An immunohistochemical study of pro-somatostatin-derived peptides in the human brain

Bouras, Constantin; Magistretti, Pierre J.; Morrison, John H.; Constantinidis, J

doi:10.1016/0306-4522(87)92959-9

Cited by 97 publications

(54 citation statements)

References 55 publications

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“…Neverthe less, the data suggest a loss of SRIF-positive cell bodies in the parahippocampal cortex in accordance with previous reports [31,32,37,38,40], The preservation of SRIFpositive cell bodies in the hippocampus and their relative alteration in the parahippocampal cortex of patients with AD contrast with other qualitative [34. 72, 73] and semiquantitative [30] investigations but are in agreement with observations of Armstrong et al [37,73]. That SRIFimmunostained neuronal cell bodies are spared in the pathological hippocampus is compatible with the general morphological characteristics of SRIF-positive neurons (cross-sectional area, orientation and absence of neurofi brillary tangles) when compared to controls (table 3, fig.…”

Section: Srif and Npy Invmmocytochemistry In Brains Of Patients With Adsupporting

confidence: 81%

Hippocampal and Parahippocampal Somatostatin 28 and Neuropeptide Y Containing Neurons in Alzheimer's Disease (Part 2 of 2)

Cervera-Pierot

Hirsch

Javoy‐Agid

et al. 1992

Dement Geriatr Cogn Disord

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The somatostatinergic innervation, and by comparison that of neuropeptide Y, was examined by immunocytochemistry, in the hippocampal formation of 6 patients with clinically and neuropathologically confirmed diagnosis of Alzheimer's disease (AD) and 4 matched controls. The quantitative assessment of the somatostatin and neuropeptide Y immunoreactive cell perikarya was conducted on regularly spaced sections covering the span of the whole hippocampus and parahippocampal cortex. The estimated total number of somatostatin or neuropeptide Y containing neurons was similar in the hippocampal formation of patients with AD and controls. By contrast, the density of the somatostatinergic fibers and terminals as estimated by the optical density of the somatostatin neuropil, significantly decreased by 30-45% in all the hippocampal subregions and the parahippocampal cortex, whereas the density of the neuropeptide Y immunoreactive neuropil significantly decreased (45%) only in the parahippocampal cortex. Numerous enlarged fibers containing somatostatin or neuropeptide Y, some of which were observed within senile plaques, were detected in the brain of patients with AD. These data suggest that in AD, somatostatin and neuropeptide Y containing cell bodies in the hippocampus and parahippocampal gyrus are anatomically preserved, in spite of an altered terminal field.

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Section: Srif and Npy Invmmocytochemistry In Brains Of Patients With Adsupporting

confidence: 81%

Hippocampal and Parahippocampal Somatostatin 28 and Neuropeptide Y Containing Neurons in Alzheimer's Disease (Part 2 of 2)

Cervera-Pierot

Hirsch

Javoy‐Agid

et al. 1992

Dement Geriatr Cogn Disord

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“…According to primate studies, specific neuronal classes in which somatostatin would be found are likely to be double-bouquet interneurons (de Lima and Morrison, 1989), a subclass of interneurons which is incidentally known to be resistant to the degenerative process of AD until late in the disease (Hof et al, 1993). SRIF-containing interneurons are primarily found in layer III, V and VI and immunoreactive fibers are distributed in all layers (Braak et al, 1985;Beal and Martin, 1986;Bouras et al, 1986;Hornung et al, 1992). Thus, localization of PC1 and PC2 is consistent with their putative role in activation of regulatory peptides in vivo, such as proSRIF.…”

Section: Discussionmentioning

confidence: 99%

The proprotein convertase PC2 is involved in the maturation of prosomatostatin to somatostatin-14 but not in the somatostatin deficit in Alzheimer's disease

et al. 2003

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Abstract-A somatostatin deficit occurs in the cerebral cortex of Alzheimer's disease patients without a major loss in somatostatin-containing neurons. This deficit could be related to a reduction in the rate of proteolytic processing of peptide precursors. Since the two proprotein convertases (PC)1 and PC2 are responsible for the processing of neuropeptide precursors directed to the regulated secretory pathway, we examined whether they are involved first in the proteolytic processing of prosomatostatin in mouse and human brain and secondly in somatostatin defect associated with Alzheimer's disease. By size exclusion chromatography, the cleavage of prosomatostatin to somatostatin-14 is almost totally abolished in the cortex of PC2 null mice, while the proportions of prosomatostatin and somatostatin-28 are increased. By immunohistochemistry, PC1 and PC2 were localized in many neuronal elements in human frontal and temporal cortex. The convertases levels were quantified by Western blot, as well as the protein 7B2 which is required for the production of active PC2. No significant change in PC1 levels was observed in Alzheimer's disease. In contrast, a marked decrease in the ratio of the PC2 precursor to the total enzymatic pool was observed in the frontal cortex of Alzheimer patients. This decrease coincides with an increase in the binding protein 7B2. However, the content and enzymatic activity of the PC2 mature form were similar in Alzheimer patients and controls. Therefore, the cortical somatostatin defect is not due to convertase alteration occuring during Alzheimer's disease. Further studies will be needed to assess the mechanisms involved in somatostatin deficiency in Alzheimer's disease.

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“…Reacting epitopes were found by radioimmunoassay (RIA) to be located on amino acids 5 to 12 [ 18], No cross reactivity by adsorption experiments was found with the following pep tides: Leu-enkephalin, Met-enkephalin, ß-endorphin, Sub stance P, Dynorphin(l-13), VIP, CCK, Eledoisin, Neu rotensin, Vasopressin, Neuropeptide Y, Physalaemin, and S-sleep inducing peptide [4]. Crossreactivity of S320 with SST fragments, other than S S T 1-12 was tested in RIAs; reactivity with SST 15-28 was absent and minimal (0.01%) with SST1-28 [I].…”

Section: Antiseramentioning

confidence: 96%

Somatostatin 1–12 immunoreactivity is decreased in the hypothalamic lateral tuberal nucleus of Huntington's disease patients

et al. 1996

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The hypothalamic lateral tuberal nucleus (NTL) can be recognized in man and higher primates, only. The function of this nucleus is unknown, but the NTL is affected in a variety of human neurodegenerative diseases, including Huntington's disease (HD) and Alzheimer's disease. In the present study we demonstrate an abundant presence of somatostatin 1-12 (SST1-12) immunoreactivity in both neurites and perikarya of the NTL. This immunoreactivity could be visualized best after microwave pretreatment. In HD brains, NTL SST1-12 immunoreactivity was greatly reduced, providing further evidence of the presence of SST1-12 as an intrinsic neuropeptide in the NTL. Although striatal SST neurons escape destruction in HD, our study demonstrates that not all SST neurons are resistant to the degenerative process in this disease.

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An immunohistochemical study of pro-somatostatin-derived peptides in the human brain

Cited by 97 publications

References 55 publications

Hippocampal and Parahippocampal Somatostatin 28 and Neuropeptide Y Containing Neurons in Alzheimer's Disease (Part 2 of 2)

Hippocampal and Parahippocampal Somatostatin 28 and Neuropeptide Y Containing Neurons in Alzheimer's Disease (Part 2 of 2)

The proprotein convertase PC2 is involved in the maturation of prosomatostatin to somatostatin-14 but not in the somatostatin deficit in Alzheimer's disease

Somatostatin 1–12 immunoreactivity is decreased in the hypothalamic lateral tuberal nucleus of Huntington's disease patients

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