Disease relevance of Neurons

• HBGF-2 is also a nerve cell survival molecule, for it potentiates the survival of primary cultures of embryonic chick ciliary ganglion cells but not of embryonic neural retina cells [1].
• The fusion of bone-marrow-derived proinsulin-expressing cells with nerve cells underlies diabetic neuropathy [2].
• The present studies show that the values of Km and Vmax and the sensitivity of phosphodiesterase activity to divalent ions change in cyclic AMP-induced differentiated neuroblastoma cells, and therefore we propose that the reverse may be true during malignant transformation of nerve cells [3].
• The degree of neurofibrillary tangle formation, granulovascuolar degeneration, and nerve cell loss was quantified in serial sections of the hippocampal formation from the brains of 5 adults dying with Down syndrome (monogolism) [4].
• In this study, we examined whether versican, a recognized anti-cell adhesive molecule for various mesenchymal and nerve cell types, influences prostate cancer cell adhesion to extracellular matrix components [5].

Psychiatry related information on Neurons

• Huntington's disease (HD) is a dominantly inherited fatal disorder characterised by premature death of nerve cells [6].
• Secondly, alpha-synuclein is present in Lewy bodies of affected nerve cells in the predominant sporadic type of Parkinson's disease as well as in dementia with Lewy bodies [7].
• In Alzheimer's disease, this protein is present in the somatodendritic compartment of certain nerve cells, where it forms a portion of paired helical filament, the major constituent of the neurofibrillary tangle [8].
• The results indicate that the activity of 5-HT nerve cells adjacent to the ventrolateral surface of the medulla oblongata and projecting to the spinal cord serves to elevate pain threshold [9].
• The mother's dietary choline during a critical period in brain development of her infant influences the rate of birth and death of nerve cells in this center [10].

High impact information on Neurons

• In situ hybridization revealed that KIF1B is expressed abundantly in differentiated nerve cells [11].
• These findings indicate that cerebral accumulation of PrPSc and its degradation products may play a role in the nerve cell degeneration that occurs in prion-related encephalopathies [12].
• Nerve growth factor, fibroblast growth factor and purpurin, have been identified as nerve-cell survival molecules [13].
• Receptors for excitatory amino-acid transmitters on nerve cells fall into two main categories associated with non-selective cationic channels, the NMDA (N-methyl-D-aspartate) and non-NMDA (kainate and quisqualate) receptors [14].
• We show that in this system cholinergic agonists activate functional ion channels, that have properties comparable to those exhibited by the peripheral AChRs in vertebrates; thus, for the first time a functional acetylcholine receptor channel has been identified in nerve cells [15].

Chemical compound and disease context of Neurons

• In the trigeminal ganglion and in the dorsal root ganglion at level C2, one-third of the TB-labeled nerve cell bodies were CGRP-immunoreactive, while only few nerve cell bodies contained SP [16].
• When an ion flux assay is used, it is possible to measure specifically the activity of the ionophore associated with the nicotinic acetylcholine receptor in cultured nerve cells (PC-12 pheochromocytoma) [17].
• Unilateral injection of kainate into the right amygdala produced epileptic seizures, as well as selective degeneration of nerve cells restricted to the ipsilateral CA3 and CA4 regions of the hippocampus, followed by the development of gliosis [18].
• Is the loss of cerebral cortical choline acetyl transferase activity in Alzheimer's disease due to degeneration of ascending cholinergic nerve cells [19].
• Excessive activation of NMDA receptors results in excitotoxic nerve cell loss, which is believed to play a critical role in the pathophysiology of Huntington's disease (HD) and several other catastrophic neurodegenerative diseases [20].

Biological context of Neurons

• Using immature cortical neurons and a clonal nerve cell line, it is shown that a decrease in GSH triggers the activation of neuronal 12-lipoxygenase (12-LOX), which leads to the production of peroxides, the influx of Ca2+, and ultimately to cell death [21].
• The data presented here show that PC-PLC also is required in oxidative glutamate-induced programmed cell death of both immature cortical neurons and a hippocampal nerve cell line, HT22 [22].
• It has been difficult to establish whether cyclic AMP-mediated protein phosphorylation in nerve cells plays a specific role in synaptic transmission [23].
• In this paper, the electrically conductive polymer--oxidized polypyrrole (PP)--has been evaluated for use as a substrate to enhance nerve cell interactions in culture as a first step toward potentially using such polymers to stimulate in vivo nerve regeneration [24].
• Nerve cells, which were obtained from fetal rats at 18 to 20 days of gestation, were plated at very low density onto polylysine-treated coverslips and were maintained in serum-free medium [25].

Anatomical context of Neurons

• This article describes current understanding of the mechanism by which synapsin I modulates communication between nerve cells and reviews the properties and putative functions of other phosphoproteins associated with synaptic vesicles [26].
• The neuropeptide Y-containing nerve cell bodies were preferentially located in the submucous ganglia [27].
• By immunohistochemical methods, immunoreactive vasoactive intestinal polypeptide and immunoreactive substance P were localized to both nerve cell bodies and nerve fibers in the ferret intestine [28].
• The effect correlated temporally with decreased mast cells and histamine, suggesting a functional role for previously reported mast cell-nerve interactions [29].
• The nerve cell bodies of the submucous plexus contained vasoactive intestinal polypeptide, substance P, leu-enkephalin, somatostatin, and 5-hydroxytryptamine but not neuropeptide Y, met-enkephalin, calcitonin gene-related peptide, and dopamine beta-hydroxylase [30].

Associations of Neurons with chemical compounds

• GABA and picrotoxinin receptors in clonal nerve cells [31].
• An initial effect of nerve growth factor on a responsive nerve cell line is to increase intracellular cyclic AMP, which in turn leads to a mobilisation of calcium ions [32].
• Desensitisation of muscarinic receptor-mediated cyclic GMP formation by cultured nerve cells [33].
• Asymmetrical displacement currents in nerve cell membrane and effect of internal fluoride [34].
• These data are compatible with the concept that noradrenaline hyperpolarizes nerve cells by decreasing resting membrane conductances to sodium and potassium ions [35].

Gene context of Neurons

• Glial cell line-derived neurotrophic factor (GDNF) induced hyperactivation of ERK and Akt in enteric nerve cells [36].
• Since leukemia inhibitory factor functions as a cholinergic differentiation factor in nerve cells, as does ciliary neurotrophic factor, these results suggest that gp130 may also play a role in the nervous system [37].
• However, a small subpopulation of synapses in any given glutamatergic nerve cell as well as all gamma-aminobutyratergic (GABAergic) synapses are largely independent of Munc13-1 [38].
• Accordingly, the promoter domain containing HF1 and HF2 is recognized by cerebellum nuclear extracts containing Engrailed and Foxa2 and has regulatory functions in primary cultures of embryonic mesmetencephalic nerve cells [39].
• A considerable portion of the TB-labeled nerve cell bodies in the superior cervical ganglion contained NPY [16].

Analytical, diagnostic and therapeutic context of Neurons

• Along similar lines, animal models have been produced that result in the formation of alpha-synuclein filaments and the degeneration of dopaminergic nerve cells [40].
• In pig fetuses VIP immunoreactive nerve cell bodies were observed already at crown-rump length of 4 cm [41].
• To determine the functions of these molecules, Schwann cell-nerve cell cultures were grown in medium containing a specific inhibitor of proteoglycan biosynthesis, 4-methylumbelliferyl-beta-D-xyloside [42].
• Molecular cloning of cDNAs for the nerve-cell specific phosphoprotein, synapsin I [43].
• Immunocytochemistry studies confirm the expression of this protein in nerve cells, a tissue in which full length dystrophin is not detected [44].

References