Abstract
Adenosine is a neurotransmitter to modulate synaptic transmission in the CNS. Currently, four adenosine receptors, A1, A2A, A2B and A3 receptor, have been cloned and characterized. Several lines of evidence have indicated that adenosine improves neurological deficits in spinal cord injury through activation of A1 receptor. Nonetheless, much less is known about the functional role of other adenosine receptors in the spinal cord. In the present study, we examined whether activation of A2A receptors affects synaptic transmission in spinal motoneurons by using the whole-cell patch-clamp technique. Bath application of an A2A receptor agonist, CGS21680 (1 μM), increased sEPSC frequency in about a half of neurons recorded at a holding potential of -70 mV. In the presence of bicuculline (20 μM), strychnine (2 μM), CNQX (10 μM) and APV (50 μM), no synaptic activity could be observed at a holding potential of -50 mV in all neurons examined. Under this condition, superfusion of CGS21680 (1 μM) induced an inward current in about 70% of neurons examined. These results indicate that the activation of presynaptic A2A receptors enhances glutamate release onto spinal motoneurons, and the activation of postsynaptic A2A receptors directly depolarizes the majority of spinal motoneurons. Thus, the activation of A2A receptors in spinal motoneurons may aggravate neural damages in spinal cord injury, in contrast to adenosine A1 receptors. [J Physiol Sci. 2007;57 Suppl:S145]
