Total number of neurons in the layers of the human entorhinal cortex

West, Mark J.; Slomianka, Lutz

doi:10.1002/(sici)1098-1063(1998)8:1<69::aid-hipo7>3.0.co;2-2

Cited by 50 publications

(14 citation statements)

References 34 publications

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“…3a, however, we find a wide range of values from ∼350,000 to ∼500,000 neurons. This wide range in the total number of neurons is not unique to the SN as there is a similar variability in the number of neurons in hippocampus [46,48] and entorhinal cortex [49] of normal subjects. Our estimation of total number of pigmented neurons in younger subjects is higher than that of previous studies (adjusted for one side of the SN): Ma et al [29] ∼150,000, and Cabello et al [7] 189,000.…”

Section: Discussionmentioning

confidence: 85%

Morphometry of the human substantia nigra in ageing and Parkinson’s disease

Rudow¹,

O’Brien

Savonenko³

et al. 2008

Acta Neuropathol

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164

117

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To investigate the relation between the loss of substantia nigra (SN) neurons in normal ageing and Parkinson's disease (PD), we measured the total number and the cell body volume of pigmented (neuromelanin) neurons in the SN. We examined young (n = 7, mean age: 19.9), middle-aged (n = grudow1@jhmi.edu. NIH Public Access NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author Manuscript 9, mean age: 50.1), and older controls from the Baltimore Longitudinal Study of Aging (n = 7, mean age: 87.6), as well as PD cases (n = 8, mean age: 74.8). On random-systematically selected paraffin Nissl-stained sections, we used the Optical Fractionator to estimate the total number of neurons on one side of the SN. Using the Nucleator probe, we measured the volume of these neurons. In young and older controls, we also estimated the total number and volume of tyrosine hydroxylase (TH) positive (+) nigral neurons. We observed a significant loss of pigmented (-28.3%, P < 0.01) and TH (+) (−36.2%, P < 0.001) neurons in older controls compared with younger subjects. Analysis of the size distribution of pigmented and TH (+) neurons showed a significant hypertrophy in older controls compared to young controls (P < 0.01). In contrast, in PD we observed a significant atrophy of pigmented neurons compared to all control groups (P < 0.01). These data suggest that neuronal hypertrophy represents a compensatory mechanism within individual SN neurons that allows for normal motor function despite the loss of neurons in normal ageing. Presumably, this compensatory mechanism breaks down or is overwhelmed by the pathological events of PD leading to the onset of the characteristic motor disturbances.

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Section: Discussionmentioning

confidence: 85%

Morphometry of the human substantia nigra in ageing and Parkinson’s disease

Rudow¹,

O’Brien

Savonenko³

et al. 2008

Acta Neuropathol

Self Cite

164

117

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“…Quantification of total number of urothelial cells (A) and total Ki-67-positive urothelial cells (B) was achieved by stereological counting (9). Reliable estimates of the number of Ki-67-positive cells contained within the developing urinary tract were determined by use of the Optical Fractionator (59,60). WT, wild-type; KO, knockout or FGF-7-null; horizontal bar is mean. }…”

Section: Discussionmentioning

confidence: 99%

Compensatory paracrine mechanisms that define the urothelial response to injury in partial bladder outlet obstruction

Lendvay

Sweet

Han

et al. 2007

American Journal of Physiology-Renal Physiology

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Diseases and conditions affecting the lower urinary tract are a leading cause of dysfunctional sexual health, incontinence, infection, and kidney failure. The growth, differentiation, and repair of the bladder's epithelial lining are regulated, in part, by fibroblast growth factor (FGF)-7 and -10 via a paracrine cascade originating in the mesenchyme (lamina propria) and targeting the receptor for FGF-7 and -10 within the transitional epithelium (urothelium). The FGF-7 gene is located at the 15q15-q21.1 locus on chromosome 15 and four exons generate a 3.852-kb mRNA. Five duplicated FGF-7 gene sequences that localized to chromosome 9 were predicted not to generate functional protein products, thus validating the use of FGF-7-null mice as an experimental model. Recombinant FGF-7 and -10 induced proliferation of human urothelial cells in vitro and transitional epithelium of wild-type and FGF-7-null mice in vivo. To determine the extent that induction of urothelial cell proliferation during the bladder response to injury is dependent on FGF-7, an animal model of partial bladder outlet obstruction was developed. Unbiased stereology was used to measure the percentage of proliferating urothelial cells between obstructed groups of wild-type and FGF-7-null mice. The stereological analysis indicated that a statistical significant difference did not exist between the two groups, suggesting that FGF-7 is not essential for urothelial cell proliferation in response to partial outlet obstruction. In contrast, a significant increase in FGF-10 expression was observed in the obstructed FGF-7-null group, indicating that the compensatory pathway that functions in this model results in urothelial repair.

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“…The left and right hemispheres were counted separately. Sampled regions in the hippocampal formation included the stratum pyramidale, the layer of pyramidal cells in the subiculum, and the middle layers in the parahippocampal gyrus, (the mesocortical Pre-β -, Pre-γ - (West and Slomianka 1998), and Priα -fi elds, as well as isocortical laminae III (lamina pyramidalis), IV (lamina granularis interna) and V (lamina ganglionaris)). The anatomical classifi cation was performed as described previously (Braak 1974(Braak , 1978.…”

Section: Confounding Factorsmentioning

confidence: 99%