Cortical projection of putative group Ib afferent fibres from the human forearm

Rossi, Alessandro; Mazzocchio, Riccardo; Parlanti, S

doi:10.1016/0006-8993(91)90574-f

Cited by 17 publications

(6 citation statements)

References 30 publications

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“…Autoradiography binding studies were performed by preincubating sections for 15 minutes in PBS buffer (pH 7.4) followed by incubation with 5 ml of respective ligand; 1 nM [ 3 H]-PIB (specific activity, SA 68 Ci/mmol, custom synthesis; GE Healthcare, Freiburg, Germany) for 45 minutes [21]; 10 nM [ 3 H]- l -deprenyl (specific activity 80 Ci/mmol, Larodan Fine Chemicals AB, Malmö, Sweden) for 1 h [22]; 5.0 nM [ 3 H]-nicotine (specific activity 75 Ci/mmol, NEN Life Science Products, Dreiech, Germany) for 40 minutes [23]; and 2 nM [ 125 I] α-bungarotoxin (specific activity 108.8 Ci/mmol, Perkin Elmer, Waltham, MA, USA) for 30 minutes [24]. To determine non-specific binding for each radioligand, adjacent sections were incubated with 1 μM of unlabeled PIB, 1 μM unlabeled deprenyl, 100 μM (−) nicotine or 1 μM unlabeled α-bungarotoxin (Tocris Bioscience, Bristol, UK), respectively.…”

Section: Methodsmentioning

confidence: 99%

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3H-Deprenyl and 3H-PIB autoradiography show different laminar distributions of astroglia and fibrillar β-amyloid in Alzheimer brain

Marutle

Gillberg

Bergfors

et al. 2013

J Neuroinflammation

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BackgroundThe pathological features in Alzheimer’s disease (AD) brain include the accumulation and deposition of β-amyloid (Aβ), activation of astrocytes and microglia and disruption of cholinergic neurotransmission. Since the topographical characteristics of these different pathological processes in AD brain and how these relate to each other is not clear, this motivated further exploration using binding studies in postmortem brain with molecular imaging tracers. This information could aid the development of specific biomarkers to accurately chart disease progression.ResultsIn vitro binding assays demonstrated increased [3H]-PIB (fibrillar Aβ) and [3H]-PK11195 (activated microglia) binding in the frontal cortex (FC) and hippocampus (HIP), as well as increased binding of [3H]-l-deprenyl (activated astrocytes) in the HIP, but a decreased [3H]-nicotine (α4β2 nicotinic acetylcholine receptor (nAChR)) binding in the FC of AD cases compared to age-matched controls. Quantitative autoradiography binding studies were also performed to investigate the regional laminar distributions of [3H]-l-deprenyl, [3H]-PIB as well as [125I]-α-bungarotoxin (α7 nAChRs) and [3H]-nicotine in hemisphere brain of a typical AD case. A clear lamination pattern was observed with high [3H]-PIB binding in all layers and [3H]-deprenyl in superficial layers of the FC. In contrast, [3H]-PIB showed low binding to fibrillar Aβ, but [3H]-deprenyl high binding to activated astrocytes throughout the HIP. The [3H]-PIB binding was also low and the [3H]-deprenyl binding high in all layers of the medial temporal gyrus and insular cortex in comparison to the frontal cortex. Low [3H]-nicotine binding was observed in all layers of the frontal cortex in comparison to layers in the medial temporal gyrus, insular cortex and hippocampus. Immunohistochemical detection in the AD case revealed abundant glial fibrillary acidic protein positive (GFAP+) reactive astrocytes and α7 nAChR expressing GFAP+ astrocytes both in the vicinity and surrounding Aβ neuritic plaques in the FC and HIP. Although fewer Aβ plaques were observed in the HIP, some hippocampal GFAP+ astrocytes contained Aβ-positive (6 F/3D) granules within their somata.ConclusionsAstrocytosis shows a distinct regional pattern in AD brain compared to fibrillar Aβ, suggesting that different types of astrocytes may be associated with the pathophysiological processes in AD.

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Section: Methodsmentioning

confidence: 99%

“…All laminar identification examinations were carried out with guidance of a classical atlas Brodman [25] and Nissl stained sections, and further assisted by autoradiograms of [ 3 H]- l -deprenyl binding, since [ 3 H]- l -deprenyl has earlier been shown to have a clear demarcation between different laminae in human brain cortex [22,26]. …”

Section: Methodsmentioning

confidence: 99%

3H-Deprenyl and 3H-PIB autoradiography show different laminar distributions of astroglia and fibrillar β-amyloid in Alzheimer brain

Marutle

Gillberg

Bergfors

et al. 2013

J Neuroinflammation

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“…The alcoholism-related changes in astrocyte numbers and their markers may be due, at least partly, to direct inhibitory effects of ethanol on astrocyte proliferation or turnover. Both in astrocytes cultured from neonatal rodents (Davies and Cox, 1991 ; Guerri and Renau-Piqueras, 1997 ; Guerri, 1998 ) or from postmortem human brain tissue autopsies (Kane et al, 1996 ) ethanol exposure causes substantial inhibition of astrocyte proliferation and synthesis of DNA and protein, including reduced expression of the major astrocyte marker GFAP. After prolonged exposure, this inhibition may lead to decreased astrocyte numbers, as well as impaired ability to perform the critical functions enumerated earlier in this review.…”

Section: Molecular Pathology Of Astrocytes In Alcohol Use Disordersmentioning

confidence: 99%

Molecular Neuropathology of Astrocytes and Oligodendrocytes in Alcohol Use Disorders

Miguel-Hidalgo

2018

Front. Mol. Neurosci.

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Postmortem studies reveal structural and molecular alterations of astrocytes and oligodendrocytes in both the gray and white matter (GM and WM) of the prefrontal cortex (PFC) in human subjects with chronic alcohol abuse or dependence. These glial cellular changes appear to parallel and may largely explain structural and functional alterations detected using neuroimaging techniques in subjects with alcohol use disorders (AUDs). Moreover, due to the crucial roles of astrocytes and oligodendrocytes in neurotransmission and signal conduction, these cells are very likely major players in the molecular mechanisms underpinning alcoholism-related connectivity disturbances between the PFC and relevant interconnecting brain regions. The glia-mediated etiology of alcohol-related brain damage is likely multifactorial since metabolic, hormonal, hepatic and hemodynamic factors as well as direct actions of ethanol or its metabolites have the potential to disrupt distinct aspects of glial neurobiology. Studies in animal models of alcoholism and postmortem human brains have identified astrocyte markers altered in response to significant exposures to ethanol or during alcohol withdrawal, such as gap-junction proteins, glutamate transporters or enzymes related to glutamate and gamma-aminobutyric acid (GABA) metabolism. Changes in these proteins and their regulatory pathways would not only cause GM neuronal dysfunction, but also disturbances in the ability of WM axons to convey impulses. In addition, alcoholism alters the expression of astrocyte and myelin proteins and of oligodendrocyte transcription factors important for the maintenance and plasticity of myelin sheaths in WM and GM. These changes are concomitant with epigenetic DNA and histone modifications as well as alterations in regulatory microRNAs (miRNAs) that likely cause profound disturbances of gene expression and protein translation. Knowledge is also available about interactions between astrocytes and oligodendrocytes not only at the Nodes of Ranvier (NR), but also in gap junction-based astrocyte-oligodendrocyte contacts and other forms of cell-to-cell communication now understood to be critical for the maintenance and formation of myelin. Close interactions between astrocytes and oligodendrocytes also suggest that therapies for alcoholism based on a specific glial cell type pathology will require a better understanding of molecular interactions between different cell types, as well as considering the possibility of using combined molecular approaches for more effective therapies.

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“…In humans, passive movement CHAPTER 4: KINESTHESIA 143 of joints as well as selective stimulation of muscle afferents evokes somatosensory cortical potentials (e.g., 42, 106). Attempts have followed to confirm a cortical projection from tendon organs with "selective" stimulation of Ib afferents (281), but the technique is insufficiently sensitive because the transverse vibration used to raise the electrical threshold of primary spindle afferents will not recruit them with certainty (see 63).…”

Section: Cortical Projectionsmentioning

confidence: 99%