Activation of adenosine A2 receptors enhances high K+-evoked taurine release from rat hippocampus: A microdialysis study

Abstract

The present study was designed to examine which type of adenosine receptors was involved in enhancement of high K(+)-evoked taurine release from in vivo rat hippocampus using microdialysis. Perfusion with 0.5 or 5.0 mM adenosine enhanced high K(+)-evoked taurine release. Perfusion with 2 microM R(-)-N6-2-phenylisopropyladenosine (PIA), a selective adenosine A1 receptor agonist, did not modulate taurine release. Perfusion with 1 microM 1,3-dipropyl-8-cyclopentylxanthine (DPCPX), a selective adenosine A1 receptor antagonist, increased taurine release. On the other hand, perfusion with 20 microM 2-[4-(2-carboxyethyl)phenethylamino]-5'-N-ethyl-carboxamide-adenos ine (CGS21680), a selective adenosine A2A receptor agonist, enhanced taurine release, while perfusion with 1 mM 3,7-dimethyl-propagylxanthine (DMPX), an adenosine A2 receptor antagonist, did not affect taurine release. These results demonstrate that adenosine enhances high K(+)-evoked taurine release via activation of adenosine A2A receptors from both neurons and glial cells of in vivo rat hippocampus.

Caffeine consumption attenuates neurochemical modifications in the hippocampus of streptozotocin‐induced diabetic rats

“…This effect of caffeine on taurine homeostasis in the hippocampus of diabetic rats may be related to the ability of adenosine receptors (the only known molecular targets of caffeine) to control osmotic swelling (Wurm et al . 2008) and taurine release from both neurons and glia (Hada et al . 1998).…”

“…These observations prompt the hypothesis that caffeine neuroprotection may also be related to this ability of caffeine to impact on osmotic adaptation of brain tissue. This effect of caffeine on taurine homeostasis in the hippocampus of diabetic rats may be related to the ability of adenosine receptors (the only known molecular targets of caffeine) to control osmotic swelling (Wurm et al 2008) and taurine release from both neurons and glia (Hada et al 1998). Thus, these effects of caffeine on diabetes-induced neurochemical profile are likely to be central effects, although caffeine consumption has been reported to have peripheral effects that may aid in the control of glucose homeostasis (van Dam and Hu 2005); however we observed that long-term caffeine intake failed to prevent hypoinsulinemia and hyperglycemia in STZ-treated rats, suggesting that these effects of caffeine on hippocampal metabolism are related to blockade of central adenosine receptors rather than peripheral actions of caffeine.…”

“…These effects are mimicked by antagonists of adenosine A 2A receptors, which are the main molecular targets of chronic caffeine consumption (Fredholm et al 1999). Adenosine receptors can control neuronal metabolism (Hammer et al 2001) and osmolarity perturbations in the brain (Hada et al 1998;Wurm et al 2008), which may occur upon chronic hyperglycemia (see above). Furthermore, the observation that the density of A 2A receptors is increased in the hippocampus of STZ-induced diabetic rats (Duarte et al 2006) bolters the interest of exploring the potential of chronic caffeine consumption to mitigate central diabetic encephalopathy.…”

“…Adenosine receptors can control neuronal metabolism (Hammer et al . 2001) and osmolarity perturbations in the brain (Hada et al . 1998; Wurm et al .…”

In vivo effects of adenosine A2 receptor agonist and antagonist on neuronal and astrocytic intermediary metabolism studied with ex vivo13C MR spectroscopy

“…It was shown that adenosine inhibited the pre‐synaptic release of excitatory neurotransmitters such as acetylcholine and glutamate via A 1 receptors (Fastbom and Fredholm 1985; Kurokawa et al . 1996) and enhanced the release of K + ‐evoked taurine release from rat hippocampus via activation of A 2a receptors (Hada et al . 1998).…”