Parvalbumin-immunoreactive neurons in the hippocampal formation of Alzheimer's diseased brain

Brady, Daniel R.; Mufson, Elliott J.

doi:10.1016/s0306-4522(97)00068-7

Cited by 106 publications

(88 citation statements)

References 37 publications

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“…Notably, in association with the putative role of Cygb in neuroprotection, a selective reduction of PV-ir neurons were observed in the hippocampus of the AD patients and transgenic animal models of AD (35)(36)(37)(38). Of note, HO-1-ir The merged image of A-C is shown.…”

Section: Discussionmentioning

confidence: 83%

Neurochemical phenotype of cytoglobin-expressing neurons in the rat hippocampus

2014

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Abstract. Cytoglobin (Cygb), a novel oxygen-binding protein, is expressed in the majority of tissues and has been proposed to function in nitric oxide (NO) metabolism in the vasculature and to have cytoprotective properties. However, the overall functions of Cygb remain elusive. Cygb is also expressed in a subpopulation of brain neurons. Recently, it has been shown that stress upregulates Cygb expression in the brain and the majority of neuronal nitric oxide synthase (nNOS)-positive neurons, an enzyme that produces NO, co-express Cygb. However, there are more neurons expressing Cygb than nNOS, thus a large number of Cygb neurons remain uncharacterized by the neurochemical content. The aim of the present study was to provide an additional and more detailed neurochemical phenotype of Cygb-expressing neurons in the rat hippocampus. The rat hippocampus was chosen due to the abundance of Cygb, as well as this limbic structure being an important target in a number of neurodegenerative diseases. Using triple immunohistochemistry, it was demonstrated that nearly all the parvalbumin-and heme oxygenase 1-positive neurons co-express Cygb and to a large extent, these neuron populations are distinct from the population of Cygb neurons co-expressing nNOS. Furthermore, it was shown that the majority of neurons expressing somastostatin and vasoactive intestinal peptide also co-express Cygb and nNOS. Detailed information regarding the neurochemical phenotype of Cygb neurons in the hippocampus can be a valuable tool in determining the function of Cygb in the brain.

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Section: Discussionmentioning

confidence: 83%

Neurochemical phenotype of cytoglobin-expressing neurons in the rat hippocampus

2014

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“…Parvalbumin-positive neurons are preferentially vulnerable in Alzheimer's disease (Inaguma et al, 1992;Brady and Mufson, 1997). Because of the early effect on the entorhinal cortex (Braak and Braak, 1991), transneuronal dendritic alterations similar to what has been observed after entorhinal cortex lesion are prominent features of this disease (Einstein et al, 1994).…”

Section: Discussionmentioning

confidence: 85%

CXCR3-Dependent Microglial Recruitment Is Essential for Dendrite Loss after Brain Lesion

Rappert¹,

Bechmann²,

Pivneva³

et al. 2004

J. Neurosci.

230

202

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Microglia are the resident macrophage population of the CNS and are considered its major immunocompetent elements. They are activated by any type of brain pathology and can migrate to the lesion site. The chemokine CXCL10 is expressed in neurons in response to brain injury and is a signaling candidate for activating microglia and directing them to the lesion site. We recently identified CXCR3, the corresponding receptor for CXCL10, in microglia and demonstrated that this receptor system controls microglial migration. We have now tested the impact of CXCR3 signaling on cellular responses after entorhinal cortex lesion. In wild-type mice, microglia migrate within the first 3 d after lesion into the zone of axonal degeneration, where 8 d after lesion denervated dendrites of interneurons are subsequently lost. In contrast, the recruitment of microglia was impaired in CXCR3 knock-out mice, and, strikingly, denervated distal dendrites were maintained in zones of axonal degeneration. No differences between wild-type and knock-out mice were observed after facial nerve axotomy, as a lesion model for assessing microglial proliferation. This shows that CXCR3 signaling is crucial in microglia recruitment but not proliferation, and this recruitment is an essential element for neuronal reorganization.

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“…Although Alzheimer's disease (AD) is well-established to be associated with widespread reductions in hippocampal volume, at least one study has indicated that loss of interneurons in AD is more prevalent in DG and CA1-2, rather than CA3 [125]. It is possible that CA2 volume reduction distinguishes AD from Mild Cognitive Impairment (MCI), since a selective reduction in the CA1-2 border region has been reported in MCI [126], indicative of CA2's importance in cognitive processing.…”

Section: Box 4: Ca2 In Diseasementioning

confidence: 99%

Updating hippocampal representations: CA2 joins the circuit

Jones

McHugh

2011

Trends in Neurosciences

114

106

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The hippocampus integrates the encoding, storage and recall of memories, binding the spatiotemporal and sensory information that constitutes experience and keeping episodes in their correct context. The rapid and accurate processing of such daunting volumes of continuouslychanging data relies on dynamically assigning different aspects of mnemonic processing to specialized, interconnected networks corresponding to the anatomical subfields of dentate gyrus (DG), CA3 and CA1. However, differentially processed information ultimately has to be reintegrated into conjunctive representations, and this is unlikely to be achieved by unidirectional, sequential steps through a DG-CA3-CA1 loop. In this Review, we highlight recently discovered anatomical and physiological features that are likely to necessitate updates to the hippocampal circuit diagram, particularly by incorporating the oft-neglected CA2 region.3

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Parvalbumin-immunoreactive neurons in the hippocampal formation of Alzheimer's diseased brain

Cited by 106 publications

References 37 publications

Neurochemical phenotype of cytoglobin-expressing neurons in the rat hippocampus

Neurochemical phenotype of cytoglobin-expressing neurons in the rat hippocampus

CXCR3-Dependent Microglial Recruitment Is Essential for Dendrite Loss after Brain Lesion

Updating hippocampal representations: CA2 joins the circuit

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