ROLE OF THE GABA CHLORIDE-ION CHANNEL COMPONENT ON AGGRESSIVE-BEHAVIOR IN THE MALE CRAB

Picrotoxin blocking effects on GABA-induced inhibition of lateral merus display in the male crab Carcinus mediterraneus suggest that the chloride ion channel component of the GABA molecule is involved in the control of this defensive behavior. The low GABA doses (3 and 5-mu/g body weight) inhibited lateral merus display as early as 10 min after drug treatment while the administration of higher GABA concentrations (> 5-mu-g/g) prolonged the duration of the behavioral effects. The administration of 1-mu-g/g picrotoxin to the animals treated with the effective GABA doses (5, 10 and 20-mu-g/g) restored lateral merus display. The antagonizing activity of picrotoxin on the inhibitory GABA effects, in a temporal manner, demonstrates that GABAergic sites other than peripheral ones are probably participating with the regulation of this agonistic posture. Quantitative autoradiography results revealed interesting receptor levels changes of the specific chloride ion channel antagonist [S-35] t-butylbicyclophosphorothionate in the different brain areas of the male crab displaying lateral merus with respect to normal nonreactive animals. Elevated receptor binding levels were encountered in the middle and posterior brain area whereas low levels were obtained at the anterior level. Both the behavioral and autoradiographic results suggest that the defensive type of aggression behavior in crustacean may not only be mediated by a peripherally controlled GABA-gated chloride ion flux but also by a central GABAergic mechanism.