Effects of an NO synthase inhibitor on aggressive and sexual behavior in male crickets

Abstract

The mechanisms of the effects of some types of behavior on others have received little study. The present investigation addresses the phenomenon present in male crickets of the species Gryllus bimaculatus, consisting of the powerful activation by transient flight (3 min) of aggression to another male and of the female courtship program. We found that flight did not evoke these behavioral changes in males injected with the NO synthase inhibitor LNNA. The intensity and duration of fights with another male, the frequency of ritual singing by the victor, and the intensity with which the victor pursued the vanquished only increased significantly after flight in control male crickets injected with Ringer's solution, but not in experimental crickets. Similarly, flown males injected with LNNA were no different from unflown males in terms of the intensity of female courtship (the latent period and relative duration of courtship singing); in controls, the latent period was significantly shorter and the duration of singing was significantly greater in flown crickets. LNNA had no effect on aggressive or sexual behavior in unflown males. These results demonstrate that flight may increase NO synthesis, making a significant contribution to the formation of the flight-evoked behavioral state.

The Decision to Fight or Flee – Insights into Underlying Mechanism in Crickets

“…Dyakonova and Krushinskii (2006) report that treatment with an NO-synthesis inhibitor prohibits the aggression promoting effects of flying in crickets, indicating that NO enhances aggressiveness. Iwasaki et al (2007) in contrast, report that inhibiting NO-synthesis relieves the loser effect, but has no effect on socially naive crickets.…”

Adding up the odds—Nitric oxide signaling underlies the decision to flee and post-conflict depression of aggression

“…Although NO acts to suppress aggression in mammals and is implicated in inappropriate aggression in human mental disorders ( 4 , 13 , 14 ), its specific behavioral function in normal aggressive behavior is unknown ( 13 ). The insect NO/cGMP signaling pathway is similar to that in mammals ( 15 ), but it is unclear whether this promotes ( 16 ) or suppresses aggression ( 17 ). Our study reveals that the sensory impact of aversive experiences during fighting activates the NO signaling pathway, which promotes the decision to flee and leads to post-conflict depression of aggression that is characteristic for social defeat in many animal species ( 18 ).…”

Cupiennin 1a, an antimicrobial peptide from the venom of the neotropical wandering spider Cupiennius salei, also inhibits the formation of nitric oxide by neuronal nitric oxide synthase

“…The isoforms of NOS are homodimers with subunits of 130–160 kDa, differing in amino acid sequence identity, but sharing an overall three‐component construction, namely: (a) an N‐terminal catalytic oxygenase domain that binds heme, tetrahydrobiopterin and l ‐arginine; (b) a C‐terminal reductase domain that binds FMN, FAD and NADPH; and (c) an intervening CaM‐binding region that regulates electronic communication between the oxygenase and reductase domains [16,17]. NOS enzymes are found in most life‐forms [16,17], including bacteria [18–21] and insects [22–24].…”