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Intracellular mGluR5 can mediate synaptic plasticity in the hippocampus.
J Neurosci
March 2014
Department of Anatomy and Neurobiology, Washington University School of Medicine, St. Louis, Missouri 63110, and Department of Psychiatry and Taylor Family Institute for Innovative Psychiatric Research, Washington University School of Medicine, St. Louis, Missouri 63110.
Metabotropic glutamate receptor 5 (mGluR5) is widely expressed throughout the CNS and participates in regulating neuronal function and synaptic transmission. Recent work in the striatum led to the groundbreaking discovery that intracellular mGluR5 activation drives unique signaling pathways, including upregulation of ERK1/2, Elk-1 (Jong et al., 2009) and Arc (Kumar et al.
View Article and Find Full Text PDFMy first 20 years in neuroscience.
Fiziol Zh (1994)
September 2011
O.O. Bogomoletz Institute of Physiology, National Academyof Sciences of Ukraine, Kiev.
Intriguing facts were obtained in the first electrophysiological investigations (1964) that the action potentials (AP) produced by direct depolarization of the cell membrane in different species of mollusks showed specific relations to changes in external ionic composition. In Helix neurons, the generation of AP was well maintained in sodium-free solutions with high calcium or barium content. The amplitude of the spike overshoot in the case was linearly related to the logarithm of calcium concentration.
View Article and Find Full Text PDFUptake of ibuprofen, indomethacin and ketoprofen into isolated rabbit parietal cells.
J Pharm Pharmacol
May 2000
Division of Pharmaceutics, College of Pharmacy, The University of Iowa, Iowa City 52245, USA.
In the United States and other countries, non-steroidal anti-inflammatory drugs (NSAIDs) can be purchased without a prescription. Due to their widespread use, the drugs' most common side effect, gastric toxicity, becomes a more serious concern. Gastric toxicity can occur directly by contact with mucous membranes or indirectly by the inhibition of prostaglandin production in the gastric mucosa.
View Article and Find Full Text PDF[Cortisone-induced osteoporosis: from physiopathology to treatment].
Rev Med Interne
March 1992
Service de Rhumatologie, CHRU Angers.
Corticosteroid-induced osteoporosis, the principal cause of "secondary" osteoporosis, is usually observed in patients under prolonged systemic corticosteroid therapy and results from the multiple effects exerted by these drugs on bone cell metabolism. Corticosteroids reduce the intestinal absorption of calcium and its tubular reabsorption, thereby negativating the calcium balance and inducing a parathyroid reaction. This reaction is responsible for an increase in bone cell remodelling, but the main manifestation of the direct effect of corticosteroids on bone is osteoblast depression, so that there is disparity between bone resorption and formation, which in turn is responsible for bone tissue deficit.
View Article and Find Full Text PDFSodium-calcium exchange in vascular smooth muscle of Wistar-Kyoto and stroke-prone spontaneously hypertensive rats.
J Hypertens Suppl
December 1988
University of Michigan, Department of Physiology, Ann Arbor 48109.
The role of the sodium-calcium (Na-Ca) exchange in vascular smooth muscle contraction was examined in tail artery rings isolated from stroke-prone spontaneously hypertensive rats (SHRSP) and in normotensive Wistar-Kyoto rats (WKY). The rings were repeatedly stimulated with noradrenaline (1 microM) in physiological salt solution (Na = 130 mM), until two successive contractions were of the same magnitude. The rings were then placed in physiological salt solution with reduced sodium concentrations (65 mM or 0 mM, replaced isosmotically with sucrose), and the noradrenaline stimulations continued.
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