N-methyl-D-aspartate-evoked adenosine and inosine release from neurons requires extracellular calcium.

The nucleoside adenosine (ADO) is a neuromodulator in brain. ADO and its metabolite inosine (INO) have been shown to increase cell viability in stroke models. During ischemia, extracellular levels of both ADO and INO are increased.

Transgenic expression of human equilibrative nucleoside transporter 1 in mouse neurons.

Transgenic mice that express human equilibrative nucleoside transporter subtype 1 (hENT1) under the control of a neuron-specific enolase promoter have been generated. Southern blot and PCR revealed the presence of the transgene in five founder mice. Mice from each founder line were examined by reverse transcriptase (RT)-PCR and found to express hENT1 in RNA isolated from whole brain, cerebral cortex, striatum, hippocampus, and cerebellum but not liver, kidney, heart, lung or skeletal muscle.

Adenosine produced by neurons is metabolized to hypoxanthine by astrocytes.

Adenosine (ADO) is an important neuromodulator in brain. During pathophysiological events such as stroke or brain trauma, ADO levels can increase up to 100-fold. We tested the hypothesis that astrocytes are important for the removal of ADO produced by neurons and for the metabolism of ADO to inosine (INO) and hypoxanthine (HX).

Astrocytes affect the profile of purines released from cultured cortical neurons.

Adenosine (ADO) is produced by cultured neurons and astrocytes, albeit by different pathways, during in vitro stroke models (Parkinson and Xiong [2004] J. Neurochem. 88:1305-1312).

Gene expression for enzymes and transporters involved in regulating adenosine and inosine levels in rat forebrain neurons, astrocytes and C6 glioma cells.

In brain, levels of adenosine increase up to 100-fold during cerebral ischemia. Based on in vitro studies, both astrocytes and neurons contribute to this adenosine release. Neurons release adenosine per se whereas astrocytes release adenine nucleotides that are metabolized to adenosine extracellularly.

The effect of acidosis on adenosine release from cultured rat forebrain neurons.

During cerebral ischemia, dysregulated glutamate release activates N-methyl-d-aspartate (NMDA) receptors which promotes excitotoxicity and intracellular acidosis. Ischemia also induces cellular adenosine (ADO) release, which activates ADO receptors and reduces neuronal injury. The aim of this research was to determine if decreasing intracellular pH (pH(i)) enhances ADO release from neurons.

Cancer-selective therapy of the future: apoptin and its mechanism of action.

Classical chemotherapy, that specifically targets rapidly proliferating cells, has been in existence for over eighty years and has proven to be fully successful in only a limited number of cancers. Thus, this review focuses on a novel, emerging approach for cancer therapy that uses alternative, and more unique features of cancer cells. This new approach facilitates the selective targeting of cancer, while sparing normal, non-transformed cells.

Effects of clozapine plus lamotrigine on phencyclidine-induced hyperactivity.

There is growing evidence from both uncontrolled and controlled clinical studies that lamotrigine (LTG) significantly augments clozapine (CLZ) in the treatment of refractory schizophrenia (RS) [Dursun, S.M., McIntosh, D.

Astrocytes and neurons: different roles in regulating adenosine levels.

Objectives: Adenosine is an endogenous nucleoside that signals through G-protein coupled receptors. Extracellular adenosine is required for receptor activation and two pathways have been identified for formation and cellular release of adenosine. The CLASSICAL pathway relies on intracellular formation of adenosine from adenine nucleotides and cellular efflux of adenosine via equilibrative nucleoside transporters (ENTs).