We have previously found that quail selectively bred to exhibit long (LTI) or short (STI) tonic immobility responses to manual restraint differed with respect to the affinity of binding at the diazepam-sensitive benzodiazepine binding site. In the current study, binding at other components of the GABAA-benzodiazepine receptor complex was investigated. Whereas the lines did not differ in either number or affinity of GABAA receptors, we found that GABA caused significantly greater enhancement of [3H]flunitrazepam binding in the forebrains of LTI than in STI birds. There was also significantly higher binding to the diazepam-insensitive component (alcohol binding site) of the GABAA-benzodiazepine complex in the forebrain of the LTI line. It is not known, however, whether this difference in the lines is due to differences in number or affinity of these sites. It is discussed whether these manifold differences between the lines in binding at the forebrain sites of the GABAA-benzodiazepine complex could be founded on subunit differences, and whether differences in benzodiazepine binding could underlie the genetically determined behavioural differences in tonic immobility.