Parvalbumin-immunoreactive neurons in the cortex in Pick's disease

Arai, Heii; Noguchi, Iwahide; Makino, Yutaka; Kosaka, Kenji; Cw, Heizmann; Iizuka, Ryo

doi:10.1007/bf00314780

Cited by 23 publications

(9 citation statements)

References 6 publications

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“…These results are interesting because parvalbumin-containing neurons form a subpopulation of GABAergic neurons (Celio, 1986;Kosaka et al, 1987;DeFelipe et al, 1989;Hendry et al, 1989;Lewis and Lund, 1990;VanBrederode et al, 1990;Demeulemeester et al, 1991), and also because previous reports focusing on the isocortex indicate that in AD there is no change in the density of these cells (Ferrer et al? 1991;Fonseca et al, 1993;Hof et al, 1993) but, rather, changes in their morphology (Arai et al, 1987;Satoh et al, 1991;Fonseca et al, 1993). A single biochemical report describes a decrease of >50%# in the quantity of parvalbumin in the parahippocampal gyrus (Inaguma et al, 1992).…”

Section: Discussionmentioning

confidence: 99%

“…Such changes are known to occur in AD in other cortical areas (Hyman et al, 1987;Masliah et al, 1993). On the other hand, and even though as in the isocortex (Arai et al, 1987;Satoh, 1992;Fonseca et al, 1993), some of the parvalbumin neurons remaining had morphological abnormalities in their processes, it is difficult to explain how the density of these cells is maintained in these latest grades of pathology. Differential vulnerability of parvalbumin neurons in cortical layers is not an unusual occurrence in the cerebral cortex.…”

Section: Grades 3 Andmentioning

confidence: 99%

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Contingent Vulnerability of Entorhinal Parvalbumin-Containing Neurons in Alzheimer’s Disease

Solodkin

Veldhuizen²,

Hoesen

1996

J. Neurosci.

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Calcium-binding proteins containing local circuit neurons are distributed ubiquitously in the human cerebral cortex where they colocalize with a subpopulation of cells that contain GABA. Several reports using a variety of pathological models, including Alzheimer's disease (AD), have suggested that cells containing calcium-binding proteins are resistant to pathological insults. In this report, we test the hypothesis that AD pathology can differentially affect parvalbumin-containing cells depending on their location in the entorhinal cortex and the state of projection neurons with which they are associated. Using cases with different quantities of AD pathology, we determined the density of immunostaining for parvalbumin in the entorhinal cortex, and we correlated this with the concomitant pathological lesions in the various layers of this cortex. Our results show a clear decrease in parvalbumin immunostaining in some parts of the entorhinal cortex when AD neuropathological markers are present. As the density of pathological markers in the entorhinal cortex becomes greater and more widespread, there is a decrease of parvalbumin immunostaining in additional layers, although in all cases, some cells persist. Parvalbumin-containing neurons are clearly vulnerable in AD, but not because of neurofibrillary tangle formation. Instead, they are rendered vulnerable only after substantial loss of projection neurons; only then do they, too, become part of the lesion.

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Section: Discussionmentioning

confidence: 99%

Section: Grades 3 Andmentioning

confidence: 99%

Contingent Vulnerability of Entorhinal Parvalbumin-Containing Neurons in Alzheimer’s Disease

Solodkin

Veldhuizen²,

Hoesen

1996

J. Neurosci.

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“…Changes in the functional architecture of local circuits within the human prefrontal cortex and in the cingulate cortices (posterior and anterior divisions) have been identified as underlying neuropsychiatric disorders such as Pick's disease (Arai et al, 1991), Alzheimers disease (Braak and Braak, 1993), and in schizophrenia (Vogt and Gabriel, 1993;Akbarian et al, 1995;Benes, 1995).…”

Section: Human Mpfc and Neuropsychiatric Disordersmentioning

confidence: 99%

Local circuit neurons in the medial prefrontal cortex (areas 24a,b,c, 25 and 32) in the monkey: I. Cell morphology and morphometrics

1996

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This paper provides a comprehensive morphological description of local circuit neurons in the medial prefrontal cortex (mPFC: areas 24a, 24b, 24c, 25 and 32) of the monkey. Cortical interneurons were identified immunocytochemically by the expression of the calcium binding proteins calretinin (CR), parvalbumin (PV) and calbindin D-28k (CB). Interneurons were also identified using GABA immunocytochemistry. The areal and laminar distributions of CR, PV, and CB cells were consistent across mPFC; their morphological characteristics identified them as local circuit neurons. Throughout layers 2-6: CR immunoreactivity labelled double bouquet and bipolar neurons, PV was localised in large and small basket neurons and in chandelier (axoaxonic) cells, while CB immunoreactivity was present in double bouquet, Martinotti, and neurogliaform neurons. In addition, some cells in layer 1 (including Cajal-Retzius neurons) were CR immunoreactive. Calbindin immunoreactivity also labelled a population of large nonpyramidal neurons deep in the cortex. Other types of CR, PV and CB cells were also immunolabelled. A small population of layer 3 pyramidal cells was weakly CB immunoreactive. Peak cell densities occurred in layer 2/upper layer 3 for CR+ neurons and in upper to midlayer 3 for CB+ cells. PV+ neuron density peaked in midcortex. These observations support and extend a similar study of monkey prefrontal cortex (Condé et al. [1994] J. Comp. Neurol. 341:95-116). The morphologies and combined cortical depth distributions of CR+, PV+, and CB+ neurons were similar to GABA-immunolabelled cells. Local circuit neurons in mPFC displaying NADPH diaphorase activity composed less than 0.25% of the total neuron population, and were distributed in two horizontal strata, in mid- to lower layer 3 and in lower layer 5/upper layer 6. CR, PV and CB immunoreactivity was colocalised in NADPH diaphorase-reactive neurons. The interrelationships between CR+, PV+ and CB+ neurons were investigated using dual immunocytochemistry. CR+ puncta were found to be closely associated with the cell bodies and proximal processes of PV+ neurons, whereas CR+ puncta were located more distally over processes from CB+ cells. Additionally, PV+ puncta were found closely apposed to PV+ somata and processes and CR+ puncta abutted against CR+ cell bodies. The companion paper (Gabbott and Bacon [1996] J. Comp. Neurol.) presents quantitative data regarding the areal and laminar distributions of the identified cell classes in mPFC. Such data provide a realistic structural framework with which to investigate neuronal operations in monkey mPFC.

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“…In the cortex, PN-wearing interneurons are often associated with the calciumbinding protein parvalbumin (PV) and the potassium channel subunit Kv3.1b (Ha¨rtig et al, 1995(Ha¨rtig et al, , 1999. In the brainstem PNs are widely expressed and especially associated with fast-spiking neurons (Arai et al, 1991;Caicedo et al, 1996;Lohmann and Friauf, 1996;Dodson et al, 2003;Elezgarai et al, 2003). In this regard the calyx of Held-MNTB principal neuron complex shows one of the fastest synaptic transmission pathways in the mammalian brain (von Gersdorff and .…”

Section: Introductionmentioning

confidence: 98%

Unique features of extracellular matrix in the mouse medial nucleus of trapezoid body – Implications for physiological functions

et al. 2013

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Parvalbumin-immunoreactive neurons in the cortex in Pick's disease

Cited by 23 publications

References 6 publications

Contingent Vulnerability of Entorhinal Parvalbumin-Containing Neurons in Alzheimer’s Disease

Contingent Vulnerability of Entorhinal Parvalbumin-Containing Neurons in Alzheimer’s Disease

Local circuit neurons in the medial prefrontal cortex (areas 24a,b,c, 25 and 32) in the monkey: I. Cell morphology and morphometrics

Unique features of extracellular matrix in the mouse medial nucleus of trapezoid body – Implications for physiological functions

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