Activation of adenosine A1 and A2 receptors differentially modulates calcium channels and glycinergic synaptic transmission in rat brainstem

Umemiya, Masashi; Berger, Albert J.

doi:10.1016/0896-6273(94)90429-4

Cited by 98 publications

(88 citation statements)

References 24 publications

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“…Tonic extracellular concentrations of adenosine in the PAG were insufficient to modulate GABAergic synaptic transmission. Application of the AÔ adenosine receptor antagonist DPCPX did not alter GABAergic synaptic transmission, as has been demonstrated in the thalamus (Ulrich & Huguenard, 1995) and hypoglossal neurons (Umemiya & Berger, 1994). In contrast, tonic adenosine inhibition of synaptic transmission has been observed in the hippocampus (Dunwiddie & Diao, 1994) and ventral tegmental area (Bonci & Williams, 1996).…”

Section: Discussionmentioning

confidence: 94%

Inhibition by adenosine receptor agonists of synaptic transmission in rat periaqueductal grey neurons

Bagley

Vaughan

Christie

1999

The Journal of Physiology

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The midbrain periaqueductal grey (PAG) plays a pivotal role in integrating the analgesic and cardiovascular responses of an animal to threat, stress or pain (Bandler & Shipley, 1994). The PAG contains a moderate density of AÔ adenosine receptors and adenosine uptake sites (Glass et al. 1996). While the functional effects of adenosine in the PAG are unknown, centrally administered adenosine receptor agonists produce analgesia (for review see Sawynok & Sweeney, 1989) and modulate cardiovascular responses (Barraco et al. 1986). The PAG is also an important site for acute opioid actions (Yaksh et al. 1976) and the expression of some signs of opioid withdrawal (for review see Christie et al. 1997). Extracellular adenosine concentrations are also increased in several brain regions during opioid withdrawal (Bonci & Williams, 1996;Chieng & Williams, 1998). Adenosine inhibits synaptic transmission in the central nervous system (Phillis et al. 1975;Uchimura & North, 1991). We have recently reported that ì_opioid, GABAB and ORLÔ receptor activation inhibits GABAergic and glutamatergic synaptic transmission in the PAG (Vaughan & Christie, 1997; Vaughan et al. 1997a,b). However, the effects of adenosine on synaptic transmission in the PAG are unknown. In the present study, the actions of adenosine on GABAergic and glutamatergic synaptic transmission were characterized in rat PAG using the thin slice patch-clamp technique. METHODSSprague-Dawley rats, 12-30 days old, were anaesthetized with halothane, killed by cervical dislocation and their brains quickly removed and immersed in ice-cold extracellular solution containing (mÒ): NaCl, 126; KCl, 2•5; NaHµPOÚ, 1•4; MgClµ, 1•2; CaClµ, 2•4; glucose, 11; and NaHCO×, 25; equilibrated with 95% Oµ:5% COµ. A vibratome was used to prepare coronal midbrain slices (250-300 ìm thickness) containing the PAG, which were placed in a holding chamber containing extracellular solution maintained at 34°C. Brain slices were placed in a recording chamber (1•5 ml volume) mounted on the stage of an upright microscope (Olympus BH_2 with a fixed-stage modification) and viewed using a water immersion objective (Zeiss, ²40). Slices were continuously superfused (2 ml min¢) with extracellular solution (34°C). Neurons located in

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Section: Discussionmentioning

confidence: 94%

Inhibition by adenosine receptor agonists of synaptic transmission in rat periaqueductal grey neurons

Bagley

Vaughan

Christie

1999

The Journal of Physiology

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“…Facilitation of neurotransmitter release appears to result from the interaction of adenosine A 2 receptors and P-type calcium channels (Umemiya and Berger, 1994). Utilizing the concept of adenosine A 2 receptor participation in excitatory neurotransmitter release, Gao and Phillis (1994) demonstrated that acute administration of a potent and weakly selective adenosine A 2 receptor antagonist, CGS 15943, at 0.1 mg/kg prior to 5 min ischemia in gerbils results in a substantial attenuation of neural damage in the CA1 sector of the hippocampus and in a marked reduction of postischemic neurological deficit (hyperactivity).…”

Section: Discussionmentioning

confidence: 99%

Cerebral ischemia in gerbils: effects of acute and chronic treatment with adenosine A2A receptor agonist and antagonist

Lubitz¹,

Lin

Jacobson³

1995

European Journal of Pharmacology

132

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Despite significant progress in understanding of the potential of adenosine A 1 receptor-based therapies in treatment of cerebral ischemia and stroke, very little is known about the effect of selective stimulation of adenosine A 2A receptors on the outcome of a cerebrovascular arrest. In view of a major role played by adenosine A 2 receptors in the regulation of cerebral blood flow, we have investigated the effect of both acute and chronic administration of the selective adenosine receptor agonist 2-[(2-aminoethylamino)-carbonylethylphenylethylamino]-5′-Nethylcarboxoamidoadenosine (APEC) and antagonist 8-(3-chlorostyryl)caffeine (CSC) on the outcome of 10 min ischemia in gerbils. Acute treatment with APEC improved recovery of postischemic blood flow and survival without affecting neuronal preservation in the hippocampus. Acute treatment with CSC had no effect on the cerebral blood flow but resulted in a very significant protection of hippocampal neurons. Significant improvement of survival was present during the initial 10 days postischemia. Due to subsequent deaths of animals treated acutely with CSC, the end-point mortality (14 days postischemia) in this group did not differ statistically from that seen in the controls. It is, however, possible that the late mortality in the acute CSC group was caused by the systemic effects of brain ischemia that are not subject to the treatment with this drug. Chronic treatment with APEC resulted in a statistically significant improvement in all studied measures. Although chronic treatment with CSC improved postischemic blood flow, its effect on neuronal preservation was minimal and statistically insignificant. Mortality remained unaffected. The results indicate that the acute treatment with adenosine A 2A receptor antagonists may have a limited value in treatment of global ischemia. However, since administered CSC has no effect on the reestablishment of postischemic blood flow, treatment of stroke with adenosine A 2A receptor antagonists may not be advisable. Additional studies are necessary to elucidate whether chronically administered drugs acting at adenosine A 2 receptors may be useful in treatment of stroke and other neurodegenerative disorders.

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“…Thus, the role of A2 A Rs in GABAergic neurotransmission apparently varies considerably. The only report of A2R modulation of glycine release was in the brainstem, but this could have been attributable to A2 B R activation (Umemiya and Berger, 1994). A2 A Rs have been shown to influence autonomic homeostatic mechanisms through a neuromodulatory role in several brainstem nuclei (Barraco et al, 1993).…”

Section: Introductionmentioning

confidence: 99%

Input-Specific Modulation of Neurotransmitter Release in the Lateral Horn of the Spinal Cord via Adenosine Receptors

Brooke

Deuchars²,

Deuchars³

2004

J. Neurosci.

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Activation of adenosine A1 and A2 receptors differentially modulates calcium channels and glycinergic synaptic transmission in rat brainstem

Cited by 98 publications

References 24 publications

Inhibition by adenosine receptor agonists of synaptic transmission in rat periaqueductal grey neurons

Inhibition by adenosine receptor agonists of synaptic transmission in rat periaqueductal grey neurons

Cerebral ischemia in gerbils: effects of acute and chronic treatment with adenosine A2A receptor agonist and antagonist

Input-Specific Modulation of Neurotransmitter Release in the Lateral Horn of the Spinal Cord via Adenosine Receptors

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