RESUMO
Nitric oxide (NO) is a molecule involved in plasticity across levels and systems. The role of NOergic pathways in stress-induced sensitization (SIS) of behavioral responses, in which a particular stressor triggers a state of hyper-responsiveness to other stressors after an incubation period, was assessed in adult zebrafish. In this model, adult zebrafish acutely exposed to a fear-inducing conspecific alarm substance (CAS) and left undisturbed for an incubation period show increased anxiety-like behavior 24â¯h after exposure. CAS increased forebrain glutamate immediately after stress and 30â¯min after stress, an effect that was accompanied by increased nitrite levels immediately after stress, 30â¯min after stress, 90â¯min after stress, and 24â¯h after stress. CAS also increased nitrite levels in the head kidney, where cortisol is produced in zebrafish. CAS-elicited nitrite responses in the forebrain 90â¯min (but not 30â¯min) after stress were prevented by a NOS-2 blocker. Blocking NOS-1 30â¯min after stress prevents SIS; blocking NOS-2 90â¯min after stress also prevents stress-induced sensitization, as does blocking calcium-activated potassium channels in this latter time window. Stress-induced sensitization is also prevented by blocking guanylate cyclase activation in both time windows, and cGMP-dependent channel activation in the second time window. These results suggest that different NO-related pathways converge at different time windows of the incubation period to induce stress-induced sensitization.