Age-related changes in calbindin-D28k, calretinin, and parvalbumin-immunoreactive neurons in the human cerebral cortex

Bu, Jing; Sathyendra, Vikram; Nagykery, Nicholas; Geula, Changiz

doi:10.1016/s0014-4886(03)00094-3

Cited by 122 publications

(92 citation statements)

References 52 publications

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“…With the exception of the cingulate cortex, the present work provides evidence for the stable expression of PV regardless of age within many neocortical areas (e.g. somatosensory and retrosplenial cortices) - minimally within the age ranges presently observed - which is consistent with findings seen across aging human populations [69]. However, it is possible that PV within these cortical regions may mature at an earlier developmental time point not included in the present work.…”

Section: Discussionsupporting

confidence: 86%

Developmental Age Differentially Mediates the Calcium-Binding Protein Parvalbumin in the Rat: Evidence for a Selective Decrease in Hippocampal Parvalbumin Cell Counts

Ganguly

Keary²,

Kania³

et al. 2016

Dev Neurosci

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Local circuit GABAergic neurons, including parvalbumin (PV)-containing basket cells, likely play a key role in the development, physiology, and pathology of neocortical circuits. Regionally selective and well-defined decreases in PV have been described in human postmortem schizophrenic brain tissue in both the hippocampus and prefrontal cortex. Animal models of schizophreniform dysfunction following acute and/or chronic ketamine treatment have also demonstrated decreases in PV expression. Conflicting reports with respect to PV immunoreactivity following acute and chronic ketamine treatments in rodents question the utility of using PV as a biological marker of pathology-related dysfunction. The current literature lacks sufficient and systematic characterization of normative PV expression in pharmacologically and behaviorally naïve rodent tissue. In order to understand developmental changes in PV and its putative role in neuropathology, we examined the baseline distribution of the number of cells expressing this protein at distinct developmental ages. The present study examined PV cell counts across the septotemporal axis of the CA1, CA3, and dentate gyrus (DG) regions of the hippocampus, as well as within the retrosplenial, somatosensory, and prefrontal cortices, in 1-, 6-, and 12-month-old naïve rats. Our findings suggest that the hippocampal PV+ cell number significantly decreases as a function of age with considerable regional (CA1, CA3, and DG) and septotemporal variation, a finding that was specific to the hippocampus. Additionally, we observed a modest increase in PV cell number within the prefrontal (anterior cingulate) cortex, which is in line with findings indicating a delayed developmental maturation of this region. The present work highlights decreases in PV+ cell counts within the hippocampus across development, and points to the need for a greater understanding of the role of PV and local circuit developmental changes, as well as consideration of their development when modeling developmentally related neuropathological disorders (e.g. schizophrenia, autism).

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Section: Discussionsupporting

confidence: 86%

Developmental Age Differentially Mediates the Calcium-Binding Protein Parvalbumin in the Rat: Evidence for a Selective Decrease in Hippocampal Parvalbumin Cell Counts

Ganguly

Keary²,

Kania³

et al. 2016

Dev Neurosci

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“…Decreases in the presence of parvalbumin-ir neurons have been described in several major illnesses of the human brain such as schizophrenia and epilepsy (for review see Woo and Lu, 2006;Lewis et al, 2005). On the other hand, in human neocortex from individuals without any signs of neurological or psychiatric disorders, Bu et al (2003) found no agerelated changes in PV-immunoreactivity with aging in contrast to a decrease in the number of calbindin-and calretinin-ir neurons.…”

Section: Introductionmentioning

confidence: 61%

Changes in parvalbumin immunoreactivity with aging in the central auditory system of the rat

Ouda¹,

Druga²,

Syka³

2008

Experimental Gerontology

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“…4). Calbindin, together with parvalbumin (PV) and calretinin (CR), constitutes the calciumbinding proteins that label GABAergic and pyramidal-shaped neurons in various areas of the brain (Iacopino and Christakos, 1990;Leuba et al, 1998;Bu et al, 2003). These calcium-binding proteins regulate intracellular calcium concentrations due to their calcium buffering capacities.…”

Section: Neuropathological Features Of Tg-bctf99/b6 As An Ad Modelmentioning

confidence: 99%

“…Mice deficient in CB were found to show impairments in spatial learning and LTP (Molinari et al, 1996). Moreover, in aging or neurodegenerative brains, CB expression was reduced, and this may be related to pathologic changes (Iacopino and Christakos, 1990;Leuba et al, 1998;Bu et al, 2003). Despite the development of numerous AD models, the correlation between CB depletion and cognitive deficits has been described only recently in transgenic lines expressing mutant forms of human APP (Palop et al, 2003;Lee et al, 2004).…”

Section: Neuropathological Features Of Tg-bctf99/b6 As An Ad Modelmentioning

confidence: 99%

Progressive neuronal loss and behavioral impairments of transgenic C57BL/6 inbred mice expressing the carboxy terminus of amyloid precursor protein

Lee

Song

et al. 2006

Neurobiology of Disease

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Age-related changes in calbindin-D28k, calretinin, and parvalbumin-immunoreactive neurons in the human cerebral cortex

Cited by 122 publications

References 52 publications

Developmental Age Differentially Mediates the Calcium-Binding Protein Parvalbumin in the Rat: Evidence for a Selective Decrease in Hippocampal Parvalbumin Cell Counts

Developmental Age Differentially Mediates the Calcium-Binding Protein Parvalbumin in the Rat: Evidence for a Selective Decrease in Hippocampal Parvalbumin Cell Counts

Changes in parvalbumin immunoreactivity with aging in the central auditory system of the rat

Progressive neuronal loss and behavioral impairments of transgenic C57BL/6 inbred mice expressing the carboxy terminus of amyloid precursor protein

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