resonance imaging and histopathology demonstrated consistent and significant loss of tissue on the left parietal cortex by the central sulcus covering the sensorimotor area. The results sug...

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“…42,46,47,74 However, the literature is far from agreement on how the hippocampus is affected by trauma. In the current study, our finding of an unaltered number of migrating neuroblasts in the hippocampus of children following TBI is similar to the results of Chirumamilla and colleagues, 11 who did not observe increased neurogenesis in the hippocampus of adult rats 48 hours after fluid percussion injury.…”

Section: Discussionmentioning

confidence: 99%

Maturation-dependent response of neurogenesis after traumatic brain injury in children

Taylor

Smith²,

Harris

et al. 2013

PED

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Object Traumatic brain injury (TBI) is the leading cause of acquired disability in children, yet innate repair mechanisms are incompletely understood. Given data from animal studies documenting neurogenesis in response to trauma and other insults, the authors investigated whether similar responses could be found in children of different ages after TBI. Methods Immunohistochemistry was used to label doublecortin (DCX), a protein expressed by immature migrating neuroblasts (newborn neurons), in specimens from patients ranging in age from 3 weeks to 10 years who had died either after TBI or from other causes. Doublecortin-positive (DCX+) cells were examined in the subventricular zone (SVZ) and periventricular white matter (PWM) and were quantified within the granule cell layer (GCL) and subgranular zone (SGZ) of the dentate gyrus to determine if age and/or injury affect the number of DCX+ cells in these regions. Results The DCX+ cells decreased in the SVZ as patient age increased and were found in abundance around a focal subacute infarct in a 1-month-old non-TBI patient, but were scarce in all other patients regardless of age or history of trauma. The DCX+ cells in the PWM and dentate gyrus demonstrated a migratory morphology and did not co-localize with markers for astrocytes, microglia, or macrophages. In addition, there were significantly more DCX+ cells in the GCL and SGZ of the dentate gyrus in children younger than 1 year old than in older children. The density of immature migrating neuroblasts in infants (under 1 year of age) was significantly greater than in young children (2–6 years of age, p = 0.006) and older children (7–10 years of age, p = 0.007). Conclusions The main variable influencing the number of migrating neuroblasts observed in the SVZ, PWM, and hippocampus was patient age. Trauma had no discernible effect on the number of migrating neuroblasts in this cohort of patients in whom death typically occurred within hours to days after TBI.

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Increased number of new neurons in the olfactory bulb and hippocampus of adult non-human primates after focal ischemia

Cited by 56 publications

References 44 publications

Antidepressant-Induced Neurogenesis in the Hippocampus of Adult Nonhuman Primates

Antidepressant-Induced Neurogenesis in the Hippocampus of Adult Nonhuman Primates

Impaired Arm Function and Finger Dexterity in a Nonhuman Primate Model of Stroke

Maturation-dependent response of neurogenesis after traumatic brain injury in children

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