ALTERED SENSORY BEHAVIORS IN MICE FOLLOWING MANIPULATION OF ENDOGENOUS SPINAL ADENOSINE NEUROTRANSMISSION

Adenosine or adenosine analogs injected intrathecally (i.t.) induce si gnificant antinociception. Recent studies support the existence of an endogenous spinal system that can modulate nociceptive input by releas ing adenosine. Inhibition of adenosine metabolism by administration of an adenosine kinase inhibitor, in the present study, decreased behavi or induced by putative pain neurotransmitters providing additional sup port for an endogenous purinergic system. Conversely, administration o f high doses of methylxanthines (i.t.), adenosine receptor antagonists , induced behavior similar to that induced by pain neurotransmitters. Methylxanthine (i.t.)-induced behavior was partially inhibited by anta gonists of receptors for pain neurotransmitters. These observations ar e consistent with the hypothesis that an endogenous purinergic system tonically modulates nociceptive input involving a variety of chemical mediators. Preliminary studies also revealed methylxanthine-induced al lodynia and suggested spinal purinergic systems may have a broader rol e in discriminating sensory input.