N-methyl-d-aspartate, kainate and quisqualate release endogenous adenosine from rat cortical slices

Hoehn, Katja; White, Thomas D.

doi:10.1016/0306-4522(90)90280-h

Cited by 73 publications

(37 citation statements)

References 54 publications

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“…Spiperone, which is devoid of affinity for al and 62 receptors (see Walker et al, 1990) but is active on putative 63 sites (Booth et al, 1993;Myers et al, 1994) 1990a, b;G6thert & Fink, 1989;Hoehn & White, 1990;Roman et al, 1991;Monnet et al, 1992a;Fink & G6thert, 1992;Malva et al, 1994).…”

Section: Introductionmentioning

confidence: 99%

Differentiation of σ ligand‐activated receptor subtypes that modulate NMDA‐evoked [³H]‐noradrenaline release in rat hippocampal slices

Monnet

Costa

Bowen

1996

British J Pharmacology

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1It is now widely accepted that there are two classes of sigma (a) binding sites, denoted and°2, and recently 3 subtype has been proposed. Selective c, and c2 receptor agonists are known to modulate the neuronal response to N-methyl-D-aspartate (NMDA) Conversely, N,N-dipropyl-2-[4-methoxy-3-(2-phenylethoxy)phenyl]-ethylamine monohydrochloride (NE-100) blocked the effects of (+)-pentazocine as well as those of BD-737, but not those of DTG. 5 The present results provide in vitro functional evidence for a a receptor type preferentially sensitive to BD-737, reduced haloperidol, BD-1008 and also to NE-100, that differs from the already identified ci, ci2 and ci3 sites.

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Section: Introductionmentioning

confidence: 99%

Differentiation of σ ligand‐activated receptor subtypes that modulate NMDA‐evoked [³H]‐noradrenaline release in rat hippocampal slices

Monnet

Costa

Bowen

1996

British J Pharmacology

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“…At this point it appears that we can identify several different possible mechanisms underlying adenosine release: (1) a calcium-dependent mechanism demonstrable in potassium-stimulated cortical slices (Hoehn and White, 1990a), synaptosomes (MacDonald and White, 1985) cerebellar neuronal cultures (Philibert and Dutton, 1989) and embryonic chick retinal neuronal cultures (Paes de Carvalho et al, 1990); (2) a calciumindependent mechanism that is demonstrable using veratridine stimulation (MacDonald and White, 1985) metabolic poisoning (Meghji et al, 1989) as well as glutamate receptor stimulation (both NMDA and non-NMDA receptors) (Hoehn and White, 1990~) and that probably utilizes the bidirectional nucleoside transporter (Meghji et al, 1989); (3) a glutamate uptake-activated mechanism demonstrable in synaptosomes (Hoehn and White, 1990b); and (4) a mechanism dependent upon the hydrolysis of extracellular ATP that is itself released as a consequence of calcium-dependent (potassium stimulation) and calcium-independent (veratridine stimulation) processes (White, 1978).…”

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confidence: 99%

Beta-adrenergic receptor-mediated regulation of extracellular adenosine in cerebral cortex in culture

Knowles

et al. 1994

J. Neurosci.

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Adenosine is an important inhibitory neuromodulator in the CNS, yet the sources of extracellular adenosine have yet to be well characterized. In this study we show that beta-adrenergic stimulation of cortical cultures results in the extracellular accumulation of cAMP as well as adenosine, and that the extracellular adenosine derives from extracellular cAMP. The concentration dependence of isoproterenol in evoking cAMP secretion was determined by radioimmunoassay, and the EC50 for this effect was found to be approximately 100 nM. In order to investigate the effect of beta-adrenergic stimulation on the regulation of extracellular adenosine, the effect of isoproterenol in stimulating the extracellular accumulation of adenine-containing compounds was examined by HPLC. Isoproterenol stimulated cAMP secretion in both astrocyte cultures and astrocyte-rich mixed cultures of astrocytes and neurons. However, no extracellular cAMP was detectable in neuron- enriched astrocyte-poor cultures. Extracellular adenosine increased in response to isoproterenol in the astrocyte-rich mixed cultures, but not in the neuron-enriched astrocyte-poor cultures. After 30 min exposure to isoproterenol, the concentration of adenosine in the extracellular medium increased by 47% in 56 experiments in the mixed astrocyte-rich cultures. In order to establish whether the adenosine that accumulates in response to isoproterenol stimulation actually derives from extracellular cAMP, phosphodiesterase inhibitors were tested for their ability to block isoproterenol-stimulated adenosine accumulation. Isobutylmethylxanthine (IBMX; 100 microM), RO 20–1724 (180 microM), carbazeran (10 microM), dipyridamole (10 microM), and trifluoperazine (10 microM) had no inhibitory effect on the isoproterenol-stimulated accumulation of extracellular adenosine. However 100 microM IBMX plus 180 microM RO 20–1724 effectively blocked isoproterenol-stimulated adenosine accumulation and, as expected, increased extracellular cAMP. As a further test of the origin of isoproterenol-stimulated adenosine accumulation, we attempted to block this phenomenon by blocking cAMP secretion itself. For this purpose probenecid, a known inhibitor of cAMP secretion in many different cell types, was used. We found that probenecid at 1 mM blocked isoproterenol-stimulated adenosine accumulation. These studies suggest that one potentially important source of extracellular adenosine in the cerebral cortex is endogenous extracellular cAMP, secreted from astrocytes in response to beta- adrenergic receptor stimulation. Since the receptors of neuromodulators other than norepinephrine may also be coupled to adenylyl cyclase in the cerebral cortex, there may be several neuromodulatory systems that regulate extracellular adenosine levels by this mechanism.

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“…Adenosine release by activation of NMDA, AMPA and kainate receptors also has been demonstrated in cortical slices (Hoehn and White 1990; Craig and White 1993a, 1993b; White 1996), hippocampal slices (Pedata et al . 1991) and in the striatum (Delaney et al .…”

Section: Discussionmentioning

confidence: 87%

“…In brain, both adenosine and glutamate are released in pathological conditions. Activation of glutamate receptors produces excitatory effects and facilitates adenosine release in various brain tissues (Hoehn and White 1990; Pedata et al . 1991; Delaney et al .…”

Section: Discussionmentioning

confidence: 99%

“…The expression of glutamate receptors on both elements from which adenosine release occurs, and the endogenous release of excitatory amino acids in formalin‐induced inflammation raises the question as to whether excitatory amino acids can evoke adenosine release peripherally. This is an especially intriguing possibility because, in the central nervous system, activation of both NMDA and non‐NMDA receptors increases extracellular adenosine levels in rat cortex (Hoehn and White 1990; White 1996), hippocampus (Arens et al . 1992; Latini et al .…”

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confidence: 99%

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Intraplantar injection of glutamate evokes peripheral adenosine release in the rat hind paw: involvement of peripheral ionotropic glutamate receptors and capsaicin‐sensitive sensory afferents

Liu

White

Sawynok

2002

Journal of Neurochemistry

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Glutamate receptors have been identified on the peripheral terminals of both primary sensory afferents and sympathetic post-ganglionic neurons, and activation of these receptors produces peripheral sensitization and enhances nociception. Adenosine is an endogenous agent that has a regulatory effect on pain. In brain and spinal cord, adenosine release can be promoted by excitatory amino acids. In the present study, we used in vivo microdialysis to determine whether glutamate also can release adenosine in peripheral tissues. Rats were anesthetized with pentobarbital and microdialysis probes were implanted into the subcutaneous tissue of the plantar aspect of the rat hind paw. Subcutaneous injection of glutamate (50 lL, 0.3-100 lmol) evoked a short-lasting adenosine release immediately following drug injection. Co-administration of either the N-methyl-D-aspartate (NMDA) receptor antagonist, dizocipine maleate (MK-801, 1 nmol) or the non-NMDA receptor antagonist, 6-cyano-7-nitroquinoxaline (CNQX, 10 nmol) with glutamate blocked such release, suggesting an involvement of peripheral ionotropic glutamate receptors in this response. Systemic pre-treatment with capsaicin, a neurotoxin selective for unmyelinated sensory afferents, significantly reduced glutamate-evoked peripheral adenosine release, but release was not affected by systemic pre-treatment with 6-hydroxydopamine, a neurotoxin selective for sympathetic nerve efferents. Neither MK-801 nor CNQX blocked 5% formalin-evoked adenosine release, suggesting adenosine release by formalin is not secondary to ionotropic glutamate receptor activation. We conclude that administration of glutamate evokes peripheral adenosine release, and that peripheral ionotropic glutamate receptors on unmyelinated sensory afferents are involved in such release. The released adenosine may provide a negative feedback control on nociception.

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N-methyl-d-aspartate, kainate and quisqualate release endogenous adenosine from rat cortical slices

Cited by 73 publications

References 54 publications

Differentiation of σ ligand‐activated receptor subtypes that modulate NMDA‐evoked [³H]‐noradrenaline release in rat hippocampal slices

Differentiation of σ ligand‐activated receptor subtypes that modulate NMDA‐evoked [³H]‐noradrenaline release in rat hippocampal slices

Beta-adrenergic receptor-mediated regulation of extracellular adenosine in cerebral cortex in culture

Intraplantar injection of glutamate evokes peripheral adenosine release in the rat hind paw: involvement of peripheral ionotropic glutamate receptors and capsaicin‐sensitive sensory afferents

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N-methyl-d-aspartate, kainate and quisqualate release endogenous adenosine from rat cortical slices

Cited by 73 publications

References 54 publications

Differentiation of σ ligand‐activated receptor subtypes that modulate NMDA‐evoked [3H]‐noradrenaline release in rat hippocampal slices

Differentiation of σ ligand‐activated receptor subtypes that modulate NMDA‐evoked [3H]‐noradrenaline release in rat hippocampal slices

Beta-adrenergic receptor-mediated regulation of extracellular adenosine in cerebral cortex in culture

Intraplantar injection of glutamate evokes peripheral adenosine release in the rat hind paw: involvement of peripheral ionotropic glutamate receptors and capsaicin‐sensitive sensory afferents

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Differentiation of σ ligand‐activated receptor subtypes that modulate NMDA‐evoked [³H]‐noradrenaline release in rat hippocampal slices

Differentiation of σ ligand‐activated receptor subtypes that modulate NMDA‐evoked [³H]‐noradrenaline release in rat hippocampal slices