Blockade of central β‐adrenoceptors attenuates tremor induced by 5‐hydroxytryptamine (5‐HT)‐receptor activation in rats

Hallberg, Heléne

doi:10.1111/j.1748-1716.1987.tb08087.x

Cited by 10 publications

(7 citation statements)

References 21 publications

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“…142 Tremor in rats is attenuated after blockage of centrally located ␤ 2 -adrenoceptors. 143 Occurrence of tremor in cats after intracaudate injection of amphetamines, 144 mescaline, tetrabenazine, bretylium, 145 or morphine 146 has been reported. Serotonin depletion and blockage of 5-HT receptors but not catecholamine depletion prevents the amphetamine syndrome in rats; for that reason, Sloviter et al suggest that it is mediated through activated 5-HT receptors.…”

Section: Miscellaneous Tremorogensmentioning

confidence: 99%

Animal models of tremor

1999

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Section: Miscellaneous Tremorogensmentioning

confidence: 99%

Animal models of tremor

1999

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“…The latter drug has also found a clinical use in the treatment of migraine (Anthony, 1978;Weber & Reinmuth, 1972) and anxiety states (Heiser & DeFrancisco, 1976;Linken, 1971 (Young et al, 1975;Taylor et al, 1981;Kuroda et al, 1988) an interference with 5-HT systems may be important (Hallberg, 1987).…”

Section: Introductionmentioning

confidence: 99%

“…It remains unclear, however, whether any of these effects of propranolol are due to actions at fl-adrenoceptors or whether other receptor populations are involved with an intermediate situation on pathways involved in the control of tremor and cerebrovascular tone. While it has been proposed that antagonism of fl-adrenoceptors is involved in the antitremor activity (Young et al, 1975;Taylor et al, 1981;Kuroda et al, 1988) an interference with 5-HT systems may be important (Hallberg, 1987).…”

Section: Introductionmentioning

confidence: 99%

Changes in neurotransmitter sensitivity in the mouse neocortical slice following propranolol and theophylline administration

Málly

Connick

Stone

1991

British J Pharmacology

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The mouse neocortical slice has been used to examine the sensitivity of neurones to isoprenaline, 5‐hydroxytryptamine (5‐HT) and adenosine acutely and following chronic treatment of animals with propranolol or theophylline. While having little effect alone, all three agonists enhanced the d.c. depolarizing potential produced by N‐methyl‐d‐aspartate (NMDA). The effect of (−)‐isoprenaline (0.2 μm) was shared by (+)‐isoprenaline at the much higher concentration of 10 μm. Superfusion of slices with theophylline or 8‐phenyltheophylline blocked responses to adenosine with evidence of selectivity. A single injection of theophylline 24 h before slice preparation did not alter agonist sensitivity, but when administered daily at 100 mg kg−1 for 14 days, the xanthine caused a loss of sensitivity to adenosine and (−)‐isoprenaline but not 5‐HT. The lower dose of theophylline, 10 mg kg−1 daily, also led to a loss of adenosine responses but no change of sensitivity to the amines. Following the 14 day treatment with theophylline at 100 mg kg−1 daily in two groups of mice, responses to adenosine recovered to control levels after 20 days. Propranolol superfusion blocked responses to both isomers of isoprenaline and 5‐HT but did not affect sensitivity to adenosine. Chronic treatment with propranolol at 25 mg kg−1 daily for 14 days induced a loss of sensitivity to (−)‐isoprenaline and 5‐HT but not adenosine. A lower dose of 5 mg kg−1 daily caused no change in responses to adenosine or 5‐HT, but yielded an increased sensitivity to (−)‐isoprenaline. The results are discussed with respect to reports of receptor up‐regulation in binding studies; caution is clearly required in extrapolating from such work to receptor activity in a functional system, especially in the case of theophylline and adenosine.

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“…Ablad et al. 1973, Borg et al 1975, Hallberg 1987. Thus, the effect appears to be mediated by blockade of P,-adrenoceptors rather than P,-adrenoceptors, a notion given further support by the reduction in tremor found in rats treated with the lipophilic P,-antagonist ICI 118, 551 (Bilski et al 1983) (calculated distribution coefficient 95, P. Johansson, pers.…”

Section: Plasma Concentrations Of P-antagonistsmentioning

confidence: 97%

“…In a recent study by Ogren et al (1985), alaproclate, a 5-HT-uptake inhibitor, was found to potentiate oxotremorine-induced tremor in rats, suggesting that a serotonergic mechanism participates in this kind of tremor. Since tremor induced by activation of central 5-HT-systems also appears to be modulated by central P,-adrenoceptors (Hallberg 1986(Hallberg , 1987, it is tempting to suggest that centrally located /I,-adrenoceptors may modulate a mechanism that is common to the tremor models studied.…”

Section: Plasma Concentrations Of P-antagonistsmentioning

confidence: 99%

Modulation of oxotremorine‐induced tremor by central β‐adrenoceptors

Hallberg¹,

Almgren²

1987

Acta Physiologica Scandinavica

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The muscarinic agonist oxotremorine was used to induce tremor in rats pretreated with methylatropine. An objective assessment of tremor intensity was accomplished by means of an accelerometer-based recording system. The non-selective, lipophilic beta-adrenoceptor antagonist propranolol dose-dependently suppressed tremor intensity, whereas the R-isomer of propranolol was without effect, verifying beta-adrenoceptor involvement. Since the hydrophilic, non-selective beta-antagonist nadolol was ineffective, the effect appears to be located inside the blood-brain barrier. The beta 2-selective antagonist ICI 118, 551 dose-dependently reduced tremor intensity, whereas selective blockade of beta 1-adrenoceptors with metoprolol had no effect, indicating the participation of a beta 2-adrenoceptor. On the other hand, the lipophilic beta 2-agonist clenbuterol dose-dependently enhanced tremor induced by oxotremorine. Determination of circulating plasma catecholamine concentrations revealed that the effect of beta-antagonists on tremor was not secondary to an effect on the oxotremorine-induced rise in catecholamine levels. Thus, the results suggest that beta 2-adrenoceptors located inside the blood-brain barrier are able to modulate oxotremorine-induced tremor in rats.

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Blockade of central β‐adrenoceptors attenuates tremor induced by 5‐hydroxytryptamine (5‐HT)‐receptor activation in rats

Cited by 10 publications

References 21 publications

Animal models of tremor

Animal models of tremor

Changes in neurotransmitter sensitivity in the mouse neocortical slice following propranolol and theophylline administration

Modulation of oxotremorine‐induced tremor by central β‐adrenoceptors

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