| 1. |
- Carlberg, Mats, et al.
(författare)
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Presence of 3 4-dihydroxyphenylalanine and 3,4,5-trihydroxyphenylalanine in a coelenterate nervous system: possible tyrosinase-mediated accumulation.
- 1987
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Ingår i: Neurochemistry International. - : Elsevier BV. - 0197-0186. ; 11, s. 161-167
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Tidskriftsartikel (refereegranskat)abstract
- 3,4-dihydroxyphenylalanine (DOPA), 3,4,5-trihydroxyphenylalanine (5-OH-DOPA), 5-S-cysteinylDOPA (5-SC.D) and 2-S-cysteinylDOPA (2-SC.D) in the tentacles of the sea anemone, Metridium senile, were studied by the combined use of differential centrifugation of tissue homogenates, ultracentrifugation on sucrose density gradients, HPLC and electron microscopy. DOPA, 5-OH-DOPA and o-diphenol:O2 oxidoreductase (Tyrosinase) were enriched in fractions containing membranes and subcellular particles, and the cysteinylDOPAs in the cytosol fractions. Ultrastructurally studied fractions rich in DOPA and 5-OH-DOPA contained large numbers of highly osmium-reducing vesicles. Identical structures were localized in ectodermal nerves and epidermal sensory cells.The results suggest that previous findings of catecholderivatives in the tentacles of Metridium and other sea anemone species by histochemical methods, are explained by a tyrosinase-based accumulation of DOPA and 5-OH-DOPA in the ectodermal nerve net. These substances are confined in specific compartments (vesicles) in the neurons and sensory cells.
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| 2. |
- del Carmen Boyano-Adánez, María, et al.
(författare)
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Effect of calmodulin antagonists on phospholipase D activity in SH-SY5Y cells.
- 2002
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Ingår i: Neurochemistry International. - 0197-0186. ; 40:3, s. 261-268
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Tidskriftsartikel (refereegranskat)abstract
- The aim of this study was to investigate the involvement of calmodulin in phospholipase D activation in SH-SY5Y cells. Cells prelabelled with [3H]-palmitic acid were incubated with calmodulin antagonists and/or other compounds. Phosphatidylethanol, a specific marker for phospholipase D activity, and phosphatidic acid were analysed. The calmodulin antagonists, calmidazolium and trifluoperazine, induced an extensive increase in phosphatidylethanol formation, and thus increased basal phospholipase D activity, in a dose- and time-dependent manner. The effect of calmidazolium on carbachol-induced activation of muscarinic receptors was also studied. Calmidazolium did not significantly affect the amount of phosphatidylethanol formed following carbachol addition. However, taking into account the increase in basal activity observed after calmidazolium addition, calmidazolium probably inhibits the muscarinic receptor-induced phospholipase D activation. In addition to phosphatidylethanol, basal phosphatidic acid levels were also increased after calmidazolium and trifluoperazine addition. Incubation with calmidazolium (10 microM) for 10 min induced a two-fold increase in phosphatidic acid. The calmidazolium-induced increase in basal phospholipase D activity was not affected by the protein kinase inhibitors H7 and staurosporine. On the other hand tyrosine kinase inhibitors abolished the calmidazolium-induced activation of phospholipase D. Calmidazolium also induced tyrosine phosphorylation in parallel to the phospholipase D activation. In conclusion, our data indicate that calmodulin antagonists induce phospholipase D activity in SH-SY5Y cells via a tyrosine kinase dependent pathway. This may point to a negative control of phospholipase D by calmodulin although a calmodulin-independent mechanism cannot be excluded. Calmodulin antagonists may be useful tools to further elucidate the mechanisms of phospholipase D regulation.
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| 3. |
- Ding, W Q, et al.
(författare)
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Acute ethanol exposure attenuates expression of junD in human neuroblastoma cells
- 1998
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Ingår i: Neurochemistry International. - 0197-0186. ; 33:6, s. 525-530
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Tidskriftsartikel (refereegranskat)abstract
- This study describes the effects of acute ethanol exposure on the mRNA levels of c-jun,junB and junD in the human neuroblastoma SH-SY5Y cell line. An acute exposure to 100 mM ethanol did not influence the basal and phorbol ester-induced expression of c-jun and junB, whereas the basal mRNA level of junD was attenuated by 30%. This effect was dose- and time-dependent with maximal inhibition being detected 2 h after 100 mM ethanol treatment and the mRNA levels gradually returned towards normal afterwards. Ethanol also inhibited phorbol ester-induced expression of junD. The fact that ethanol did not influence degradation of the junD mRNA suggests that acute ethanol suppresses the transcription of the gene. These results indicate that acute ethanol exerts different effects on expression of Jun transcription factors, suggesting that as compared to c-jun and junB, the junD gene may be more sensitive to acute ethanol treatment in neuronal cells.
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| 4. |
- Ehinger, B, et al.
(författare)
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Retinal indoleamine accumulating neurons
- 1980
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Ingår i: Neurochemistry International. - : Elsevier BV. - 0197-0186. ; 1C, s. 29-209
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Tidskriftsartikel (refereegranskat)abstract
- A previously unknown set of neurons, characterized by their ability to accumulate indoleamines, has been identified in the retina of Cebus monkeys, rabbits, cats, pigeons, chicken, goldfish and lampreys. They are not demonstrable with presently available techniques in humans, Cynomolgus monkeys, cows, pigs and rats. The neurons are called indoleamine accumulating neuron and form a subset of amacrine cells, distinguishable from all other subsets of amacrines with known transmitter. By electron microscopy they have been shown to be contacted by bipolar cells in the dyad arrangement and to form reciprocal contacts on the bipolar cells. A procedure is available for destroying selectively the processes of the indoleamine accumulating neurons. The indoleamine accumulating neurons do not show any formaldehyde induced fluorescence in the normal animals or in animals in which the 5-hydroxytryptamine concentration in the brain has been elevated pharmacologically, and the 5-hydroxytryptamine concentration in the normal retina is too low to make it a likely neurotransmitter. What little is present is presumably in blood platelets in most cases (chicken may be an exception). The rate limiting enzyme in the 5-hydroxytryptamine synthesis, tryptophan hydroxylase, is not detectable in the retina. 5-hydroxytryptamine does not elicit any increase in retinal cyclic AMP. There is an energy dependent, high affinity uptake system for indoleamines but the effect of various inhibitors is different from that on the uptake into brain tissue. Several lines of evidence thus disfavour 5-hydroxytryptamine as a retinal neurotransmitter. Nevertheless, the active uptake of indoleamines suggests that the transmitter of the indoleamine accumulating neurons is an indole which, however, at present remains unidentified.
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| 5. |
- Perez, M T, et al.
(författare)
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Stimulation-evoked release of purines from the rabbit retina
- 1988
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Ingår i: Neurochemistry International. - : Elsevier BV. - 0197-0186. ; 13:3, s. 18-307
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Tidskriftsartikel (refereegranskat)abstract
- The evoked release of purines from rabbit retinae preloaded with [(3)H]adenosine was studied in vitro. Potassium (8.6-43.6 mM) and ouabain (1 or 10 microM) increased the release of radioactivity in a concentration-dependent manner. The K(+)-evoked release was significantly reduced when the superfusion was carried out at 2-4 degrees C. The effect of K(+) (8.6, 13.6 and 23.6 mM) and of ouabain (1 microM) were completely abolished when the retinae were superfused with a Ca(2+)-free medium containing 0.1 mM EGTA. Calcium removal only partially reduced the effect of higher K(+) and ouabain concentrations (43.6 mM and 10 microM, respectively). Further, the effect of K(+) was found to be independent of extracellular Ca(2+) when retinae were pretreated with ouabain for 30 min. Stimulation of the retina with light flashes induced a small, persistent increase in the release of radioactivity observable for several minutes after the end of stimulation. The superfusate contained mainly hypoxanthine and inosine. There were no significant changes in the relative proportions of the different purine compounds released before or in response to either K(+) (23.6 mM) or ouabain (10 microM) stimulation. Potassium stimulation significantly increased the release of adenosine, inosine and hypoxanthine. Addition of the adenosine deaminase inhibitor, erythro-9-(2-hydroxy-3-nonyl)adenine (EHNA), significantly increased the relative proportions of released endogenous adenosine and inosine. The results indicate that K(+) stimulation induces the release of purines from the rabbit retina by a Ca(2+)- and energy-dependent process. Light flashes also induce a purine release. The results suggest an active role for adenosine in retinal neurotransmission.
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| 6. |
- Tornqvist, K, et al.
(författare)
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Simultaneous immunohistochemistry and autoradiography of peptides and 5-hydroxytryptamine in bird retina
- 1983
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Ingår i: Neurochemistry International. - : Elsevier BV. - 0197-0186. ; 5:5, s. 86-579
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Tidskriftsartikel (refereegranskat)abstract
- A method was developed for the simultaneous demonstration of two specific cellular constituents. Cryostat sections of formaldehyde fixed tissue from retinae treated with ((3)H)-5-hydroxytryptamine were subjected to immunohistochemistry and subsequent autoradiography. The method takes advantage of the very efficient and specific uptake mechanism that many types of neurons possess which makes it possible to label them with radioactivity. With this method a study was made on the possible co-occurrence in the avian retina of 5-hydroxytryptamine on one hand and somatostatin, glucagon and substance P on the other. Substance P and 5-hydroxytryptamine were investigated in pigeon retina whereas 5-hydroxytryptamine and somatostatin or glucagon were investigated in chicken retina. Though a large number of cell bodies were examined no co-occurrence of 5-hydroxytryptamine and any of the peptides was found. The sensitivity of the method allows an assertion that if present, double labelled neurons are likely to number less than 0.5-1% of the respective populations.
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