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M Vainio

Publications and source records attributed to M Vainio.

15 recordsLinked to original sources
PubMed2006

Selective tuning of cortical sound-feature processing by language experience.

In 'quantity-languages', such as Japanese or Finnish, sound duration is linguistically relevant. We showed that quantity-language speakers were superior to speakers of a non-quantity language in discriminating the duration of even non-speech sounds. In contrast, there was no group difference in the discrimination of sound frequency. This result, obtained both by behavioural and neural indices at attentive and automatic levels of processing, indicates precise feature-specific tuning of the auditory-cortex functions by the mother tongue.

Acoustic Stimulation↗
PubMed2000

The role of adenosine A(1) receptors in the ATP-evoked Ca(2+) response in rat thyroid FRTL-5 cells.

The effect of adenosine A(1) receptor activation on the ATP-induced increase in intracellular free Ca(2+) was studied in control and protein kinase C down-regulated Fisher rat thyroid (FRTL-5) cells. Long-term phorbol ester treatment, which leads to protein kinase C down-regulation, enhanced the ATP-evoked extracellular Ca(2+) influx. The increased Ca(2+) influx was antagonized by the adenosine A(1) receptor antagonist 8-cyclopentyl-1, 3-dipropylxanthine (DPCPX). [3H]DPCPX binding studies revealed that phorbol ester-treatment increased the number of adenosine A(1) receptors. The adenosine A(1) receptor-mediated inhibition of the cyclic AMP formation was not affected by the increased receptor number. We conclude that the enhanced ATP-evoked Ca(2+) influx in protein kinase C down-regulated cells is mediated by adenosine formed by hydrolysis of ATP, and that this adenosine interacts with the increased number of A(1) receptors. The mechanism by which adenosine enhances Ca(2+) entry is not known. Thus, the larger number of adenosine A(1) receptors broadens the spectrum of adenosine A(1) receptor affected signaling systems in FRTL-5 cells.

Adenosine Deaminase↗
PubMed2000

Extracellular ATP-mediated phospholipase A(2) activation in rat thyroid FRTL-5 cells: regulation by a G(i)/G(o) protein, Ca(2+), and mitogen-activated protein kinase.

We investigated the mechanism of phospholipase A(2) (PLA(2)) activation in response to the P2 receptor agonist ATP in rat thyroid FRTL-5 cells. The PLA(2) activity was determined by measuring the release of [(3)H]-arachidonic acid (AA) from prelabeled cells. ATP evoked a dose- and time-dependent AA release. This release was totally inhibited by pertussis toxin (PTX) treatment, indicating the involvement of a G(i)/G(o) protein. The AA release was also diminished by chelating extracellular Ca(2+) with EGTA or by inhibiting influx of Ca(2+) using Ni(2+). Although the activation of protein kinase C (PKC) by 12-phorbol 13-myristate acetate (PMA) alone did not induce any AA release, the ATP-evoked AA release was significantly reduced when PKC was inhibited by GF109203X or by a long incubation with PMA to downregulate PKC. Both the ATP-evoked AA release and the mitogen-activated protein kinase (MAP kinase) phosphorylation were decreased by the MAP kinase kinase (MEK) inhibitor PD98059. Furthermore, the ATP-evoked MAP kinase phosphorylation was also inhibited by GF109203X and by downregulation of PKC, suggesting a PKC-mediated activation of MAP kinase. Inhibiting Src-like kinases by PP1 attenuated both the MAP kinase phosphorylation and the AA release. These results suggest that these kinases are involved in the regulation of MAP kinase and PLA(2) activation. Elevation of intracellular cAMP by TSH or by dBucAMP did not induce a phosphorylation of MAP kinase. Furthermore, neither the ATP-evoked AA release nor the MAP kinase phosphorylation were attenuated by TSH or dBucAMP. Taken together, our results suggest that ATP regulates the activation of PLA(2) by a G(i)/G(o) protein-dependent mechanism. Moreover, Ca(2+), PKC, MAP kinase, and Src-like kinases are also involved in this regulatory process.

Adenosine Triphosphate↗
PubMed2000

Thyrotropin regulates adenosine A(1) receptor expression in rat thyroid FRTL-5 cells.

The effect of thyrotropin (TSH), on adenosine A(1) receptor expression in thyroid FRTL-5 cells was examined by [(3)H]-1, 3-dipropyl-,8-cyclopentyl xanthine ([(3)H]-DPCPX) binding on cells in suspension and on membrane preparation, and by in situ mRNA labelling. The estimated K(D) for intact cells was 0.19 nM and about 47,000 binding sites per cell were found in cells constantly grown in the presence of TSH. Three days deprivation of TSH decreased the number of [(3)H]-DPCPX binding sites without any significant effect of K(D). Reintroduction of TSH to the cells returned the higher level of A(1) receptors both in suspension binding studies on whole cells and on membrane preparations. In situ hybridization revealed that TSH evoked an increase in the number of cells densely labelled with a probe against A(1) receptor mRNA. The potency of the A(1) receptor agonist N(6)-cyclohexyladenosine (CHA) as an inhibitor of cyclic AMP formation induced by forskolin was increased in TSH-treated cells, with a shift in the IC(50) from 2.05 nM in TSH-deprived cells to 0.14 nM in TSH-treated cells. Since the activation of A(1) receptors inhibits TSH-mediated cyclic AMP signalling, our results suggest a regulatory feedback mechanism between signalling via adenosine A(1) receptors and TSH receptors.

Adenylyl Cyclases↗
PubMed1999

Sphingosylphosphorylcholine activates Gq, Gi-2, and Gi-3 in thyroid FRTL-5 cells: implications for the activation of calcium fluxes and Na+-H+ exchange.

In the present investigation of rat thyroid FRTL-5 cells, we show using reverse-transcriptase PCR that these cells express both Edg-1 and Edg-5. We show using a [35S]GTPgammaS-binding assay that sphingosylphosphorylcholine (SPC), which binds to both Edg-1 and EDG-5, activates Gq, Gi-2, and Gi-3 proteins. SPC potently increases intracellular free calcium concentrations ([Ca2+]i). This effect is mediated through both Gq and Gi proteins, as the mobilization of sequestered calcium was insensitive to pertussis toxin (i.e., mediated by Gq), while the SPC-evoked calcium entry was inhibited by pretreatment with pertussis toxin (i.e., mediated by Gi). Furthermore, SPC in a concentration-dependent manner increases intracellular pH in acidified cells via a Na+-H+ exchange mechanism. The enhanced activation of Na+-H+ exchange is independent of both an increase in [Ca2+]i and an activation of protein kinase C. The effect of SPC on Na+-H+ exchange is insensitive to pertussis toxin, suggesting an effect mediated via Gq.

Animals↗
PubMed1999

Pre-attentive detection of vowel contrasts utilizes both phonetic and auditory memory representations.

Event-related brain potentials (ERP) were recorded to infrequent changes of a synthesized vowel (standard) to another vowel (deviant) in speakers of Hungarian and Finnish language, which are remotely related to each other with rather similar vowel systems. Both language groups were presented with identical stimuli. One standard-deviant pair represented an across-vowel category contrast in Hungarian, but a within-category contrast in Finnish, with the other pair having the reversed role in the two languages. Both within- and across-category contrasts elicited the mismatch negativity (MMN) ERP component in the native speakers of either language. The MMN amplitude was larger in across- than within-category contrasts in both language groups. These results suggest that the pre-attentive change-detection process generating the MMN utilized both auditory (sensory) and phonetic (categorical) representations of the test vowels.

Acoustic Stimulation↗
PubMed1999

In the dose range of 0.5-2.0 mg/kg, acetylsalicylic acid does not affect prostacyclin production in hypertensive pregnancies.

OBJECTIVE: To determine the dose of acetylsalicylic acid (ASA), that inhibits the production of the vasoconstrictive, aggregatory thromboxane A2 while sparing the production of the vasodilatory antiaggregatory prostacyclin. DESIGN: A controlled study comparing the effects of three doses of ASA on the production of thromboxane A2 and prostacyclin. METHODS: Seven pregnant hypertensive patients and five non-pregnant healthy women received 0.5, 1.0 and 2.0 mg/kg/day of ASA, each dose for 10-12 days, the treatment periods following each other immediately. Seven normotensive pregnant women served as controls and were given no ASA. Blood and urine samples were taken at baseline and after the treatment periods to determine serum thromboxane B2 and the urinary 2.3-dinor-6-ketoprostaglandin F1alpha and 11-dehydrothromboxaneB2, the major stable metabolites of prostacyclin and thromboxane A2, respectively. RESULTS: The urinary excretion of 11-dehydrothromboxaneB2 was significantly higher in both hypertensive (34.9+/-18.3 pg/micromol creatinine) and normotensive (39.3+/-14.4 pg/micromol creatinine) pregnant women than in non-pregnant women (14.8+/-6.4 pg/micromol creatinine). The urinary excretion of 2.3-dinor-6-ketoprostaglandinF1alpha was also higher in normotensive pregnant women (93.9+/-50.9 pg/micromol creatinine) than in non-pregnant women (18.2+/-11.3 pg/micromol creatinine). The excretion rate of 2.3-dinor-6-ketoprostaglandinF1alpha in hypertensive patients was lower than in normotensive pregnant women (44.7+/-24.2 pg/micromol creatinine). At baseline the urinary 2.3-dinor-6-ketoprostaglandin F1alpha/11-dehydrothromboxaneB2 ratio was almost the same in the hypertensive patients (1.6) and in the non-pregnant women (1.2). The ratio was 2.6 in normotensive pregnant women. In the hypertensive group, already the lowest dose of ASA inhibited urinary 11-dehydrothromboxaneB2 excretion significantly. Because none of the doses of ASA inhibited 2.3-dinor-6-ketoprostaglandinF1alpha production, the 2.3-dinor-6-ketoprostaglandinF1alpha/11-dehydrothromboxaneB2 ratio was shifted in the favor of prostacyclin at all dose levels. In the non-pregnant women, even the highest dose level of ASA failed to affect the ratio. CONCLUSION: In the dose range of 0.5-2.0 mg/kg/day, ASA has a favorable effect on the ratio of prostacyclin to thromboxane A2 in hypertensive pregnancies.

Aspirin↗
PubMed1997

Language-specific phoneme representations revealed by electric and magnetic brain responses.

There is considerable debate about whether the early processing of sounds depends on whether they form part of speech. Proponents of such speech specificity postulate the existence of language-dependent memory traces, which are activated in the processing of speech but not when equally complex, acoustic non-speech stimuli are processed. Here we report the existence of these traces in the human brain. We presented to Finnish subjects the Finnish phoneme prototype /e/ as the frequent stimulus, and other Finnish phoneme prototypes or a non-prototype (the Estonian prototype /õ/) as the infrequent stimulus. We found that the brain's automatic change-detection response, reflected electrically as the mismatch negativity (MMN), was enhanced when the infrequent, deviant stimulus was a prototype (the Finnish /ö/) relative to when it was a non-prototype (the Estonian /õ/). These phonemic traces, revealed by MMN, are language-specific, as /õ/ caused enhancement of MMN in Estonians. Whole-head magnetic recordings located the source of this native-language, phoneme-related response enhancement, and thus the language-specific memory traces, in the auditory cortex of the left hemisphere.

Acoustic Stimulation↗
PubMed1997

Adenosine inhibits DNA synthesis stimulated with TSH, insulin, and phorbol 12-myristate 13-acetate in rat thyroid FRTL-5 cells.

Adenosine has been shown to modulate cell proliferation in FRTL-5 thyroid cells, although the mechanisms by which this interaction occurs is still unclear. In the present study we investigated the effects of adenosine on the 3H-thymidine incorporation, cell cycle kinetics, and expression of the transcription factor c-Fos in cells stimulated via three different mitogenic pathways, i.e., by thyroid stimulating hormone (TSH) [adenosine 3',5'-cyclic monophosphate(cAMP)], insulin (tyrosine kinase), or phorbol 12-myristate 13-acetate (protein kinase C). Addition of adenosine to cells grown in medium containing hormones and serum did not inhibit the incorporation of 3H-thymidine. If adenosine was added to hormone-deprived cells together with any of the tested mitogens, the stimulation of the 3H-thymidine incorporation was inhibited in a dose-dependent manner. The inhibition was significantly lower when the cells were preincubated with TSH or insulin for 48 h. Flow cytometric studies showed that adenosine evoked an inhibition of the cells in the G0/G1 phase. Submaximal doses of adenosine (10 nM-10 microM) were able to induce c-Fos expression in FRTL-5 cells. However, the mitogen-induced expression of c-Fos was not reduced by maximal dose of adenosine (100 microM). The effect of adenosine on DNA synthesis was not dependent on pertussis toxin-sensitive G-proteins. In addition, adenosine A1- or A2- receptor antagonists did not block the effect of adenosine. The effect of adenosine was abolished by treatment of the cells with adenosine deaminase, suggesting that the observed effect was not mediated by a metabolite of adenosine. The results suggest that adenosine is an effective blocker of mitogen-evoked DNA synthesis of FRTL-5 cells, provided that adenosine is administered simultaneously with the mitogen.

Adenosine↗
PubMed1997

Sphingosine 1-phosphate mobilizes sequestered calcium, activates calcium entry, and stimulates deoxyribonucleic acid synthesis in thyroid FRTL-5 cells.

Sphingosine 1-phosphate (SPP) potently mobilizes sequestered calcium and is a mitogen in several cell types. In the present investigation, we have evaluated the effect of SPP on intracellular free calcium concentration ([Ca2+]i) and synthesis of DNA in thyroid FRTL-5 cells. SPP rapidly and transiently mobilized sequestered calcium and stimulated entry of extracellular calcium. The entry of calcium, but not the mobilization, was in part inhibited by pretreatment with pertussis toxin (Ptx), and by activation of protein kinase C. SPP did not stimulate the production of inositol 1,4,5-trisphosphate. SPP stimulated the incorporation of 3H-thymidine in a time- and dose-dependent manner. The effect was not inhibited by Ptx. Furthermore, SPP stimulated the activation of the proto-oncogene c-fos. SPP rapidly tyrosine-phosphorylated an approximately 66 kDa protein. This phosphorylation persisted for at least 1 h. Pretreatment of the cells with genistein abolished the SPP-evoked tyrosine phosphorylation, and attenuated the SPP-evoked increase in [Ca2+]i. Furthermore, the SPP-evoked activation of Na+-H+ exchange was inhibited by genistein. The phosphorylation was not attenuated by pretreatment of the cells with Ptx. SPP per se did not affect cellular cAMP levels but attenuated the TSH-evoked increase in cAMP. As the effect of SPP might be due to activation of phospholipase D, we tested whether phosphatidic acid (PA) mobilized calcium or stimulated the incorporation of 3H-thymidine. PA mobilized sequestered calcium but did not stimulate calcium entry. PA very modestly enhanced the incorporation of 3H-thymidine. Our results suggest, that SPP stimulates DNA synthesis and activates entry of calcium in FRTL-5 cells. The effect on calcium entry appears to be dependent, at least in part, on one or several tyrosine kinases.

Animals↗
PubMed1996

Purinergic agonists stimulate the secretion of endothelin-1 in rat thyroid FRTL-5 cells.

The aim of the present study was to investigate the mechanisms regulating endothelin-1 (ET-1) secretion in rat thyroid FRTL-5 cells. ET-1 was found to be secreted after stimulation with adenosine and ATP. The release of ET-1 was sensitive to pertussis toxin, indicating a role of G-proteins in the stimulus-secretion coupling. The stimulation evoked by ATP or adenosine was inhibited by the P1-receptor antagonist 8-cyclopentyl-1,3-dipropylxanthine (DPCPX), and in the presence of adenosine deaminase the adenosine- and ATP-mediated ET-1 secretion was abolished. These evidences suggest a role of a P1-adenosine receptor in the secretion of ET-1. Increasing cyclic AMP with forskolin decreased the adenosine-mediated secretion. In addition, the intracellular calcium chelator BAPTA or inhibition of calcium entry with Ni2+ prevented the response. Protein kinase C (PKC) is also partly involved in ET-1 secretion in FRTL-5 cells. Activation of PKC with the phorbol ester phorbol 12-myristate 13-acetate (PMA) stimulated the secretion of ET-1 in a time- and dose-dependent manner. Furthermore, downregulation of PKC decreased the secretion of ET-1 stimulated by adenosine. In conclusion, ET-1 secretion in FRTL-5 cells is stimulated via a pertussis toxin-sensitive P1-receptor pathway which is modulated by several signal transduction mechanisms including cAMP, Ca2+, and PKC.

Adenosine↗
PubMed1994

Electromagnetic stimulation of the auditory system of deaf patients.

Electromagnetically induced auditory perception was investigated in 18 deaf patients who were candidates for cochlear implants. In the extracranial magnetic stimulation (EMS) procedure, patients were stimulated with time-varying magnetic field brief pulses from a coil positioned at the i) auricle, ii) the mastoid, and iii) the temporal lobe area. EMS elicited auditory sensations in 26 ears (of 14 patients/subjects). The lowest threshold of auditory sensation (TAS) was found to be at the 20% EMS level, with a range of 20-50% of the maximum level (2.0 Tesla), and approximately equal sensitivity in each coil position. Eleven of the subjects hearing EMS-induced sound perceived changes in pitch while 6 heard "clicks" or clicks and tones. Spearman Rho correlation analysis showed a mild negative correlation between the EMS/TAS and the pre-implant FFA, best tone threshold (BTT), and direct promontorial electrical stimulation (ES) thresholds at 250 Hz and 500 Hz. No correlation was found between EMS or ES and performance on the pre-implant or post-implant psychacoustic tests (MAC VIII or 3-Digit speech tests) or the measurements of the thickness of cutaneous and osseous tissue from the stimulation sites at the mastoid and ear canal to the cochlear and 8th nerve. A fair positive correlation was found between the EMS/TAS and the post-implant (6 months) ES threshold when the electrodes allocated the 500 Hz frequency range were stimulated. A mild positive correlation between the pre-cochlear-implant promontorial electrical stimulation (ES) at 250 Hz and the four frequency tone average (FFA: 0.5, 1, 2, 4 kHz) was also found.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗