| 1. |
- Jankowska, Elzbieta, et al.
(författare)
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Effects of Monoamines on Transmission from Group II Muscle Afferents in Sacral Segments in the Cat Szabo Läckberg, Z. & Dyrehag, L.E.
- 1994
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Ingår i: European Journal of Neuroscience. - : Wiley. - 0953-816X .- 1460-9568. ; 6, s. 1058-1061
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Tidskriftsartikel (refereegranskat)abstract
- The effects of one 5‐HT1A serotonin agonist (8‐OH‐DPAT) and of two α2 noradrenaline agonists (tizanidine and B‐HT 933) were tested on the transmission between group II muscle afferents and spinal neurons in the sacral segments of the spinal cord in the cat. These agonists have previously been found to depress transmission from group II muscle afferents either in the dorsal horn or in the intermediate zone of midlumbar segments, and this study addressed the question of whether their actions in the sacral segments are similarly selective. The drugs were applied ionophoretically and their effects were tested on field potentials evoked from group II muscle afferents. As judged by changes in the amplitude of the early components of these field potentials, the transmission is effectively depressed by the serotonin agonist (to 56 ± 26% after 2 min of ionophoresis of 8‐OH‐DPAT) but not by the noradrenaline agonists (to 97 ± 12% after 6 min of ionophoresis of B‐HT 933 and to 95 ± 17% after 6 min of ionophoresis of tizanidine). These data suggest that transmission from group II muscle spindle afferents in the sacral segments is under control of serotonin releasing neurons, as in the dorsal horn of midlumbar segments, but leave open the question of the similarities or differences in the mechanisms (pre‐and/or postsynaptic) of this control. Copyright © 1994, Wiley Blackwell. All rights reserved
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| 2. |
- Kokaia, Zaal, et al.
(författare)
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Brain insults in rats induce increased expression of the BDNF gene through differential use of multiple promoters
- 1994
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Ingår i: European Journal of Neuroscience. - : Wiley. - 1460-9568 .- 0953-816X. ; 6:4, s. 587-596
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Tidskriftsartikel (refereegranskat)abstract
- The rat brain-derived neurotrophic factor (BDNF) gene consists of four short 5'-exons linked to separate promoters and one 3'-exon encoding the mature BDNF protein. Using in situ hybridization we demonstrate here that kindling-induced seizures, cerebral ischaemia and insulin-induced hypoglycaemic coma increase BDNF mRNA levels through insult- and region-specific usage of three promoters within the BDNF gene. Both brief (2 min) and longer (10 min) periods of forebrain ischaemia induced significant and major increases only of exon III mRNA in the dentate gyrus. Following hypoglycaemic coma (1 and 30 min), exon III mRNA was markedly elevated in the dentate gyrus and, in addition, exon I mRNA showed a moderate increase. Single and recurrent (n = 40) hippocampal seizures significantly increased expression of exon I, II and III mRNAs in the dentate gyrus granule cells. After recurrent seizures, including generalized convulsions, there were also major increases of both exon I and III mRNAs in the CA3 region, amygdala, piriform cortex and neocortex, whereas in the hippocampal CA1 sector marked elevations were detected only for exon III mRNA. The insults had no effect on the level of exon IV mRNA in the brain. The region- and insult-specific pattern of promoter activation might be of importance for the effectiveness of protective responses as well as for the regulation of plastic changes following brain insults.
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| 3. |
- Smits, Anja, et al.
(författare)
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PDGF-BB exerts trophic activity on cultured GABA interneurons from the newborn rat cerebellum.
- 1993
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Ingår i: European Journal of Neuroscience. - 0953-816X .- 1460-9568. ; 5:8, s. 986-94
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Tidskriftsartikel (refereegranskat)abstract
- Platelet-derived growth factor (PDGF) is a well known mitogen for mesenchyme-derived cells and glial cells. Its presence in neuronal cells of the central nervous system has only recently been described. We have shown earlier that neurons of newborn rat brains in culture express PDGF beta-receptors and that PDGF-BB, a homodimer of PDGF B-chain, increases survival and promotes neurite outgrowth of newborn cerebellar cells (Smits et al., Proc. Natl Acad. Sci. USA, 88, 8159-8163, 1991). In this study, the effects of PDGF on early postnatal rat cerebellar cells were further explored. By using chemically defined serum-free medium, we have established primary cell cultures of rat cerebella (postnatal day 4-5) containing 70-80% neuronal cells. During the first 10 days in vitro, no difference in total cell number was found between PDGF-BB-treated and untreated cultures. After this time period, however, increased survival of the PDGF-BB-treated cells was found. Within the first 10 days in vitro, the addition of PDGF-BB to the cultures resulted in a relative increase in survival of interneurons expressing glutamic acid decarboxylase (GAD), the GABA biosynthetic enzyme. Moreover, addition of PDGF-BB in the untreated cell culture resulted in a rapid increase of GAD mRNA. These results show that PDGF-BB acts as a trophic factor on GABAergic interneurons of the cerebellum by up-regulating GAD synthesis and prolonging the survival of these cells. Furthermore, in situ hybridization revealed that there are scattered cells present in the early postnatal cerebellum that express PDGF beta-receptor mRNA.
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