Effects of adenosine on depolarization-induced release of various radiolabelled neurotransmitters from slices of rat corpus striatum

Harms, Herman H.; Wardeh, George; Mulder, Arie H.

doi:10.1016/0028-3908(79)90107-2

Cited by 206 publications

(34 citation statements)

References 16 publications

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“…of acetylcholine (Harms et al, 1979;Pedata et al, 1983;Spignoli et al, 1984;Jackisch et al, 1984b), noradrenaline (Harms et al, 1978;Fredholm et al, 1983;Jackisch et al, 1985a) and 5-hydroxytryptamine (Harms et al, 1979;Feuerstein et al, 1985) from CNS tissue slices is inhibited by adenosine. The adenosine receptors which inhibit the stimulation-evoked release of these neurotransmitters in the rabbit hippocampus have been characterized as A,-receptors (Jackisch et al, 1984b;1985a;Feuerstein et al, 1985).…”

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

British J Pharmacology

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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

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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

British J Pharmacology

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“…11 In addition, adenosine is also able to depress the release of inhibitory neurotransmitters in several brain regions. 13 -32 These observations have suggested that adenosine has a "universal" depressor effect in the CNS. However, our present results in the NTS (which are the first to demonstrate an increase in glutamate release by adenosine) and studies by others documenting an increase of dopamine 49 and acetylcholine 50 by purines, seriously challenge this concept and indicate that regional brain differences are present.…”

Section: -45mentioning

confidence: 99%

Cardiovascular excitatory effects of adenosine in the nucleus of the solitary tract.

et al. 1991

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Adenosine is an inhibitory neuromodulator in several brain regions. In the nucleus tractus soUtarius (NTS), however, adenosine exerts excitatory cardiovascular effects. The purpose of the present study was to elucidate the involvement of other endogenous mechanisms that could contribute to the final hemodynamic response to adenosine in this nucleus. In normotensive Sprague-Dawley rats, intra-NTS microinjection of adenosine (23 nmol/60 nl) decreased blood pressure and heart rate. These effects were blocked by prior administration of the specific adenosine receptor antagonist l,3-dipropyl-8-p-sulfophenylxanthine (0.92 nmol) and by the two glutamate receptor antagonists kynurenic acid and glutamic diethylester. The specificity of the adenosine-glutamate interaction in the NTS was demonstrated with adrenergic and angiotensin receptor antagonists that did not affect the adenosine response and by experiments with glutamate receptor antagonists that did not affect nicotine actions in the NTS. Furthermore, an increase in glutamate levels was demonstrated during perfusion of adenosine through a microdiatysis probe in the NTS of anesthetized rabbits. These findings indicate that adenosine increases the release of glutamate in the NTS and, thus, are at variance with the concept of a "universal" inhibitory effect of adenosine in the central nervous system. (Hypertension 1991;18:494-502)

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“…89 Tissue levels of adenosine in the central nervous system have been shown to increase during hypoxia 10 and seizures." Adenosine inhibits the release of many neurotransmitters, including acetylcholine, 12 " 192 HYPERTENSION VOL 11, No 2, FEBRUARY 1988 rine, 1516 dopamine, 17 GABA, 18 and L-glutamate, 19 both in the central nervous system and in peripheral tissues. Adenosine also has a marked depressive action on the firing of neurons in virtually all regions of the central nervous system tested.…”

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confidence: 99%

Purinergic receptors in the brainstem mediate hypotension and bradycardia.

et al. 1988

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SUMMARY Adenosine acts at many sites to modulate neuronal activity. The purpose of this study was to investigate a possible role for adenosine as a neuromodnlator of brainstem cardiovascular control. Microinjections of adenosine (0-2.3 nmol) were made stereotaxically into various brainstem sites. Injection of adenosine into the nucleus tractus solitarii (NTS) produced dose-related decreases in heart rate and systolic and diastolic blood pressures. Maximal changes occurred 90 seconds after injection. Injection into the area postrema also produced decreased heart rate and systolic and diastolic blood pressures. No significant effect occurred following injection into the Cl area. Adenosine 5-triphosphate and its analogue, /3,-y-methylene adenosine 5-triphosphate also produced doserelated and potent vasodepressor and bradycardia effects in the NTS. Injection of l,3-dipropyl-8-psulfophenylxanthine (0.92 nmol), a potent adenosine receptor antagonist, produced no effect itself, but abolished for 45 minutes the actions of further injections of adenosine and adenosine 5'-triphosphate (but not L-glutamate) in both the NTS and area postrema. Thus, NTS and area postrema injections of adenosine decrease blood pressure and heart rate in anesthetized normotensive rats through adenosine receptors located in these areas. These findings support a role for endogenous adenosine as a central modulator in cardiovascular control. (Hypertension 11: 191-197, 1988) KEY WORDS • adenosine • adenosine 5'-triphosphate • central nervous system • nucleus tractus solitarii • area postrema • rats • nucleosides • purines • purinergic neurotransmission A UTONOMIC cardiovascular control is achieved / \ in the medulla oblongata through integration X \ . of input from higher centers with afferent input from receptors in chest and neck structures.1 This afferent input travels in the vagus and glossopharyngeal nerves and terminates principally in the nucleus tractus solitarii (NTS). NTS neurons have projections to many rostral and ventral sites. The Cl area in the ventrolateral medulla, which contributes to the tonic control over sympathetic outflow, receives some of these NTS projections.2 Stimulation of the NTS produces inhibition of sympathetic tone, while stimulation of the Cl area leads to an increase in sympathetic activation.

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Effects of adenosine on depolarization-induced release of various radiolabelled neurotransmitters from slices of rat corpus striatum

Cited by 206 publications

References 16 publications

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

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

Cardiovascular excitatory effects of adenosine in the nucleus of the solitary tract.

Purinergic receptors in the brainstem mediate hypotension and bradycardia.

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Effects of adenosine on depolarization-induced release of various radiolabelled neurotransmitters from slices of rat corpus striatum

Cited by 206 publications

References 16 publications

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

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

Cardiovascular excitatory effects of adenosine in the nucleus of the solitary tract.

Purinergic receptors in the brainstem mediate hypotension and bradycardia.

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

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