n(6)-cyclopentyladenosine and Ischemic-Attack--Transient

n(6)-cyclopentyladenosine has been researched along with Ischemic-Attack--Transient* in 2 studies

Other Studies

2 other study(ies) available for n(6)-cyclopentyladenosine and Ischemic-Attack--Transient

Article	Year
Acetylcholine output from the ischemic rat cerebral cortex: effects of adenosine agonists. Brain research, 1993, Jun-11, Volume: 613, Issue:2 The efflux of acetylcholine (ACh) from the ischemic rat cerebral cortex was examined using the cortical cup technique and an HPLC with electrochemical detection assay. Four vessel occlusion of the cerebral circulation caused a rapid increase in ACh efflux into the cortical superfusates, which was then sustained during the 20 min period of occlusion. Reperfusion was associated with a rapid return of ACh efflux to basal levels. The A1 and A2 selective adenosine receptor agonists, N6-cyclopentyladenosine (10(-8) and 10(-10) M) and CGS 21680 (10(-8)), failed to significantly alter ischemia-evoked release of ACh. Because ACh is known to enhance NMDA receptor mediated neuronal depolarization and intracellular Ca2+ levels, and to potentiate L-glutamate-induced neural degeneration, the present findings suggest that ACh could contribute to ischemic brain injury. Topics: Acetylcholine; Adenosine; Animals; Antihypertensive Agents; Cerebral Cortex; Chromatography, High Pressure Liquid; Ischemic Attack, Transient; Male; Phenethylamines; Rats; Rats, Sprague-Dawley; Receptors, Purinergic P1; Receptors, Purinergic P2; Time Factors	1993
Adenosine receptor agonists inhibit the release of gamma-aminobutyric acid (GABA) from the ischemic rat cerebral cortex. Brain research, 1992, Jun-05, Volume: 582, Issue:1 The effects of CPA (a selective A1 receptor agonist), NECA (a mixed A1 and A2 receptor agonist), and CGS 21680 (a selective A2 receptor agonist) on the ischemia-evoked release of gamma-aminobutyric acid (GABA) from rat cerebral cortex was investigated with the cortical cup technique. Cerebral ischemia (20 min) was elicited by four vessel occlusion. In control animals, superfusate GABA increased from a basal level of 206 +/- 26 nM (mean +/- S.E.M., n = 18) to 10,748 +/- 3,876 nM during the reperfusion period. Pretreatment with adenosine receptor agonists failed to affect basal levels of GABA release. However, CPA (10(-10) M), NECA (10(-9) M), and CGS 21680 (10(-8) M) significantly suppressed the ischemia-evoked release of GABA. The ability to block the ischemia-evoked release of GABA was not evident when the adenosine receptor agonists were administered at higher concentrations. Thus, the selective activation of either A1 or high-affinity A2a adenosine receptors results in an inhibition of ischemia-evoked GABA release. Topics: Adenosine; Adenosine-5'-(N-ethylcarboxamide); Analysis of Variance; Animals; Cerebral Cortex; Dose-Response Relationship, Drug; Electroencephalography; gamma-Aminobutyric Acid; Ischemic Attack, Transient; Kinetics; Male; Phenethylamines; Rats; Rats, Inbred Strains; Receptors, Purinergic; Time Factors	1992

Article

Year

Acetylcholine output from the ischemic rat cerebral cortex: effects of adenosine agonists.

Brain research, 1993, Jun-11, Volume: 613, Issue:2

The efflux of acetylcholine (ACh) from the ischemic rat cerebral cortex was examined using the cortical cup technique and an HPLC with electrochemical detection assay. Four vessel occlusion of the cerebral circulation caused a rapid increase in ACh efflux into the cortical superfusates, which was then sustained during the 20 min period of occlusion. Reperfusion was associated with a rapid return of ACh efflux to basal levels. The A1 and A2 selective adenosine receptor agonists, N6-cyclopentyladenosine (10(-8) and 10(-10) M) and CGS 21680 (10(-8)), failed to significantly alter ischemia-evoked release of ACh. Because ACh is known to enhance NMDA receptor mediated neuronal depolarization and intracellular Ca2+ levels, and to potentiate L-glutamate-induced neural degeneration, the present findings suggest that ACh could contribute to ischemic brain injury.

Topics: Acetylcholine; Adenosine; Animals; Antihypertensive Agents; Cerebral Cortex; Chromatography, High Pressure Liquid; Ischemic Attack, Transient; Male; Phenethylamines; Rats; Rats, Sprague-Dawley; Receptors, Purinergic P1; Receptors, Purinergic P2; Time Factors

1993

Adenosine receptor agonists inhibit the release of gamma-aminobutyric acid (GABA) from the ischemic rat cerebral cortex.

Brain research, 1992, Jun-05, Volume: 582, Issue:1

The effects of CPA (a selective A1 receptor agonist), NECA (a mixed A1 and A2 receptor agonist), and CGS 21680 (a selective A2 receptor agonist) on the ischemia-evoked release of gamma-aminobutyric acid (GABA) from rat cerebral cortex was investigated with the cortical cup technique. Cerebral ischemia (20 min) was elicited by four vessel occlusion. In control animals, superfusate GABA increased from a basal level of 206 +/- 26 nM (mean +/- S.E.M., n = 18) to 10,748 +/- 3,876 nM during the reperfusion period. Pretreatment with adenosine receptor agonists failed to affect basal levels of GABA release. However, CPA (10(-10) M), NECA (10(-9) M), and CGS 21680 (10(-8) M) significantly suppressed the ischemia-evoked release of GABA. The ability to block the ischemia-evoked release of GABA was not evident when the adenosine receptor agonists were administered at higher concentrations. Thus, the selective activation of either A1 or high-affinity A2a adenosine receptors results in an inhibition of ischemia-evoked GABA release.

Topics: Adenosine; Adenosine-5'-(N-ethylcarboxamide); Analysis of Variance; Animals; Cerebral Cortex; Dose-Response Relationship, Drug; Electroencephalography; gamma-Aminobutyric Acid; Ischemic Attack, Transient; Kinetics; Male; Phenethylamines; Rats; Rats, Inbred Strains; Receptors, Purinergic; Time Factors

1992