The Experts below are selected from a list of 33 Experts worldwide ranked by ideXlab platform
Martti Raisanen - One of the best experts on this subject based on the ideXlab platform.
-
Nialamide an mao inhibitor increases urinary excretion of endogenously produced bufotenin in man
Biological Psychiatry, 1992Co-Authors: Jorma Karkkainen, Martti RaisanenAbstract:Abstract Nialamide, an MAO inhibitor, was given per os (PO) to a normal man who volunteered in two separate trials (total intake 300 mg and 1000 mg, respectively), and his bufotenin excretion was followed by consecutive urine samples. In both experiments the excretion rose well above the values measured from the same test subject when not taking Nialamide (median 0.089 nmol/mmol creatinine, range 0.002–1.78). At its highest, the excretion was 16.5 nmol/mmol creatinine, and the maximum urinary output was 495 nmoles (56 μg) in 24 hr. The levels of bufotenin in plasma required for the excretion of the latter amounts are not far from those that produce psychic symptoms in man.
Jorma Karkkainen - One of the best experts on this subject based on the ideXlab platform.
-
Nialamide an mao inhibitor increases urinary excretion of endogenously produced bufotenin in man
Biological Psychiatry, 1992Co-Authors: Jorma Karkkainen, Martti RaisanenAbstract:Abstract Nialamide, an MAO inhibitor, was given per os (PO) to a normal man who volunteered in two separate trials (total intake 300 mg and 1000 mg, respectively), and his bufotenin excretion was followed by consecutive urine samples. In both experiments the excretion rose well above the values measured from the same test subject when not taking Nialamide (median 0.089 nmol/mmol creatinine, range 0.002–1.78). At its highest, the excretion was 16.5 nmol/mmol creatinine, and the maximum urinary output was 495 nmoles (56 μg) in 24 hr. The levels of bufotenin in plasma required for the excretion of the latter amounts are not far from those that produce psychic symptoms in man.
H. Steffens - One of the best experts on this subject based on the ideXlab platform.
-
Influence of opioids and naloxone on rhythmic motor activity in spinal cats
Experimental Brain Research, 1995Co-Authors: E. D. Schomburg, H. SteffensAbstract:The effects of l -DOPA, naloxone, and the opioids ( d -Ala^2, N -Me-Phe^4,Gly^5-ol)-enkephalin (DAGO) and d -Ser^2-Leu-enkephalin-Thr^6 (DSLET) on spinal motor rhythm generation were compared in anemically decapitated high spinal cats. After premedication with Nialamide, DOPA caused the well-known, slow rhythmic motor activity with a locomotor pattern. The cycle duration of the evoked rhythm was usually between 3.9 and 5.0 s. The opioids DAGO and DSLET, injected intravenously (1.2–2 mg/kg) or suffused over the lumbar spinal cord (10^-3–10^-4 M in Ringer's solution), severely depressed the DOPA-induced rhythmic activity, sometimes completely abolishing efferent motor activity. Naloxone (0.5–1 mg/kg i.v.) exerted different rhythm-facilitating effects, depending on the experimental condition. In the acute phase after spinalization, without paralysis and without Nialamide and DOPA, naloxone induced rhythmic movements with a main frequency of 1.2–2 Hz. In the same preparation with paralysis, naloxone induced a rhythmic motor activity with a distinctly higher frequency (main range 4.3–5.8 Hz). After premedication with Nialamide and DOPA, naloxone facilitated or, if a rhythm was absent, induced the slow-frequency DOPA type of rhythm. Given after i.v. or topical opioid application, naloxone antagonized the rhythm-depressing action of the opioid and caused an additional facilitation of rhythmic activity. Dopa and naloxone facilitated the long-latency, segmental reflex pathways from flexor reflex afferents (FRA), while the opioids depressed them. The short-latency FRA pathways were depressed by DOPA and opioids but were facilitated by naloxone.The influence of the different drugs on spinal motor rhythm generation is discussed in relation to their influence on short- and long-latency segmental pathways from FRA. If the rhythm generation induced by DOPA is based on the release of the long-latency FRA pathways, as has been proposed before, the rhythm-depressing action of opioids may be due to the suppression of these pathways, and the particular rhythm-generating function of naloxone may be related to its facilitation of short- and long-latency FRA pathways.
E. D. Schomburg - One of the best experts on this subject based on the ideXlab platform.
-
Influence of opioids and naloxone on rhythmic motor activity in spinal cats
Experimental Brain Research, 1995Co-Authors: E. D. Schomburg, H. SteffensAbstract:The effects of l -DOPA, naloxone, and the opioids ( d -Ala^2, N -Me-Phe^4,Gly^5-ol)-enkephalin (DAGO) and d -Ser^2-Leu-enkephalin-Thr^6 (DSLET) on spinal motor rhythm generation were compared in anemically decapitated high spinal cats. After premedication with Nialamide, DOPA caused the well-known, slow rhythmic motor activity with a locomotor pattern. The cycle duration of the evoked rhythm was usually between 3.9 and 5.0 s. The opioids DAGO and DSLET, injected intravenously (1.2–2 mg/kg) or suffused over the lumbar spinal cord (10^-3–10^-4 M in Ringer's solution), severely depressed the DOPA-induced rhythmic activity, sometimes completely abolishing efferent motor activity. Naloxone (0.5–1 mg/kg i.v.) exerted different rhythm-facilitating effects, depending on the experimental condition. In the acute phase after spinalization, without paralysis and without Nialamide and DOPA, naloxone induced rhythmic movements with a main frequency of 1.2–2 Hz. In the same preparation with paralysis, naloxone induced a rhythmic motor activity with a distinctly higher frequency (main range 4.3–5.8 Hz). After premedication with Nialamide and DOPA, naloxone facilitated or, if a rhythm was absent, induced the slow-frequency DOPA type of rhythm. Given after i.v. or topical opioid application, naloxone antagonized the rhythm-depressing action of the opioid and caused an additional facilitation of rhythmic activity. Dopa and naloxone facilitated the long-latency, segmental reflex pathways from flexor reflex afferents (FRA), while the opioids depressed them. The short-latency FRA pathways were depressed by DOPA and opioids but were facilitated by naloxone.The influence of the different drugs on spinal motor rhythm generation is discussed in relation to their influence on short- and long-latency segmental pathways from FRA. If the rhythm generation induced by DOPA is based on the release of the long-latency FRA pathways, as has been proposed before, the rhythm-depressing action of opioids may be due to the suppression of these pathways, and the particular rhythm-generating function of naloxone may be related to its facilitation of short- and long-latency FRA pathways.
Arto Palkama - One of the best experts on this subject based on the ideXlab platform.
-
SYMPATHETIC NERVES TO THE RAT CORNEA
Acta Ophthalmologica, 2009Co-Authors: Timo Tervo, Arto PalkamaAbstract:The adrenergic innervation of the rat cornea was investigated by using the formaldehyde induced fluorescence (FIF) technique. The fluorescent nerves were observed mainly in the corneal stroma. Either cervical sympathectomy or pre-treatment with reserpine completely abolished the fluorescence of the adrenergic nerves of the cornea. After a stereotactic coagulation of the ophthalmic division of the trigeminal nerve, no adrenergic fibres were visible in the cornea and the number of the fluorescent iridic nerves was also reduced to a marked extent. On the other hand, ciliary ganglionectomy seemed to have no effect on the adrenergic fibres of the cornea. When the rats had been pre-treated with a monoamine oxidase inhibitor, Nialamide, and noradrenaline, not only was there an increase in the intensity of the specific fluorescence, but also in the number of adrenergic nerves in the cornea. The epithelium was also shown to contain adrenergic nerves by administering high doses of Nialamide combined with noradrenaline, both intravenously as well as topically on the cornea, under the protection of propranolol. It may be concluded that the rat cornea receives its adrenergic innervation along the posterior ciliary nerves. The short ciliary nerves do not appear to carry sympathetic nerves to the cornea.