Plasticity of neuropeptide Y in the dentate gyrus after seizures, and its relevance to seizure-induced neurogenesis

Scharfman, Helen E.; Gray, William Peter

doi:10.1007/3-7643-7417-9_15

Cited by 27 publications

(28 citation statements)

References 79 publications

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“…NPY expression was found markedly increased in hilar GABAergic interneurons, granule cells and sprouted mossy fibers (Bellmann et al, 1991;Chafetz et al, 1995;Lurton and Cavalheiro, 1997;Scharfman et al, 1999Scharfman et al, , 2002Sperk et al, 1992;Takahashi et al, 2000;Vezzani et al, 1996). NPY in the dentate gyrus can influence synaptic transmission and neurogenesis, demonstrates remarkable plasticity after seizures (Scharfman and Gray, 2006), and may have an anticonvulsive action (Furtinger et al, 2001;Klapstein and Colmers, 1997;Vezzani et al, 1999). In the present study, epileptic animals demonstrated alterations in NPY IR in both cortex and hippocampus; however, the significance of these changes is not known at present.…”

Section: Discussioncontrasting

confidence: 50%

Changes in neuropeptide Y protein expression following photothrombotic brain infarction and epileptogenesis

Kharlamov

Kelly

2007

Brain Research

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This study characterized morphological changes in the cortex and hippocampus of Sprague-Dawley rats following photothrombotic infarction and epileptogenesis with emphasis on the distribution of neuropeptide Y (NPY) expression. Animals were lesioned in the left sensorimotor cortex and compared with age-matched naïve and sham-operated controls by immunohistochemical techniques at 1, 3, 7, and 180 days post-lesioning (DPL). NPY immunostaining was assessed by light microscopy and quantified by the optical fractionator technique using unbiased stereological methods. At 1, 3, and 7 DPL, the number of NPY-positive somata in the lesioned cortex was increased significantly compared to controls and the contralateral cortex. At 180 DPL, lesioned epileptic animals with frequent seizure activity demonstrated significant increases of NPY expression in the cortex, CA1, CA3, hilar interneurons, and granule cells of the dentate gyrus. In addition to NPY immunostaining, neuronal degeneration, cell death/cell loss, and astroglial response were assessed with cell-specific markers. Nissl and NeuN staining showed reproducible infarctions at each investigated time point. FJB-positive somata were most abundant in the infarct core at 1 DPL, decreased markedly at 3 DPL, and virtually absent by 7 DPL. Activated astroglia were detected in the cortex and hippocampus following lesioning and the development of seizure activity. In summary, NPY protein expression and morphological changes following cortical photothrombosis were time-, region-and pathologic state-dependent. Alterations in NPY expression may reflect reactive or compensatory responses of the rat brain to acute infarction and to the development and expression of epileptic seizures.

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Section: Discussioncontrasting

confidence: 50%

Changes in neuropeptide Y protein expression following photothrombotic brain infarction and epileptogenesis

Kharlamov

Kelly

2007

Brain Research

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“…Considering these, it is plausible that multiple other NSC mitogenic factors also display subdued response to injury in the middle-aged and aged hippocampi. This may include FGF-2, EGF, VEGF neurogenesin-1, wnt proteins, cysteine protease cystatin C expressed on reactive astrocytes and microglia, serotonin 1A receptors and neuropeptide Y (Radley & Jacobs, 2003;Ueki et al, 2003;Howell et al, 2005Howell et al, , 2007Lie et al, 2005;Pirttila et al, 2005;Scharfman & Gray, 2006;Rai et al, 2007). Lower levels of neurotrophic factors in the injured middle-aged and aged hippocampi are also supported by the observation that pretreatment and grafting of fetal hippocampal cell grafts with neurotrophic factors FGF-2 and/or BDNF improves their survival in the injured middle-aged and aged hippocampi, in comparison to the poor survival observed for untreated fetal hippocampal cell grafts in these locations (Zaman & Shetty, 2002, 2003Rao et al, 2006b).…”

Section: Potential Reasons For Altered Plasticity Of Nscs In the Middmentioning

confidence: 99%

Plasticity of hippocampal stem/progenitor cells to enhance neurogenesis in response to kainate‐induced injury is lost by middle age

2007

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SummaryA remarkable up-regulation of neurogenesis through increased proliferation of neural stem/progenitor cells (NSCs) is a well-known plasticity displayed by the young dentate gyrus (DG) following brain injury. To ascertain whether this plasticity is preserved during aging, we quantified DG neurogenesis in the young adult, middleaged and aged F344 rats after kainic acid induced hippocampal injury. Measurement of new cells that are added to the dentate granule cell layer (GCL) between post-injury days 4 and 15 using 5′ ′ ′ ′ -bromodeoxyuridine labeling revealed an increased addition of new cells in the young DG but not in the middle-aged and aged DG. Quantification of newly born neurons using doublecortin immunostaining also demonstrated a similar trend. Furthermore, the extent of ectopic migration of new neurons into the dentate hilus was dramatically increased in the young DG but was unaltered in the middle-aged and aged DG. However, there was no change in neuronal fate-choice decision of newly born cells following injury in all age groups. Similarly, comparable fractions of new cells that are added to the GCL after injury exhibited 5-month survival and expressed the mature neuronal marker NeuN, regardless of age or injury at the time of their birth. Thus, hippocampal injury does not adequately stimulate NSCs in the middle-aged and aged DG, resulting in no changes in neurogenesis after injury. Interestingly, rates of both neuronal fate-choice decision and long-term survival of newly born cells remain stable with injury in all age groups. These results underscore that the ability of the DG to increase neurogenesis after injury is lost as early as middle age.

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“…Remarkably, these stem cells can lead to abnormal growths if a normal animal is used, but in an animal that has had seizures, the stem cells become GCs and tumors do not appear to develop (Carpentino et al, 2008). Infusion of neuropeptide Y may be a particularly effective strategy after such stem cell infusion, because it stimulates precursor division (Howell et al, 2003;Scharfman and Gray, 2006;2007) and reduces seizures (Noe et al, 2006). There are four distinct stem cell-based approaches for treating TLE.…”

Section: Temporal Lobe Epilepsymentioning

confidence: 99%

Stem Cell in Neurological Disorders

Kishk¹,

Abokrysha²

2011

Stem Cells in Clinic and Research

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Plasticity of neuropeptide Y in the dentate gyrus after seizures, and its relevance to seizure-induced neurogenesis

Cited by 27 publications

References 79 publications

Changes in neuropeptide Y protein expression following photothrombotic brain infarction and epileptogenesis

Changes in neuropeptide Y protein expression following photothrombotic brain infarction and epileptogenesis

Plasticity of hippocampal stem/progenitor cells to enhance neurogenesis in response to kainate‐induced injury is lost by middle age

Stem Cell in Neurological Disorders

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