Differential localization of nadph-diaphorase and calbindin-D28k within the cholinergic neurons of the basal forebrain, striatum and brainstem in the rat, monkey, baboon and human

Geula, Changiz; Schatz, C; Mesulam, Marsel

doi:10.1016/0306-4522(93)90266-i

Cited by 175 publications

(128 citation statements)

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“…Firstly, low concentrations of Ab may effectively modulate cholinergic neurotransmission (Abe et al, 1994;Kar et al, 1996;Auld et al, 1998). Cholinergic neurons of the rat basal forebrain are devoid of Ca 2+ -binding`buffer' proteins, such as calbindin-D28k and parvalbumin (Geula et al, 1993;Van der Zee & Luiten, 1994), which have been shown to be excito-protective by attenuating the intracellular Ca 2+ overload (Mattson et al, 1991;Harkany et al, 1995a). Secondly, Kuner et al (1998) reported that Ab directly binds p75 NTR and thereby initiates a neurotoxic cascade through subsequent activation of nuclear factor kB.…”

Section: Discussionmentioning

confidence: 99%

β‐Amyloid neurotoxicity is mediated by a glutamate‐triggered excitotoxic cascade in rat nucleus basalis

Harkany

Ábrahám

Timmerman

et al. 2000

Eur J of Neuroscience

259

151

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β-Amyloid neurotoxicity is mediated by a glutamate-triggered excitotoxic cascade in rat nucleus basalis Harkany, T.; Ábrahám, I.; Timmerman, W.; Laskay, G.; Tóth, B.; Sasvári, M.; Kónya, C.; Sebens, J.B.; Korf, Jakob; Nyakas, C. Link to publication in University of Groningen/UMCG research database Citation for published version (APA): Harkany, T., Ábrahám, I., Timmerman, W., Laskay, G., Tóth, B., Sasvári, M., ... Luiten, P. G. M. (2000). β-Amyloid neurotoxicity is mediated by a glutamate-triggered excitotoxic cascade in rat nucleus basalis. European Journal of Neuroscience, 12, 2735-2745. CopyrightOther than for strictly personal use, it is not permitted to download or to forward/distribute the text or part of it without the consent of the author(s) and/or copyright holder(s), unless the work is under an open content license (like Creative Commons).Take-down policy If you believe that this document breaches copyright please contact us providing details, and we will remove access to the work immediately and investigate your claim.Downloaded from the University of Groningen/UMCG research database (Pure): http://www.rug.nl/research/portal. For technical reasons the number of authors shown on this cover page is limited to 10 maximum. SummaryWhereas a cardinal role for b-amyloid protein (Ab) has been postulated as a major trigger of neuronal injury in Alzheimer's disease, the pathogenic mechanism by which Ab deranges nerve cells remains largely elusive. Here we report correlative in vitro and in vivo evidence that an excitotoxic cascade mediates Ab neurotoxicity in the rat magnocellular nucleus basalis (MBN). In vitro application of Ab to astrocytes elicits rapid depolarization of astroglial membranes with a concomitant inhibition of glutamate uptake. In vivo Ab infusion by way of microdialysis in the MBN revealed peak extracellular concentrations of excitatory amino acid neurotransmitters within 20±30 min. Ab-triggered extracellular elevation of excitatory amino acids coincided with a signi®cantly enhanced intracellular accumulation of Ca 2+ in the Ab injection area, as was demonstrated by 45 Ca 2+ autoradiography. In consequence of these acute processes delayed cell death in the MBN and persistent loss of cholinergic ®bre projections to the neocortex appear as early as 3 days following the Ab-induced toxic insult. Such a sequence of Ab toxicity was effectively antagonized by the N-methyl-D-aspartate (NMDA) receptor ligand dizocilpine maleate (MK-801). Moreover, Ab toxicity in the MBN decreases with advancing age that may be associated with the age-related loss of NMDA receptor expression in rats. In summary, the present results indicate that Ab compromises neurons of the rat MBN via an excitotoxic pathway including astroglial depolarization, extracellular glutamate accumulation, NMDA receptor activation and an intracellular Ca 2+ overload leading to cell death.

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Section: Discussionmentioning

confidence: 99%

β‐Amyloid neurotoxicity is mediated by a glutamate‐triggered excitotoxic cascade in rat nucleus basalis

Harkany

Ábrahám

Timmerman

et al. 2000

Eur J of Neuroscience

259

151

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“…In humans, the mesencephalic locomotor region is located in the dorsolateral portion of the midbrain [8].…”

Section: Introductionmentioning

confidence: 99%

Correlation of midbrain diameter and gait disturbance in patients with idiopathic normal pressure hydrocephalus

et al. 2005

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The clinical elements of the NPH gait can be summarized as a hypokinetic gait which is characterized by diminished gait velocity, reduced stride length, reduced step height, and dynamic disequilibrium [17,28,31,34]. Patients with many other neurodegenerative diseases, such as Parkinson's disease, subcortical arteriosclerotic encephalopathy, progressive supranuclear palsy (PSP), and corticobasal degeneration, may develop hypokinetic gait during the disease progression [4,35,37] ■ Abstract Background and purpose Although gait disturbance is an important feature of idiopathic normal pressure hydrocephalus (NPH), only tentative theories have been offered to explain its pathophysiology. It has been suggested that the mesencephalic locomotor region is the anatomical substrate for the development of the hypokinetic NPH gait. To investigate this possibility, we evaluated the correlation between gait disturbance and midbrain diameter. Methods We enrolled 21 patients with NPH and 20 age-matched control subjects for the study. The maximal diameter of the midbrain and pons, and the width of the lateral and third ventricles were measured using midsagittal T1-weighted MRI and axial T2-weighted MRI, respectively. Gait disturbance, cognitive dysfunction, and incontinence were semiquantified. Results The maximal midbrain diameter was significantly smaller in the NPH group than in the controls (14.8 ± 0.9 vs. 17.1 ± 0.7 mm, p < 0.001). There were inverse correlations between the midbrain diameter and the widths of the two ventricles (r = -0.562, p = 0.008 for the third ventricle, and r = -0.510, p = 0.018 for the lateral ventricle). The severity of gait disturbance was negatively correlated with the midbrain diameter (r = -0.598, p = 0.004), but the degree of cognitive dysfunction and incontinence showed no significant correlation with midbrain diameter or ventricular width. Conclusions This study suggests that midbrain atrophy is significantly associated with gait disturbance in NPH.

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“…In contrast, the parvalbumin (PV) and calbindin subfamilies of CBPs, the latter including the vitamin D-dependent 28 kDa isoform of calbindin (CB) and calretinin (CR), exhibit restricted tissue-specific expression patterns in vertebrates (5,6). During the past decades, PV, CB, and CR received significant attention because of their exquisite developmentally regulated cell type-specific expression in the mammalian nervous system (6)(7)(8).…”

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confidence: 99%

Secretagogin is a Ca ²⁺ -binding protein specifying subpopulations of telencephalic neurons

Mulder

Zilberter²,

Spence

et al. 2009

Proc. Natl. Acad. Sci. U.S.A.

144

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The Ca 2؉ -binding proteins (CBPs) parvalbumin, calbindin, and calretinin are phenotypic markers of terminally differentiated neurons in the adult brain. Although subtle phylogenetic variations in the neuronal distribution of these CBPs may occur, morphologically and functionally diverse subclasses of interneurons harbor these proteins in olfactory and corticolimbic areas. Secretagogin (scgn) is a recently cloned CBP from pancreatic ␤ and neuroendocrine cells. We hypothesized that scgn is expressed in the mammalian brain. We find that scgn is a marker of neuroblasts commuting in the rostral migratory stream. Terminally differentiated neurons in the olfactory bulb retain scgn expression, with scgn being present in periglomerular cells and granular layer interneurons. In the corticolimbic system, scgn identifies granule cells distributed along the dentate gyrus, indusium griseum, and anterior hippocampal continuation emphasizing the shared developmental origins, and cytoarchitectural and functional similarities of these neurons. We also uncover unexpected phylogenetic differences in scgn expression, since this CBP is restricted to primate cholinergic basal forebrain neurons. Overall, we characterize scgn as a neuronspecific CBP whose distribution identifies neuronal subtypes and hierarchical organizing principles in the mammalian brain.cortex ͉ development ͉ interneuron ͉ neurogenesis ͉ stem cell T he ability to release neurotransmitters at chemical synapses, to integrate the activity of diverse synaptic inputs and trigger molecular mechanisms underlying neuronal adaptation, as well as to maintain excitability in neurons rely on the refined spatial and temporal control of momentary changes in cytosolic [Ca 2ϩ ] (1, 2). Ca 2ϩ -binding proteins (CBPs) represent a means to effectively regulate intracellular Ca 2ϩ dynamics (3). Members of the EF-hand family of CBPs invariably contain a 3-D motif to bind Ca 2ϩ at its physiological cytosolic concentrations (4). Some ancestral representatives of this protein family, such as calmodulin, are ubiquitously expressed with a high degree of evolutionary conservation and are involved in the control of fundamental cellular functions ranging from the cell cycle, cell motility and axon polarization to synaptic signaling (3). In contrast, the parvalbumin (PV) and calbindin subfamilies of CBPs, the latter including the vitamin D-dependent 28 kDa isoform of calbindin (CB) and calretinin (CR), exhibit restricted tissue-specific expression patterns in vertebrates (5, 6). During the past decades, PV, CB, and CR received significant attention because of their exquisite developmentally regulated cell type-specific expression in the mammalian nervous system (6-8).CBPs show a unique association with newly generated neurons in the adult brain (9, 10). Neural progenitors that are born in the subependymal zone and migrate in the rostral migratory stream (RMS) to differentiate into interneurons in the olfactory bulb (OB) commonly express CR at their neuroblast stage with select subpopulations ...

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Differential localization of nadph-diaphorase and calbindin-D28k within the cholinergic neurons of the basal forebrain, striatum and brainstem in the rat, monkey, baboon and human

Cited by 175 publications

References 73 publications

β‐Amyloid neurotoxicity is mediated by a glutamate‐triggered excitotoxic cascade in rat nucleus basalis

β‐Amyloid neurotoxicity is mediated by a glutamate‐triggered excitotoxic cascade in rat nucleus basalis

Correlation of midbrain diameter and gait disturbance in patients with idiopathic normal pressure hydrocephalus

Secretagogin is a Ca ²⁺ -binding protein specifying subpopulations of telencephalic neurons

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Differential localization of nadph-diaphorase and calbindin-D28k within the cholinergic neurons of the basal forebrain, striatum and brainstem in the rat, monkey, baboon and human

Cited by 175 publications

References 73 publications

β‐Amyloid neurotoxicity is mediated by a glutamate‐triggered excitotoxic cascade in rat nucleus basalis

β‐Amyloid neurotoxicity is mediated by a glutamate‐triggered excitotoxic cascade in rat nucleus basalis

Correlation of midbrain diameter and gait disturbance in patients with idiopathic normal pressure hydrocephalus

Secretagogin is a Ca 2+ -binding protein specifying subpopulations of telencephalic neurons

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Product

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Secretagogin is a Ca ²⁺ -binding protein specifying subpopulations of telencephalic neurons