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Spinal cord, in vivo

Lapadula DM, Irwin RD, Suwita E et al. 1986. Cross-linking of neurofilament proteins of rat spinal cord in vivo after administration of 2,5-hexanedione. J Neurochem 46 1843-1850. [Pg.239]

Abrahamsson C (2000) Neuropeptide Y1- and Y2-receptor-mediated cardiovascular effects in the anaesthetized guinea pig, rat, and rabbit. J Cardiovasc Pharmacol 36 451-8 Ackley MA, Hurley RW, Virnich DE et al (2001) A cellular mechanism for the antinociceptive effect of a kappa opioid receptor agonist. Pain 91 377-88 Aimone LD, Yaksh TL (1989) Opioid modulation of capsaicin-evoked release of substance P from rat spinal cord in vivo. Peptides 10 1127-31... [Pg.429]

Donatsch P, Lowe D A, Richardson B P, and Taylor P (1977) The functional significance of sodium channels in pancreatic beta-cell membranes f Physiol 1 7, 357-376 Fagg G. E, Jones I M, and Jordan C C (1978) Descending fiber-mediated release of endogenous glutamate and glycine from the perfused cat spinal cord in vivo Brain Res 158, 159-170. [Pg.266]

Morton I K M, Stagg C F, and Webster R A (1977) Perfusion of the central canal and subarachnoid space of the cat and rabbit spinal cord in vivo Neuropharmacot 16, 1-6... [Pg.268]

Yaksh, T. L., Jessell, T. M., Gamse, R., Mudge, A. W., and Leeman, S. E., 1980, Intrathecal morphine inhibits substance P release from mammalian spinal cord in vivo. Nature 286 155-157. [Pg.236]

Antagonist potencies were determined in the cat spinal cord in vivo and frog spinal cord m vitro as summarized by Watkins et al. (1980) and Davies et al. (1979). [Pg.240]

The second technique is the hemisected spinal cord in vitro, initially of amphibia but now more commonly of neonatal rats [6]. Grease-seals or suction electrodes are used to record DC potentials or synaptic responses from ventral or dorsal roots. Since compounds are usually added to the bathing solution, more quantitative information from this in vitro preparation can be obtained than fi-om microelectrophoresis experiments in vivo. [Pg.246]

The 2,3-benzodiazepine, GYKI 52466, was first shown to block spinal reflexes [61] and subsequently to block responses to AMPA on spinal neurones in vivo [63]. Following electrophoretic ejection of GYKI 52466, responses to kainate were reduced in parallel with those to AMPA whereas those to NMDA were unaffected. The block is clearly non-competitive on cortical slices and presumably will also be on spinal cord tissue when tested in vitro. [Pg.247]

Motor neurons provide a compelling example of how a single class of neurons can be supported by an extraordinarily wide range of factors. More than 15 growth factors have been shown in vitro or in vivo to sustain these cells. Some of these are derived from the muscle target, while others are elaborated by ensheathing Schwann cells and by cells resident within the spinal cord. It is likely that motor neurons rely upon multiple factors for their survival and different subpopulations of motor neurons may exhibit unique combinations of trophic factor dependence [4]. [Pg.483]

Nogo-A neutralizing antibodies lead to axonal growth and functional recovery in vivo. After cell culture experiments, the next step was to show the ability to block myelin inhibitors and achieve axonal regrowth after spinal cord injury. The monoclonal antibody IN-1 was initially raised against myelin fractions enriched for... [Pg.522]

Sharp T, Bramwell SR, Lambert P, et al Effect of short- and long-term administration of lithium on the release of endogenous 5-HT in the hippocampus of the rat in vivo and in vitro. Neuropharmacology 30 977-984, 1991 Sharpley AL, Cowen PJ Effect of the pharmacological treatment on sleep of depressed patients. Biol Psychiatry 37 85-98, 1995 Sharpley AL, Walsh AES, Cowen PJ Nefazodone—a novel antidepressant— may increase REM sleep. Biol Psychiatry 31 1070-1073, 1992 Shaw DM, Harris B, Lloyd AT, et al A comparison of the antidepressant action of citalopram and amitriptyline. Br J Psychiatry 149 515-517, 1986 Shaw PJ, Ince PG A quantitative autoradiographic study of H-3-Kainate binding sites in the normal human spinal-cord, brain stem, motor cortex. Brain Res 641 39-45, 1994... [Pg.743]

Martens, D.J., Seaberg, R.M., van der Kooy, D. (2002). In vivo infusions of exogenous growth factors into the fourth ventricle of the adult mouse brain increase the proliferation of neural progenitors around the fourth ventricle and the central canal of the spinal cord. Eur JNeurosci, 16, 1045-57. [Pg.30]

Ex vivo Locomotor recovery and cell migration Four injections of 35 HuCNS-SCs were injected into spinal cord injured NOD/SCID mice 9 days after contusion HuCNS-SC engraftment was associated with loco-motor recovery at 16 weeks ost-treatment. By 17 weeks post-treatment, cells had migrated days after con-tusion away from the lesion epicenter, in sagittal sections, with some transplanted cells found > 1 cm from the lesion epicenter 623960-... [Pg.53]

Matos, F. F., Rollema, H., Brown, J. L., Basbaum, A. I. Do opioids evoke the release of serotonin in the spinal cord An in vivo microdialysis study of the regulation of extracellular serotonin in the rat, Pain 1992, 48, 439-447. [Pg.282]

Tsukada (30) have examined developmental changes of the enzyme in chick brain and spinal cord. Enzymic activity appears at about the eighteenth day of incubation and increases rapidly until 3 days after hatching in the brain and between 18 and 21 days of incubation in the spinal cord. These are precisely the periods of active myelination in the brain and spinal cord of the chick, respectively. Similarly, brain tissue of the newborn rat is devoid of cyclic phosphate diesterase activity it appears at about 8 days after birth and increases dramatically between the tenth and thirty-fifth day of life (29). This coincides precisely with the development of myelin in this species. The diesterase is essentially absent in the brain of the jimpy mouse (31), a lethal mutant devoid of myelin in the central nervous system. It is also absent from the spinal cord of this mutant. The enzyme is about 50% deficient in brain tissue of the quaking mouse (29), a mutant with partial deficiency of myelin. There is no activity in nerve fibers and ganglia from a variety of invertebrates such as squid, octopus, crab, shrimp, and starfish. Nerve tissue in these organisms is nonmyelinated. All these observations point to an intimate association of the enzyme with myelin in vivo. [Pg.365]

In vitro, urotensin II is a potent constrictor of vascular smooth muscle its activity depends on the type of blood vessel and the species from which it was obtained. Vasoconstriction occurs primarily in arterial vessels, where urotensin II can be more potent than endothelin 1, making it the most potent known vasoconstrictor. In vivo, urotensin II has complex hemodynamic effects, the most prominent being regional vasoconstriction and cardiac depression. The extent to which the peptide is involved in the regulation of vascular tone and blood pressure in humans is not clear recent studies have produced conflicting results. The actions of urotensin II are mediated by G protein-coupled receptors that are widely distributed in the brain, spinal cord, heart, vascular smooth muscle, skeletal muscle, and pancreas. Some effects of the peptide including vasoconstriction are mediated by the phospholipase C/IP3/DAG signal transduction pathway. [Pg.433]

Bian, F., Li, Z., Offord, J., Davis, M. D., McCormick, J., Taylor, C. P, et al. (2006) Calcium channel alpha2-delta type 1 subunit is the major binding protein for pregabalin in neocortex, hippocampus, amygdala, and spinal cord an ex vivo autoradiographic study... [Pg.53]

Pohl, M., Ballet, S., Collin, E., Mauborgne, A., Bourgoin, S., Benoliel, J. J., Hamon, M., and Cesselin, F. (1997). Enkephalinergic and dynorphinergic neurons in the spinal cord and dorsal root ganglia of the polyarthritic rat—in vivo release and cDNA hybridization studies. Brain Res. 749, 18-28. [Pg.202]

Application of in vitro test methods have become advantageous in specific cases, such as structurally defined compounds and delayed neuropathy, since target cell data and biochemical processes associated in delayed neuropathy are known. Microscopic studies reveal that cases of OPIDN have degeneration of axons followed by demyelination of the nervous system.25,26 Epidemiologic studies have indicated mild impairment of the brainstem, spinal cord, and peripheral nerve functions in Gulf War veterans.27 Such studies are consistent with the spectrum of OPIDN syndrome. The main nerve agents have been shown to inhibit NTE in vitro as well as in vivo. Sarin has been shown to produce delayed neurotoxicity when administered at higher doses in protected hens.25-27... [Pg.128]


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See also in sourсe #XX -- [ Pg.613 ]




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