Interaction between adenosine A1 and A2 receptor-mediated responses in the rat hippocampus in vitro

O’Kane, E.M.; Stone, T.W.

doi:10.1016/s0014-2999(98)00730-4

Cited by 71 publications

(43 citation statements)

References 52 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…A 1 R and A 2A R are coupled to G i/oand G s/olf -proteins, respectively (Dunwiddie and Masino, 2001). Stimulation of presynaptic A 1 Rs receptors decreases the probability of neurotransmitter release, whereas activation of presynaptic A 2A Rs enhances neurotransmitter release (Yawo and Chuhma, 1993;Wu and Saggau, 1997;O'Kane and Stone, 1998;Lopes et al, 2002;Quarta et al, 2004b).…”

Section: Introductionmentioning

confidence: 99%

“…Previous studies have provided evidence for functional antagonistic interactions between A 1 Rs and A 2A Rs that modulate glutamate release in the striatum and hippocampus (O'Kane and Stone, 1998;Lopes et al, 2002;Quarta et al, 2004b). The coexistence of both facilitatory A 2A Rs and inhibitory A 1 Rs in the same terminal is intriguing, particularly in view of their opposite functional effects.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Presynaptic Control of Striatal Glutamatergic Neurotransmission by Adenosine A₁–A_2AReceptor Heteromers

et al. 2006

View full text Add to dashboard Cite

show abstract

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Presynaptic Control of Striatal Glutamatergic Neurotransmission by Adenosine A₁–A_2AReceptor Heteromers

et al. 2006

View full text Add to dashboard Cite

show abstract

“…This suggests that the EPSP-spike dissociation is mainly caused by actions of CPA at postsynaptic sites [6] . These actions of CPA, however, are prevented by the presence of the A 2A receptor-selective agonist CGS21680, consistent with the existence of cross-talk between the two subtypes of receptor.…”

Section: Discussionmentioning

confidence: 95%

“…We have observed that activation of adenosine A 2A receptors can attenuate the adenosine A 1 receptor-mediated inhibition of EPSP spike coupling by decreasing the effects of adenosine A 1 receptor activation at postsynaptic sites [6] . In this study we attempt to determine the mechanism by which adenosine receptors dissociate EPSP spike coupling using modulators of second messenger systems, potassium channel blockers, and nitric oxide synthase inhibitors.…”

Section: Introductionmentioning

confidence: 92%

“…Several groups have previously reported an inhibitory effect of adenosine A 1 receptors on population fi eld excitatory postsynaptic potentials (fEPSPs), population spikes (PS) and the relationship between the two, i.e. EPSP spike (ES) coupling in the CA1 area of rat hippocampus (see [6] ). The fEPSP gives primarily a measure of membrane potential changes generated by excitatory synapses on the apical dendrites of CA1 pyramidal neurones.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Barium, Glibenclamide and CGS21680 Prevent Adenosine A<sub>1</sub> Receptor Changes of ES Coupling and Spike Threshold

O’Kane¹,

Stone²

2004

Neurosignals

Self Cite

View full text Add to dashboard Cite

Activation of adenosine A₁ receptors raised spike thresholds and induced a dissociation of excitatory postsynaptic potential (EPSP) spike coupling in hippocampal pyramidal neurones. This effect could be prevented by activation of A_2A adenosine receptors. The A₁ receptor agonist N⁶-cyclopentyladenosine caused a dissociation of the EPSP spike coupling recorded extracellularly and increased the threshold for spike generation measured intracellularly. These effects were prevented by the A_2A receptor agonist CGS21680. A series of agents interfering with adenylate cyclase activity, protein kinase A or C, or nitric oxide synthase had no effect on these responses to N⁶-cyclopentyladenosine. Superfusion with barium or glibenclamide prevented both the dissociation of EPSP spike coupling and the increase of spike threshold. It is concluded that a barium- and glibenclamide-sensitive potassium current may be involved in the postsynaptic effects of A₁ receptors on spike threshold, and it is suggested that a similar suppression of a potassium current by A_2A receptors could underlie the inhibition of A₁ receptor responses.

show abstract

Neuroprotection by A_2A receptor antagonists

Stone¹,

Jones²,

Smith³

2001

Drug Development Research

Self Cite

View full text Add to dashboard Cite

Activation of A 2A receptors has been shown to protect neurons in the hippocampus from damage caused by excitotoxins or from cerebral insults such as ischaemia. For example, the A 2A agonist 2-p-(2-carboxyethyl)phenethylamino-5′-N-ethylcarboxamidoadenosine hydrochloride (CGS 21680) protects the hippocampus at concentrations which are only partially blocked by the centrally acting adenosine A 1 receptor antagonist 8-cyclopentyl-1,3-dipropylxanthine (CPX), suggesting that protection is mediated largely by the A 2A receptor. However, selective antagonists at the A 2A receptor, such as 4-(2-[7-amino-2-{2-furyl}{1,2,4}triazolo{2,3-a}{1,3,5}triazin-5-yl-amino]ethyl)phenol (ZM 241385), also show protection against neuronal death produced by ischaemia or excitotoxicity. In addition, A 2A receptor antagonists can reduce damage produced by combinations of subthreshold doses of the endogenous excitotoxin quinolinic acid and free radicals. The TdT-mediated dUTP-biotin nick end labeling (TUNEL) method has revealed that, after systemic kainic acid administration, staining was apparent in the CA1 region of the hippocampus only, even though damage was present in both the CA1 and CA3a areas. In animals injected intrahippocampally, both apoptosis and damage were limited to the CA3 region. Intrahippocampal co-injection of kainate together with ZM 241385 did not induce apoptosis even though damage was apparent. This suggests that the adenosine A 2A receptor may play a role in the route by which cells die during excitotoxicity. Overall, A 2A receptor antagonists appear to be promising candidates as new drugs for the prevention of neuronal damage and death in the central nervous system. Drug Dev. Res. 52:323-330, 2001.

show abstract

Interaction between adenosine A1 and A2 receptor-mediated responses in the rat hippocampus in vitro

Cited by 71 publications

References 52 publications

Presynaptic Control of Striatal Glutamatergic Neurotransmission by Adenosine A₁–A_2AReceptor Heteromers

Presynaptic Control of Striatal Glutamatergic Neurotransmission by Adenosine A₁–A_2AReceptor Heteromers

Barium, Glibenclamide and CGS21680 Prevent Adenosine A<sub>1</sub> Receptor Changes of ES Coupling and Spike Threshold

Neuroprotection by A_2A receptor antagonists

Contact Info

Product

Resources

About

Interaction between adenosine A1 and A2 receptor-mediated responses in the rat hippocampus in vitro

Cited by 71 publications

References 52 publications

Presynaptic Control of Striatal Glutamatergic Neurotransmission by Adenosine A1–A2AReceptor Heteromers

Presynaptic Control of Striatal Glutamatergic Neurotransmission by Adenosine A1–A2AReceptor Heteromers

Barium, Glibenclamide and CGS21680 Prevent Adenosine A<sub>1</sub> Receptor Changes of ES Coupling and Spike Threshold

Neuroprotection by A2A receptor antagonists

Contact Info

Product

Resources

About

Presynaptic Control of Striatal Glutamatergic Neurotransmission by Adenosine A₁–A_2AReceptor Heteromers

Presynaptic Control of Striatal Glutamatergic Neurotransmission by Adenosine A₁–A_2AReceptor Heteromers

Neuroprotection by A_2A receptor antagonists