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Reidun Ursin - One of the best experts on this subject based on the ideXlab platform.
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Sleep-wake and eeg effects following adenosine a1 agonism and antagonism: similarities and interactions with sleep-wake and eeg effects following a serotonin reuptake inhibitor in rats.
Sleep research online : SRO, 1998Co-Authors: Reidun Ursin, Bjørn BjorvatnAbstract:Adenosine is currently being investigated as a possible mediator of a homeostatic sleep need. Reports from different laboratories suggest that both adenosine A1 agonists and selective serotonin reuptake inhibitors (SSRI) increase deep slow wave sleep (SWS-2) after an interval. In this study, the sleep-wake effects of the adenosine A1 agonist N6-cyclopentyladenosine (CPA) and the SSRI Zimeldine are directly compared in the same animals. Since the SWS-2 increase following SSRIs may be secondary to increased adenosine levels during the initially increased waking, it was also investigated whether the adenosine A1 antagonist 8-cyclopentyltheofylline (CPT) would inhibit the SWS-2 increase following the serotonin reuptake inhibitor. Both the adenosine A1 agonist CPA and the SSRI Zimeldine increased SWS-2 after an interval. Both drugs increased slow wave activity and decreased 9-20 Hz activity during SWS-2. Both the adenosine A1 antagonist CPT, Zimeldine and the two drugs combined initially increased waking and subsequently increased SWS-2 after 2 or 4 h. All treatments increased 2-6 Hz activity in SWS-2 after 2h. Thus, CPT did not antagonize the SWS-2 increase of Zimeldine. Based on the sleep and power spectral effects it is suggested that the adenosine A1 antagonist potentiated the Zimeldine effect, possibly due to antagonism of adenosine A1 inhibition of serotonin release. The data indicate that the delayed SWS-2 and slow wave activity increases following Zimeldine are not due to increased stimulation of adenosine A1 receptors following the initial sleep loss.
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Lesion of descending 5-HT pathways increases Zimeldine-induced waking in rats.
Physiology & behavior, 1995Co-Authors: Alvhild Alette Bjørkum, Dag Neckelmann, Bjørn Bjorvatn, Reidun UrsinAbstract:Abstract Sleep, waking, and EEG power spectra were investigated in rats with spinal 5,6-dihydroxytryptamine (5,6-DHT) lesions, following 20 mg/kg Zimeldine or vehicle IP injections. 5,6-DHT selectively lesioned the descending serotonergic pathways. Lesion alone did not change sleep and waking stages compared to baseline, except for a reduction in REM sleep. Consistent with earlier findings, Zimeldine in nonlesioned rats increased waking the first 2 h of recording. Zimeldine treatment in lesioned rats gave a significant additional 50% increase in waking the first 2 h and a corresponding decrease in total slow wave sleep, suggesting a potentiation of these effects. Zimeldine gave no significant changes in waking EEG power spectral density. Lesion gave a tendency to reduction between 4.0 and 15.5 Hz compared with baseline, and between 10.0 and 16.5 compared to the independent control group. In both comparisons, the combined treatment strengthened this effect, again suggesting a potentiating effect of lesion. In sleep, Zimeldine reduced power over the whole spectrum (0.5–20.0 Hz), less in the lower frequencies than in the higher frequencies.
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Sleep/waking and EEG power spectrum effects of a nonselective serotonin (5-HT) antagonist and a selective 5-HT reuptake inhibitor given alone and in combination.
Sleep, 1995Co-Authors: Bjørn Bjorvatn, Dag Neckelmann, Alvhild Alette Bjørkum, Reidun UrsinAbstract:Sleep/waking stages, electroencephalogram (EEG) power spectra and behavior were studied in rats for 8 hours following intraperitoneal administration of a nonselective serotonin (5-HT) antagonist (0.1 and 2.0 mg/kg methiothepin) and a selective 5-HT reuptake inhibitor (20 mg/kg Zimeldine), given alone and in combination. Consistent with earlier studies, Zimeldine gave a biphasic effect on sleep and waking. Waking was increased and slow wave sleep (SWS)-2 decreased initially, followed by an increase in SWS-2 in the second 2-hour period. Rapid eye movement (REM) sleep was reduced throughout the experiment. EEG power densities were generally reduced in the higher frequencies, but the effect differed somewhat in the different vigilance states and between the fronto-frontal and fronto-parietal EEG leads. Zimeldine did not change behavior. Methiothepin, at 0.1 mg/kg, gave only minor effects by itself but it blocked the initial waking increase of Zimeldine. So did 2.0 mg/kg methiothepin, but this dose markedly changed sleep/waking stages by itself : SWS-1 was profoundly increased, whereas waking, SWS-2 and REM sleep were reduced. Total SWS (TSWS) was markedly increased due to the SWS-1 increase. Because TSWS was increased while SWS-2 was decreased following 2.0 mg/kg methiothepin, it is concluded that spindle activity was facilitated, whereas slow wave activity was antagonized. Methiothepin, at 2.0 mg/kg, also markedly changed EEG power densities within TSWS and induced cataleptic behavior. It is concluded that the initial waking increase of Zimeldine depends on simultaneous activation of several different 5-HT receptor subtypes. The other Zimeldine effects were not consistently antagonized, thus the mechanisms behind these effects remain unclear.
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Diurnal differences in L-tryptophan sleep and temperature effects in the rat
Behavioural Brain Research, 1994Co-Authors: Øystein Erlend Olsen, Dag Neckelmann, Reidun UrsinAbstract:Abstract Sleep/waking and EEG power spectra were investigated for 6 h periods in rats following administration of the essential amino acid L-tryptophan (40 mg/kg), the selective serotonin uptake inhibitor Zimeldine (20 mg/kg), and following a combination of L-tryptophan and Zimeldine. In contrast to earlier studies, L-tryptophan decreased waking and increased total slow wave sleep when administered late in the light phase ( 8 1 2 h after light onset). No sleep effects were seen after early light phase injections (2 h after lights on). In agreement with earlier studies, Zimeldine initially increased wakefulness, followed by an increase in slow wave sleep-2. REM sleep was abolished after Zimeldine treatment. Zimeldine increased EEG delta activity and decreased EEG activity above 7 Hz. L-Tryptophan potentiated the Zimeldine induced increase in waking only when given early in the light phase. In a separate experiment, body temperature was monitored after L-tryptophan injections in both early and late light phase. A thermogenic effect of L-tryptophan was seen in the early light phase, while the opposite was seen in the late light phase. The data indicate diurnal differences in sleep/waking and temperature effects of a physiological dose of L-tryptophan.
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The 5-HT2 antagonist ritanserin decreases sleep in cats.
Sleep, 1993Co-Authors: Liv Sommerfelt, Reidun UrsinAbstract:Sleep and wakefulness were recorded in cats after oral administration of the 5-HT2 antagonist ritanserin at doses of 0.5 and 1.0 mg/kg (n = 6), and after 2.5 mg/kg (n = 3). A subgroup (n = 4) of the animals also received the selective 5-HT uptake inhibitor Zimeldine and a combination of ritanserin and Zimeldine. The drugs were administered shortly after light onset, and sleep was recorded for 15 hours. Waking was increased and slow wave sleep (SWS), particularly deep slow wave sleep (SWS-2), was decreased throughout the recording time after ritanserin administration. Rapid eye movement (REM) sleep latency was increased, and the amount of REM sleep was reduced. In the combination study, ritanserin reduced the delayed SWS increase following the serotonin uptake inhibitor. The findings of increased waking and decreased SWS-2 after ritanserin in cats contrasts with findings from humans and rats where slow wave sleep is increased following ritanserin administration.
Bjørn Bjorvatn - One of the best experts on this subject based on the ideXlab platform.
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Sleep-wake and eeg effects following adenosine a1 agonism and antagonism: similarities and interactions with sleep-wake and eeg effects following a serotonin reuptake inhibitor in rats.
Sleep research online : SRO, 1998Co-Authors: Reidun Ursin, Bjørn BjorvatnAbstract:Adenosine is currently being investigated as a possible mediator of a homeostatic sleep need. Reports from different laboratories suggest that both adenosine A1 agonists and selective serotonin reuptake inhibitors (SSRI) increase deep slow wave sleep (SWS-2) after an interval. In this study, the sleep-wake effects of the adenosine A1 agonist N6-cyclopentyladenosine (CPA) and the SSRI Zimeldine are directly compared in the same animals. Since the SWS-2 increase following SSRIs may be secondary to increased adenosine levels during the initially increased waking, it was also investigated whether the adenosine A1 antagonist 8-cyclopentyltheofylline (CPT) would inhibit the SWS-2 increase following the serotonin reuptake inhibitor. Both the adenosine A1 agonist CPA and the SSRI Zimeldine increased SWS-2 after an interval. Both drugs increased slow wave activity and decreased 9-20 Hz activity during SWS-2. Both the adenosine A1 antagonist CPT, Zimeldine and the two drugs combined initially increased waking and subsequently increased SWS-2 after 2 or 4 h. All treatments increased 2-6 Hz activity in SWS-2 after 2h. Thus, CPT did not antagonize the SWS-2 increase of Zimeldine. Based on the sleep and power spectral effects it is suggested that the adenosine A1 antagonist potentiated the Zimeldine effect, possibly due to antagonism of adenosine A1 inhibition of serotonin release. The data indicate that the delayed SWS-2 and slow wave activity increases following Zimeldine are not due to increased stimulation of adenosine A1 receptors following the initial sleep loss.
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Lesion of descending 5-HT pathways increases Zimeldine-induced waking in rats.
Physiology & behavior, 1995Co-Authors: Alvhild Alette Bjørkum, Dag Neckelmann, Bjørn Bjorvatn, Reidun UrsinAbstract:Abstract Sleep, waking, and EEG power spectra were investigated in rats with spinal 5,6-dihydroxytryptamine (5,6-DHT) lesions, following 20 mg/kg Zimeldine or vehicle IP injections. 5,6-DHT selectively lesioned the descending serotonergic pathways. Lesion alone did not change sleep and waking stages compared to baseline, except for a reduction in REM sleep. Consistent with earlier findings, Zimeldine in nonlesioned rats increased waking the first 2 h of recording. Zimeldine treatment in lesioned rats gave a significant additional 50% increase in waking the first 2 h and a corresponding decrease in total slow wave sleep, suggesting a potentiation of these effects. Zimeldine gave no significant changes in waking EEG power spectral density. Lesion gave a tendency to reduction between 4.0 and 15.5 Hz compared with baseline, and between 10.0 and 16.5 compared to the independent control group. In both comparisons, the combined treatment strengthened this effect, again suggesting a potentiating effect of lesion. In sleep, Zimeldine reduced power over the whole spectrum (0.5–20.0 Hz), less in the lower frequencies than in the higher frequencies.
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Sleep/waking and EEG power spectrum effects of a nonselective serotonin (5-HT) antagonist and a selective 5-HT reuptake inhibitor given alone and in combination.
Sleep, 1995Co-Authors: Bjørn Bjorvatn, Dag Neckelmann, Alvhild Alette Bjørkum, Reidun UrsinAbstract:Sleep/waking stages, electroencephalogram (EEG) power spectra and behavior were studied in rats for 8 hours following intraperitoneal administration of a nonselective serotonin (5-HT) antagonist (0.1 and 2.0 mg/kg methiothepin) and a selective 5-HT reuptake inhibitor (20 mg/kg Zimeldine), given alone and in combination. Consistent with earlier studies, Zimeldine gave a biphasic effect on sleep and waking. Waking was increased and slow wave sleep (SWS)-2 decreased initially, followed by an increase in SWS-2 in the second 2-hour period. Rapid eye movement (REM) sleep was reduced throughout the experiment. EEG power densities were generally reduced in the higher frequencies, but the effect differed somewhat in the different vigilance states and between the fronto-frontal and fronto-parietal EEG leads. Zimeldine did not change behavior. Methiothepin, at 0.1 mg/kg, gave only minor effects by itself but it blocked the initial waking increase of Zimeldine. So did 2.0 mg/kg methiothepin, but this dose markedly changed sleep/waking stages by itself : SWS-1 was profoundly increased, whereas waking, SWS-2 and REM sleep were reduced. Total SWS (TSWS) was markedly increased due to the SWS-1 increase. Because TSWS was increased while SWS-2 was decreased following 2.0 mg/kg methiothepin, it is concluded that spindle activity was facilitated, whereas slow wave activity was antagonized. Methiothepin, at 2.0 mg/kg, also markedly changed EEG power densities within TSWS and induced cataleptic behavior. It is concluded that the initial waking increase of Zimeldine depends on simultaneous activation of several different 5-HT receptor subtypes. The other Zimeldine effects were not consistently antagonized, thus the mechanisms behind these effects remain unclear.
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The 5-HT1A antagonist (-)-alprenolol fails to modify sleep or Zimeldine-induced sleep-waking effects in rats.
Pharmacology biochemistry and behavior, 1992Co-Authors: Bjørn Bjorvatn, Dag Neckelmann, Reidun UrsinAbstract:Sleep and waking in rats were studied for 8 h following administration of a selective 5-hydroxytryptamine (5-HT) reuptake inhibitor (Zimeldine), a putative 5-HT1A antagonist {L(−)-alprenolol hydrogene tartrate monohydrate [(−)-alprenolol]} and a combination of (−)-alprenolol and Zimeldine. Consistent with earlier findings, Zimeldine gave a biphasic effect on sleep and waking. Waking was increased during the first 3 h, followed by a small decrease. Deep slow-wave sleep (SWS-2) showed the opposite trend. An initial decrease in SWS-2 was followed by an increase after around 3 h. Rapid eye movement sleep was markedly suppressed and latencies to sleep increased after Zimeldine. (−)-Alprenolol had no effects on the different sleep and waking stages or latencies to sleep. The 5-HT1A antagonist also failed to modify the effects of Zimeldine administration. The behavioral syndrome induced by a selective 5-HT1A agonist [8-hydroxy-2-(di-n-propyl-amino)-tetralin (8-OH-DPAT)] was clearly antagonized by administration of (−)-alprenolol, indicating that (−)-alprenolol was an efficient 5-HT1A blocker. The data indicate that the sleep-waking effects of Zimeldine cannot easily be explained by stimulation of 5-HT1A receptors.
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Studies on sleep/wake effects of serotonin reuptake inhibitors and receptor subtype involvement
Journal of sleep research, 1992Co-Authors: Reidun Ursin, Dag Neckelmann, Bjørn Bjorvatn, Liv Sommerfelt, Alvhild Alette BjørkumAbstract:Studies with the serotonin uptake inhibitors Zimeldine and alaproclate show biphasic effects on the sleep/wake axis in rats and cats. Zimeldine induced an initial waking response succeeded by a small SWS-2 increase in rats. The waking increase was not blocked by the 5-HT2 antagonist ritanserin nor by the putative 5-HT1A antagonist (-)-alprenolol. In cats, Zimeldine induced initial behavioural changes which were succeeded by a large SWS-2 increase. Alaproclate gave similar initial responses as Zimeldine in both species, and was succeeded by a moderate sleep increase in cats but not in rats. The complex sleep/wake effects following the serotonin uptake inhibitors may result from simultaneous induction of incompatible serotonergic effects.
Dag Neckelmann - One of the best experts on this subject based on the ideXlab platform.
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Lesion of descending 5-HT pathways increases Zimeldine-induced waking in rats.
Physiology & behavior, 1995Co-Authors: Alvhild Alette Bjørkum, Dag Neckelmann, Bjørn Bjorvatn, Reidun UrsinAbstract:Abstract Sleep, waking, and EEG power spectra were investigated in rats with spinal 5,6-dihydroxytryptamine (5,6-DHT) lesions, following 20 mg/kg Zimeldine or vehicle IP injections. 5,6-DHT selectively lesioned the descending serotonergic pathways. Lesion alone did not change sleep and waking stages compared to baseline, except for a reduction in REM sleep. Consistent with earlier findings, Zimeldine in nonlesioned rats increased waking the first 2 h of recording. Zimeldine treatment in lesioned rats gave a significant additional 50% increase in waking the first 2 h and a corresponding decrease in total slow wave sleep, suggesting a potentiation of these effects. Zimeldine gave no significant changes in waking EEG power spectral density. Lesion gave a tendency to reduction between 4.0 and 15.5 Hz compared with baseline, and between 10.0 and 16.5 compared to the independent control group. In both comparisons, the combined treatment strengthened this effect, again suggesting a potentiating effect of lesion. In sleep, Zimeldine reduced power over the whole spectrum (0.5–20.0 Hz), less in the lower frequencies than in the higher frequencies.
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Sleep/waking and EEG power spectrum effects of a nonselective serotonin (5-HT) antagonist and a selective 5-HT reuptake inhibitor given alone and in combination.
Sleep, 1995Co-Authors: Bjørn Bjorvatn, Dag Neckelmann, Alvhild Alette Bjørkum, Reidun UrsinAbstract:Sleep/waking stages, electroencephalogram (EEG) power spectra and behavior were studied in rats for 8 hours following intraperitoneal administration of a nonselective serotonin (5-HT) antagonist (0.1 and 2.0 mg/kg methiothepin) and a selective 5-HT reuptake inhibitor (20 mg/kg Zimeldine), given alone and in combination. Consistent with earlier studies, Zimeldine gave a biphasic effect on sleep and waking. Waking was increased and slow wave sleep (SWS)-2 decreased initially, followed by an increase in SWS-2 in the second 2-hour period. Rapid eye movement (REM) sleep was reduced throughout the experiment. EEG power densities were generally reduced in the higher frequencies, but the effect differed somewhat in the different vigilance states and between the fronto-frontal and fronto-parietal EEG leads. Zimeldine did not change behavior. Methiothepin, at 0.1 mg/kg, gave only minor effects by itself but it blocked the initial waking increase of Zimeldine. So did 2.0 mg/kg methiothepin, but this dose markedly changed sleep/waking stages by itself : SWS-1 was profoundly increased, whereas waking, SWS-2 and REM sleep were reduced. Total SWS (TSWS) was markedly increased due to the SWS-1 increase. Because TSWS was increased while SWS-2 was decreased following 2.0 mg/kg methiothepin, it is concluded that spindle activity was facilitated, whereas slow wave activity was antagonized. Methiothepin, at 2.0 mg/kg, also markedly changed EEG power densities within TSWS and induced cataleptic behavior. It is concluded that the initial waking increase of Zimeldine depends on simultaneous activation of several different 5-HT receptor subtypes. The other Zimeldine effects were not consistently antagonized, thus the mechanisms behind these effects remain unclear.
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Diurnal differences in L-tryptophan sleep and temperature effects in the rat
Behavioural Brain Research, 1994Co-Authors: Øystein Erlend Olsen, Dag Neckelmann, Reidun UrsinAbstract:Abstract Sleep/waking and EEG power spectra were investigated for 6 h periods in rats following administration of the essential amino acid L-tryptophan (40 mg/kg), the selective serotonin uptake inhibitor Zimeldine (20 mg/kg), and following a combination of L-tryptophan and Zimeldine. In contrast to earlier studies, L-tryptophan decreased waking and increased total slow wave sleep when administered late in the light phase ( 8 1 2 h after light onset). No sleep effects were seen after early light phase injections (2 h after lights on). In agreement with earlier studies, Zimeldine initially increased wakefulness, followed by an increase in slow wave sleep-2. REM sleep was abolished after Zimeldine treatment. Zimeldine increased EEG delta activity and decreased EEG activity above 7 Hz. L-Tryptophan potentiated the Zimeldine induced increase in waking only when given early in the light phase. In a separate experiment, body temperature was monitored after L-tryptophan injections in both early and late light phase. A thermogenic effect of L-tryptophan was seen in the early light phase, while the opposite was seen in the late light phase. The data indicate diurnal differences in sleep/waking and temperature effects of a physiological dose of L-tryptophan.
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The 5-HT1A antagonist (-)-alprenolol fails to modify sleep or Zimeldine-induced sleep-waking effects in rats.
Pharmacology biochemistry and behavior, 1992Co-Authors: Bjørn Bjorvatn, Dag Neckelmann, Reidun UrsinAbstract:Sleep and waking in rats were studied for 8 h following administration of a selective 5-hydroxytryptamine (5-HT) reuptake inhibitor (Zimeldine), a putative 5-HT1A antagonist {L(−)-alprenolol hydrogene tartrate monohydrate [(−)-alprenolol]} and a combination of (−)-alprenolol and Zimeldine. Consistent with earlier findings, Zimeldine gave a biphasic effect on sleep and waking. Waking was increased during the first 3 h, followed by a small decrease. Deep slow-wave sleep (SWS-2) showed the opposite trend. An initial decrease in SWS-2 was followed by an increase after around 3 h. Rapid eye movement sleep was markedly suppressed and latencies to sleep increased after Zimeldine. (−)-Alprenolol had no effects on the different sleep and waking stages or latencies to sleep. The 5-HT1A antagonist also failed to modify the effects of Zimeldine administration. The behavioral syndrome induced by a selective 5-HT1A agonist [8-hydroxy-2-(di-n-propyl-amino)-tetralin (8-OH-DPAT)] was clearly antagonized by administration of (−)-alprenolol, indicating that (−)-alprenolol was an efficient 5-HT1A blocker. The data indicate that the sleep-waking effects of Zimeldine cannot easily be explained by stimulation of 5-HT1A receptors.
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Studies on sleep/wake effects of serotonin reuptake inhibitors and receptor subtype involvement
Journal of sleep research, 1992Co-Authors: Reidun Ursin, Dag Neckelmann, Bjørn Bjorvatn, Liv Sommerfelt, Alvhild Alette BjørkumAbstract:Studies with the serotonin uptake inhibitors Zimeldine and alaproclate show biphasic effects on the sleep/wake axis in rats and cats. Zimeldine induced an initial waking response succeeded by a small SWS-2 increase in rats. The waking increase was not blocked by the 5-HT2 antagonist ritanserin nor by the putative 5-HT1A antagonist (-)-alprenolol. In cats, Zimeldine induced initial behavioural changes which were succeeded by a large SWS-2 increase. Alaproclate gave similar initial responses as Zimeldine in both species, and was succeeded by a moderate sleep increase in cats but not in rats. The complex sleep/wake effects following the serotonin uptake inhibitors may result from simultaneous induction of incompatible serotonergic effects.
Alvhild Alette Bjørkum - One of the best experts on this subject based on the ideXlab platform.
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Sleep/waking and EEG power spectrum effects of a nonselective serotonin (5-HT) antagonist and a selective 5-HT reuptake inhibitor given alone and in combination.
Sleep, 1995Co-Authors: Bjørn Bjorvatn, Dag Neckelmann, Alvhild Alette Bjørkum, Reidun UrsinAbstract:Sleep/waking stages, electroencephalogram (EEG) power spectra and behavior were studied in rats for 8 hours following intraperitoneal administration of a nonselective serotonin (5-HT) antagonist (0.1 and 2.0 mg/kg methiothepin) and a selective 5-HT reuptake inhibitor (20 mg/kg Zimeldine), given alone and in combination. Consistent with earlier studies, Zimeldine gave a biphasic effect on sleep and waking. Waking was increased and slow wave sleep (SWS)-2 decreased initially, followed by an increase in SWS-2 in the second 2-hour period. Rapid eye movement (REM) sleep was reduced throughout the experiment. EEG power densities were generally reduced in the higher frequencies, but the effect differed somewhat in the different vigilance states and between the fronto-frontal and fronto-parietal EEG leads. Zimeldine did not change behavior. Methiothepin, at 0.1 mg/kg, gave only minor effects by itself but it blocked the initial waking increase of Zimeldine. So did 2.0 mg/kg methiothepin, but this dose markedly changed sleep/waking stages by itself : SWS-1 was profoundly increased, whereas waking, SWS-2 and REM sleep were reduced. Total SWS (TSWS) was markedly increased due to the SWS-1 increase. Because TSWS was increased while SWS-2 was decreased following 2.0 mg/kg methiothepin, it is concluded that spindle activity was facilitated, whereas slow wave activity was antagonized. Methiothepin, at 2.0 mg/kg, also markedly changed EEG power densities within TSWS and induced cataleptic behavior. It is concluded that the initial waking increase of Zimeldine depends on simultaneous activation of several different 5-HT receptor subtypes. The other Zimeldine effects were not consistently antagonized, thus the mechanisms behind these effects remain unclear.
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Lesion of descending 5-HT pathways increases Zimeldine-induced waking in rats.
Physiology & behavior, 1995Co-Authors: Alvhild Alette Bjørkum, Dag Neckelmann, Bjørn Bjorvatn, Reidun UrsinAbstract:Abstract Sleep, waking, and EEG power spectra were investigated in rats with spinal 5,6-dihydroxytryptamine (5,6-DHT) lesions, following 20 mg/kg Zimeldine or vehicle IP injections. 5,6-DHT selectively lesioned the descending serotonergic pathways. Lesion alone did not change sleep and waking stages compared to baseline, except for a reduction in REM sleep. Consistent with earlier findings, Zimeldine in nonlesioned rats increased waking the first 2 h of recording. Zimeldine treatment in lesioned rats gave a significant additional 50% increase in waking the first 2 h and a corresponding decrease in total slow wave sleep, suggesting a potentiation of these effects. Zimeldine gave no significant changes in waking EEG power spectral density. Lesion gave a tendency to reduction between 4.0 and 15.5 Hz compared with baseline, and between 10.0 and 16.5 compared to the independent control group. In both comparisons, the combined treatment strengthened this effect, again suggesting a potentiating effect of lesion. In sleep, Zimeldine reduced power over the whole spectrum (0.5–20.0 Hz), less in the lower frequencies than in the higher frequencies.
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Studies on sleep/wake effects of serotonin reuptake inhibitors and receptor subtype involvement
Journal of sleep research, 1992Co-Authors: Reidun Ursin, Dag Neckelmann, Bjørn Bjorvatn, Liv Sommerfelt, Alvhild Alette BjørkumAbstract:Studies with the serotonin uptake inhibitors Zimeldine and alaproclate show biphasic effects on the sleep/wake axis in rats and cats. Zimeldine induced an initial waking response succeeded by a small SWS-2 increase in rats. The waking increase was not blocked by the 5-HT2 antagonist ritanserin nor by the putative 5-HT1A antagonist (-)-alprenolol. In cats, Zimeldine induced initial behavioural changes which were succeeded by a large SWS-2 increase. Alaproclate gave similar initial responses as Zimeldine in both species, and was succeeded by a moderate sleep increase in cats but not in rats. The complex sleep/wake effects following the serotonin uptake inhibitors may result from simultaneous induction of incompatible serotonergic effects.
Liv Sommerfelt - One of the best experts on this subject based on the ideXlab platform.
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The 5-HT2 antagonist ritanserin decreases sleep in cats.
Sleep, 1993Co-Authors: Liv Sommerfelt, Reidun UrsinAbstract:Sleep and wakefulness were recorded in cats after oral administration of the 5-HT2 antagonist ritanserin at doses of 0.5 and 1.0 mg/kg (n = 6), and after 2.5 mg/kg (n = 3). A subgroup (n = 4) of the animals also received the selective 5-HT uptake inhibitor Zimeldine and a combination of ritanserin and Zimeldine. The drugs were administered shortly after light onset, and sleep was recorded for 15 hours. Waking was increased and slow wave sleep (SWS), particularly deep slow wave sleep (SWS-2), was decreased throughout the recording time after ritanserin administration. Rapid eye movement (REM) sleep latency was increased, and the amount of REM sleep was reduced. In the combination study, ritanserin reduced the delayed SWS increase following the serotonin uptake inhibitor. The findings of increased waking and decreased SWS-2 after ritanserin in cats contrasts with findings from humans and rats where slow wave sleep is increased following ritanserin administration.
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Studies on sleep/wake effects of serotonin reuptake inhibitors and receptor subtype involvement
Journal of sleep research, 1992Co-Authors: Reidun Ursin, Dag Neckelmann, Bjørn Bjorvatn, Liv Sommerfelt, Alvhild Alette BjørkumAbstract:Studies with the serotonin uptake inhibitors Zimeldine and alaproclate show biphasic effects on the sleep/wake axis in rats and cats. Zimeldine induced an initial waking response succeeded by a small SWS-2 increase in rats. The waking increase was not blocked by the 5-HT2 antagonist ritanserin nor by the putative 5-HT1A antagonist (-)-alprenolol. In cats, Zimeldine induced initial behavioural changes which were succeeded by a large SWS-2 increase. Alaproclate gave similar initial responses as Zimeldine in both species, and was succeeded by a moderate sleep increase in cats but not in rats. The complex sleep/wake effects following the serotonin uptake inhibitors may result from simultaneous induction of incompatible serotonergic effects.
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Behavioral, sleep-waking and EEG power spectral effects following the two specific 5-HT uptake inhibitors Zimeldine and alaproclate in cats.
Behavioural brain research, 1991Co-Authors: Liv Sommerfelt, Reidun UrsinAbstract:Sleep, waking and EEG power spectra were studied in cats for 15 h following peroral administration of placebo or 10 mg/kg and 20 mg/kg of the 5-HT reuptake inhibitors Zimeldine and alaproclate. Behavior was also observed during the initial period following drug administration. Both drugs had effects on motor behavior and initiated hallucinatory like behavior. Zimeldine increased latency to stable sleep and to SWS-2. Alaproclate increased latency to SWS-1. Both drugs increased SWS (NREM sleep) and particularly SWS-2. REM sleep latency was increased and REM sleep was reduced following both drugs. EEG slow wave activity was increased following Zimeldine. It is concluded that the 5-HT stimulation caused by the drugs yields complex effects on the sleep-waking axis, both sleep incompatible and sleep promoting effects.
