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PubMed1995

Changes in [3H]flunitrazepam binding in the brain of rats made tolerant to and dependent upon pentobarbital.

Changes in benzodiazepine binding sites labeled by [3H]flunitrazepan (FNZ) in twenty discrete brain regions of rats made tolerant to and dependent upon pentobarbital were examined. Animals were rendered tolerant by intracerebroventricular (i.c.v.) infusion with pentobarbital (300 micrograms/ 10 microliters/ hr for six days) through pre-implanted cannulae connected to osmotic mini-pumps. The pentobarbital dependence was assessed 24 hr after abrupt withdrawal from pentobarbital. In the tolerant rats, a significant increase in [3H]FNZ binding sites was found in layer IV of frontal cortex and the molecular layer of olfactory bulb. [3H]FNZ binding sites in the pentobarbital dependent rats were significantly increased in layers I-III and V-VI of frontal cortex, caudate-putamen, olfactory tubercle, globus pallidus and ventral pallidum, in addition to those observed in the tolerant group. There was, however, no significant difference in the hippocampus and several regions in the hindbrain in either pentobarbital-treated group. Taken together with characteristics of subtypes of benzodiazepine receptors and changes in GABA-benzodiazepine receptor complexes elucidated in our previous studies, these findings suggest that both types of benzodiazepine receptors are involved in the development of pentobarbital intoxication mediated by GABAA receptors.

Animals↗
PubMed1995

Interaction between [3H]flunitrazepam and [3H]GABA binding in the cerebellum of reeler mice.

It has been shown that in the cerebellum of reeler mutant mice GABA levels and GABA uptake increase while GABA binding decreases. This study shows that in the cerebellum of these mutants there is also an increase of benzodiazepine receptors. This increase is observed in cerebellar homogenates, in nuclei and in membranes. The increase in the density of central (i.e. clonazepam displacable) benzodiazepine receptors is primarily reflected in binding sites located in the GABA-receptor complex. In comparison to wild-type, GABA-modulin extracted from reeler cerebellum inhibits with a greater potency [3H]GABA binding. The increase in the central-type of benzodiazepine binding and its interaction with GABA binding, observed in cerebellar membranes, is interpreted as a functional response to the decrease in GABA binding and may reflect benzodiazepine receptor condensation and/or changes of subunit composition of the GABA/benzodiazepine receptor complex. The enhanced activity of reeler GABA-modulin reflects a functional response to the increased GABA levels in reeler cerebellum. The increase of the peripheral-type (i.e. PK 11195 displacable) of benzodiazepine receptors is probably due to metabolic changes that may accompany reeler cerebellar mutation. Differences in nuclear benzodiazepine binding between reeler and wild-type mice add a physiological importance to the nuclear binding of this drug.

Animals↗
PubMed1986

Comparative aspects of cerebellar [3H]flunitrazepam and [3H]GABA binding.

[3H]Flu and [3H]GABA binding has been studied in mice and Rabbit cerebellum (Ce). The Bmax of [3H]Flu binding in Ce membranes is similar in all mice strains examined and Rabbit. However, in Ce homogenate there are significant differences in both kd and Bmax. Subcellular distribution shows higher [3H]Flu binding in the nuclear than in the membranous fraction. However, the [3H]GABA binding is lower in the nuclear than the membranous fraction.

Animals↗
PubMed1983

Benzodiazepine receptors in fish brain: [3H]-flunitrazepam binding and modulatory effects of GABA in rainbow trout.

We have identified and partially characterised benzodiazepine binding sites in whole brain membranes of male rainbow trout. In terms of Bmax and KD values trout brain receptors are remarkably similar to those in rat and human brain. The Hill coefficient was 0.98, indicating a single binding site. GABA (10(-4) M) was able to significantly elevate binding of [3H]-FNZ through a change in KD rather than Bmax. This effect was prevented by the GABA receptor antagonist bicuculline methiodide.

Animals↗