Multiple components of the A1 adenosine receptor-adenylate cyclase system are regulated in rat cerebral cortex by chronic caffeine ingestion.

Ramkumar, Vickram; Bumgarner, Jacob R.; Jacobson, Ken; Stiles, Gary L.

doi:10.1172/jci113577

Cited by 68 publications

(38 citation statements)

References 41 publications

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“…On the other hand, absence of such alterations has been also reported (Georgiev et al, 1993;Von Lubitz et al, 1994a,b). Since prolonged exposure to adenosine m I receptor agonists causes uncoupling of G-proteins from the receptor (Ramkumar et al, 1988), downregulation of cellular levels of G-proteins, or their redistribution from the membranes to the cytosol (Milligan, 1993), it has been suggested that the regimen-dependent inversion of the therapeutic outcome may result from changes induced in G-proteins (Von Lubitz et al, 1994a,b).…”

Section: Discussionmentioning

confidence: 99%

Adenosine A3 receptor stimulation and cerebral ischemia

Lubitz

Lin

Popik

et al. 1994

European Journal of Pharmacology

271

257

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Chronic treatment with the selective adenosine A 3 receptor agonist N 6 -(3-iodobenzyl)adenosine-5'-N-methylcarboxamide (IB-MECA) administered prior to either 10 or 20 min forebrain ischemia in gerbils resulted in improved postischemic cerebral blood circulation, survival, and neuronal preservation. Opposite effects, i.e., impaired postischemic blood flow, enhanced mortality, and extensive neuronal destruction in the hippocampus were seen when IB-MECA was given acutely. Neither adenosine A 1 nor A 2 receptors are involved in these actions. The data indicate that stimulation of adenosine A 3 receptors may play an important role in the development of ischemic damage, and that adenosine A 3 receptors may offer a new target for therapeutic interventions.

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Section: Discussionmentioning

confidence: 99%

Adenosine A3 receptor stimulation and cerebral ischemia

Lubitz

Lin

Popik

et al. 1994

European Journal of Pharmacology

271

257

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“…Therefore, it is not surprising that a series of daily injections of CPA results in facilitation of learning possibly caused by downregulation of A 1 receptor sites. Conversely, therefore, chronic exposure to an adenosine receptor A 1 antagonist may upregulate them (Ramkumar et al, 1988) with the consequent impairment of memory functions. Interpretation of the results obtained when drugs were administered prior to training is more difficult.…”

Section: Discussionmentioning

confidence: 99%

Effects of chronic administration of adenosine A1 receptor agonist and antagonist on spatial learning and memory

Lubitz

Paul

Bartus

et al. 1993

European Journal of Pharmacology

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Spatial memory acquisition in Morris water maze was tested in C57BL/6 mice. Animals were injected once daily with different doses of either N 6 -cyclopentyladenosine (CPA) or 8-cyclopentyl-1,3-dipropylxanthine (CPX). Drugs were administered for 9 days either concurrently with water maze testing (drugs injected 1 h after each trial), or prior to the entire block of trials. In the latter case, 1 day without injections preceded water maze experiments. Chronic administration of CPA resulted in a significant, dose-dependent reduction of target latencies, rapid development of spatial preference, and the absence of animals unable to perform the task. CPX treated animals did not show significant performance changes, and failed to develop spatial preference. Locomotor disturbances were not the cause of the observed effects. Our results indicate that chronic treatment with agents acting at adenosine A 1 receptors results in behavioral effects that are significantly different from those observed following their acute administration. Therefore, particular caution is required in development of adenosine-based strategies targeted at neurodegenerative or cognitive disorders in which chronic treatment is advocated.

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“…Several studies have shown that chronic treatment with caffeine causes an upregulation of adenosine A, receptors (Fredholm, 1982;Johansson et al, 1993a;Shi et al, 1993). There is also evidence that receptors for other transmitters, especially GABA and ACh, as well as G,-proteins are affected (Ramkumar et al, 1988;Shi et al, 1993). Interestingly, both NGFI-A and NGFI-B proteins can bind specifically to DNA (Christy and Nathans, 1989;Wilson et al, 1991) and act as transcription factors.…”

Section: Gaba Releasementioning

confidence: 99%

Biphasic changes in locomotor behavior and in expression of mRNA for NGFI-A and NGFI-B in rat striatum following acute caffeine administration

1995

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The time course of expression of mRNA for NGFI-A and NGFI-B after a single intraperitoneal injection of saline or caffeine was examined using in situ hybridization. Administration of a high dose of caffeine (100 mg/kg) decreased locomotor behavior and increased NGFI-A and NGFI- B mRNA in the entire striatum. A lower dose of caffeine (50 mg/kg) caused a weak enhancement of both messages, which was confined to the lateral part of caudate-putamen. This dose increased horizontal, but not vertical, movement. In rats treated with the lowest dose of caffeine (25 mg/kg), the expression of both investigated genes tended to be lower than for saline-treated rats and both horizontal and vertical locomotor activity increased markedly. The reduction in the number of labeled neurons seemed to occur predominantly in enkephalin- containing neurons, which coexpress adenosine A2A receptors and dopamine D2 receptors. The decrease of mRNA for NGFI-A, NGFI-B, and jun B caused by caffeine (25 mg/kg) could be mimicked by the D2 agonist quinpirole (1 and 3 mg/kg). Moreover, caffeine could significantly decrease the expression seen following treatment with the D2 antagonist raclopride (2 mg/kg). In addition, in the parietal cortex, 25 mg/kg of caffeine caused a significant elevation of both examined immediate early genes. Thus, biphasic changes in locomotion induced by caffeine are paralleled by biphasic changes in mRNA for NGFI-A, NGFI-B, and jun B. The results also provide additional support for a functionally important interaction between adenosine and dopamine D2 receptors.

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Multiple components of the A1 adenosine receptor-adenylate cyclase system are regulated in rat cerebral cortex by chronic caffeine ingestion.

Abstract: The effects of chronic caffeine on the Al adenosine receptoradenylate cyclase system of rat cerebral cortical membranes were studied.

Cited by 68 publications

References 41 publications

Adenosine A3 receptor stimulation and cerebral ischemia

Adenosine A3 receptor stimulation and cerebral ischemia

Effects of chronic administration of adenosine A1 receptor agonist and antagonist on spatial learning and memory

Biphasic changes in locomotor behavior and in expression of mRNA for NGFI-A and NGFI-B in rat striatum following acute caffeine administration

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