Adenosine modulates depolarization-induced release of 3H-noradrenaline from slices of rat brain neocortex

3 The adenosine receptor antagonist 8-phenyltheophylline significantly increased the evoked noradrenaline release by about 15% in control slices by diminishing the inhibitory action of endogenous adenosine. In NEM-treated slices this effect of 8-phenytheophylline was not seen. In the presence of ( -)-PIA (0.1 1aM), i.e. under conditions of an increased inhibitory tone, release facilitation by 8-phenyltheophylline was decreased by NEM compared to that in the respective controls. Occupation of the

Section: Discussionmentioning

confidence: 93%

The adenosine receptor‐mediated inhibition of noradrenaline release possibly involves a N‐protein and is increased by α₂‐autoreceptor blockade

Allgaier

Hertting

Kügelgen

1987

“…Having discussed the ability of adenosine to inhibit potassium-evoked GABA release, it must be emphasized that this action seems to be much weaker than the inhibition of noradrenaline release from the same preparation reported by Harms et al (1978). Thus, while the latter group observed decreases of noradrenaline release ranging from 20% at 10'-M adenosine to 34% at 10'-M adenosine, the statistically significant depression of GABA release in the present work seems to vary from 9% at 10-M to 35% at 10' M.…”

Section: Discussionmentioning

confidence: 95%

“…1978) and adrenergic (Hedqvist & Fredholm, 1976;Clanachan, Johns & Paton, 1977;Enero & Saidman, 1977;Verhaeghe, Vanhoutte & Shepherd, 1977;Su, 1978;Paton, Bar, Clanachan & Lauzon, 1978) terminals in the peripheral nervous system. It has recently been concluded that adenosine can also reduce acetylcholine release at the synapse between motor axon collaterals and Renshaw cells (Lekic, 1977), and noradrenaline release from terminals in the cerebral cortex in vivo (Taylor & Stone, 1980) and in vitro (Harms, Wardeh & Mulder, 1978 (Bowery & Brown, 1974 …”

Section: Introductionmentioning

confidence: 99%

Adenosine Inhibition of Γ‐aminobutyric Acid Release From Slices of Rat Cerebral Cortex

Hollins

Stone

1980

157

1 The effect of purine compounds on the potassium-evoked release of '4C-labelled y-aminobutyric acid (GABA) has been studied in 400 gm slices of rat cerebral cortex in vitro. 2 Adenosine and adenosine 5' monophosphate (AMP) inhibited the release of GABA at 10-5 to 10-' M. Adenosine triphosphate (ATP) produced a significant inhibition of release only at 10-' M.3 Theophylline i0-' or 10'-M reduced the inhibitory effect of adenosine, but did not change basal release of GABA. 4 Dipyridamole 10'5 M itself reduced evoked GABA release, but did not prevent the inhibitory effect of adenosine, implying that adenosine was acting at an extracellularly directed receptor. 5 Calcium removal or antagonism by verapamil reduced the evoked release of GABA, but adenosine did not produce any further reduction of the calcium-independent release. This may indicate that the inhibitory effect of adenosine on GABA release results from interference with calcium influx or availability within the terminals.

“…Possibly the increase in ij.p. amplitude was due to an inhibition of an adenosine-tone which acts prejunctionally to depress transmitter release, in a manner similar to the 'purinergic tone' of the central nervous system (Harms et al, 1978) or the endogenous adenosine release in adipose tissue (Fredholm & Lindgren, 1984) or at the neuromuscular junction (Ribeiro & Sebastiao, 1987). Other possible explanations for the raised ij.p.…”

Section: Effects Ofxanthine Derivativesmentioning

confidence: 99%

Pre‐and postjunctional actions of purine and xanthine compounds in the guinea‐pig caecum circular muscle

Hoyle

Vladimirova

Burnstock

1988

1 The sucrose-gap technique was used to study pre-and postjunctional actions of P1-purinoceptor and P2-purinoceptor agonists and a range of xanthine derivatives in the guinea-pig caecum circular muscle.2 Adenosine, 2-chloroadenosine (2-ClAd), ATP and a,#-methylene ATP all caused concentrationdependent hyperpolarization of the smooth muscle membrane with a rank order of potency of 2-ClAd > a,fi-methylene ATP > adenosine. 3 The xanthine derivatives caffeine, theophylline, 8-phenyltheophylline and 1,3-dipropyl-8{2-amino-4-chlorophenyl) xanthine (PACPX) at submicromolar concentrations evoked depolarization of the smooth muscle membrane. At higher concentrations, all these compounds and enprofylline caused concentration-dependent hyperpolarization.4 All the purine compounds tested caused a reduction in the amplitude of the non-adrenergic, non-cholinergic inhibitory junction potential (ij.p.). For the P,-purinoceptor agonists adenosine and 2-ClAd this was almost entirely a prejunctional effect. For the P2-purinoceptor agonists this was mostly a postjunctional effect because both ATP and a,fi-methylene ATP caused significantly greater increases in the conductance of the smooth muscle membrane than did adenosine or 2-ClAd.