Increased neurogenesis and the ectopic granule cells after intrahippocampal BDNF infusion in adult rats

Scharfman, Helen E.; Goodman, Jeffrey H.; Macleod, A. P.; Phani, Sudar; Antonelli, Cara; Croll, Susan D.

doi:10.1016/j.expneurol.2004.11.016

Cited by 637 publications

(435 citation statements)

References 59 publications

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“…Indeed, the similarities do not stop with those listed above. The rate of dentate gyrus neurogenesis is increased by both estrogen and BDNF [72][73][74][75]. The influence of both estrogen and BDNF also applies to glia [76][77][78], although this is not as well documented as their effects on neurons.…”

Section: Comparison Of Estrogen and Bdnf Actions In Hippocampus-mentioning

confidence: 99%

Estrogen and brain-derived neurotrophic factor (BDNF) in hippocampus: Complexity of steroid hormone-growth factor interactions in the adult CNS

Scharfman

MacLusky

2006

Frontiers in Neuroendocrinology

270

202

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In the CNS, there are widespread and diverse interactions between growth factors and estrogen. Here we examine the interactions of estrogen and brain-derived neurotrophic factor (BDNF), two molecules that have historically been studied separately, despite the fact that they seem to share common targets, effects, and mechanisms of action. The demonstration of an estrogen-sensitive response element on the BDNF gene provided an impetus to explore a direct relationship between estrogen and BDNF, and predicted that the effects of estrogen, at least in part, might be due to the induction of BDNF. This hypothesis is discussed with respect to the hippocampus, where substantial evidence has accumulated in favor of it, but alternate hypotheses are also raised. It is suggested that some of the interactions between estrogen and BDNF, as well as the controversies and implications associated with their respective actions, may be best appreciated in light of the ability of BDNF to induce neuropeptide Y (NPY) synthesis in hippocampal neurons. Taken together, this tri-molecular cascade, estrogen-BDNF-NPY, may be important in understanding the hormonal regulation of hippocampal function. It may also be relevant to other regions of the CNS where estrogen is known to exert profound effects, such as amygdala and hypothalamus; and may provide greater insight into neurological disorders and psychiatric illness, including Alzheimer's disease, depression and epilepsy.

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Section: Comparison Of Estrogen and Bdnf Actions In Hippocampus-mentioning

confidence: 99%

Estrogen and brain-derived neurotrophic factor (BDNF) in hippocampus: Complexity of steroid hormone-growth factor interactions in the adult CNS

Scharfman

MacLusky

2006

Frontiers in Neuroendocrinology

270

202

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“…This may seem counterintuitive, as it is generally expected that excessive excitatory activity would lead to cell loss. However, numerous studies have reported increased hilar neurons in animal models of TLE and it is speculated that neurogenesis may be a compensatory response to seizure-induced cell death [34][35][36]41]. Characterization of these neurons has revealed that they exhibit properties of dentate granule cells (i.e., ectopic granule cells).…”

Section: Discussionmentioning

confidence: 99%

“…Characterization of these neurons has revealed that they exhibit properties of dentate granule cells (i.e., ectopic granule cells). These cells can be readily identified using calbindin immunohistochemistry, because granule cells are the only calbindin positive cells in the dentate gyrus [35,41,42]. Results from calbindin immunohistochemistry (Fig.…”

Section: Discussionmentioning

confidence: 99%

“…In rats, chemical or electrically induced seizures and status epilepticus result in a number of cytoarchitectural changes in the hippocampus including activation and proliferation of astrocytes [33] and neurogenesis in the dentate hilus associated with the formation of ectopic granule cells [34][35][36]. Our objective in the current study was to determine if similar changes occur in the neonatal DOM model and further to see if such changes are progressive over time by sampling animals at time points earlier than those previously examined (i.e., prior to postnatal day (PND) 90).…”

Section: Introductionmentioning

confidence: 99%

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Progressive changes in hippocampal cytoarchitecture in a neurodevelopmental rat model of epilepsy: implications for understanding presymptomatic epileptogenesis, predictive diagnosis, and targeted treatments

et al. 2017

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Epilepsies affect about 4% of the population and are frequently characterized by a prolonged Bsilent^period before the onset of spontaneous seizures. Most current animal models of epilepsy either involve acute seizure induction or kindling protocols that induce repetitive seizures. We have developed a rat model of epilepsy that is characterized by a slowly progressing series of behavioral abnormalities prior to the onset of behavioral seizures. In the current study, we further describe an accompanying progression of cytoarchitectural changes in the hippocampal formation. Groups of male and female SD rats received serial injections of a low dose of domoic acid (0.020 mg/kg) (or vehicle) throughout the second week of life. Postmortem hippocampal tissue was obtained on postnatal days 29, 64, and 90 and processed for glial fibrillary acidic protein (GFAP), NeuN, and calbindin expression. The data revealed no significant changes on postnatal day (PND) 29 but a significant increase in hilar NeuN-positive cells in some regions on PND 64 and 90 that were identified as ectopic granule cells. Further, an increase in GFAP positive cell counts and evidence of reactive astrogliosis was found on PND 90 but not at earlier time points. We conclude that changes in cellular expression, possibly due to on-going non-convulsive seizures, develop slowly in this model and may contribute to progressive brain dysfunction that culminates in a seizure-prone phenotype.

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“…Administration of neurotrophic factors is r e l e v a n t a s m a n y f a c t o r s t h a t p r o m o t e neurogenesis (e.g: BDNF, FGF-2, IGF-1) are reduced in chronic epilepsy . Supporting this, a range of studies have demonstrated that administration of neurotrophic factors to both the normal and injured adult rodent brain can enhance hippocampal neurogenesis (Lichtenwalner, et al, 2001, Yoshimura, et al, 2001, Scharfman, et al, 2005, Rai, et al, 2007, Paradiso, et al, 2009, Paradiso, et al, 2011. Performing physical exercise and environmental enrichment have also been shown to enhance hippocampal neurogenesis, potentially through increased expression of a range of mitogenic factors such as BDNF, FGF2, NGF, IGF-1 and VEGF as well as phosphorylation of cAMP-response binding protein (CREB) (Nithianantharajah, et al, 2006, Van Praag, 2008, Llorens-Martín, et al, 2009, Lafenetre, et al, 2011 and may provide an appealing noninvasive therapeutic approach for the treatment of chronic TLE (Dhanushkodi, et al, 2008, Arida, et al, 2009.…”

Section: Chronic Tlementioning

confidence: 91%

Compensatory Neurogenesis in the Injured Adult Brain

Connor¹

2012

Brain Injury - Pathogenesis, Monitoring, Recovery and Management

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Increased neurogenesis and the ectopic granule cells after intrahippocampal BDNF infusion in adult rats

Cited by 637 publications

References 59 publications

Estrogen and brain-derived neurotrophic factor (BDNF) in hippocampus: Complexity of steroid hormone-growth factor interactions in the adult CNS

Estrogen and brain-derived neurotrophic factor (BDNF) in hippocampus: Complexity of steroid hormone-growth factor interactions in the adult CNS

Progressive changes in hippocampal cytoarchitecture in a neurodevelopmental rat model of epilepsy: implications for understanding presymptomatic epileptogenesis, predictive diagnosis, and targeted treatments

Compensatory Neurogenesis in the Injured Adult Brain

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