Differences in benzodiazepine binding in quail selectively bred for differences in tonic immobility

• Published in: Pharmacology, biochemistry and behavior biochemistry and behavior, 1996-05, Vol.54 (1), p.117-121
• Main Authors: Hogg, Sandy, Mills, Andrew D., File, Sandra E.
• Format: Article
• Language: English
• Subjects: Alcohol binding site; Animals; Anti-Anxiety Agents - pharmacokinetics; Anti-Anxiety Agents - pharmacology; Azides - pharmacology; Behavioral psychophysiology; Benzodiazepines - pharmacology; Biological and medical sciences; Brain - drug effects; Brain - metabolism; Chloride uptake; Chlorine - metabolism; Computer Science; Coturnix - metabolism; Diazepam - pharmacology; Ethanol - metabolism; Fear; Flunitrazepam - pharmacokinetics; Fundamental and applied biological sciences. Psychology; GABA A receptor; gamma-Aminobutyric Acid - pharmacology; Japanese quail; Kinetics; Life Sciences; Motor Activity - genetics; Neurotransmission and behavior; Psychology. Psychoanalysis. Psychiatry; Psychology. Psychophysiology; Radioisotopes; Receptors, GABA-A - drug effects; Receptors, GABA-A - genetics; Receptors, GABA-A - metabolism
• ISSN: 0091-3057; 1873-5177
• DOI: 10.1016/0091-3057(95)02113-2

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 GABA A-benzodiazepine receptor complex was investigated. Whereas the lines did not differ in either number or affinity of GABA A 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 GABA A-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 GABA A-benzodiazepine complex could be founded on subunit differences, and whether differences in benzodiazepine binding could underlie the genetically determined behavioural differences in tonic immobility.