GABA-noradrenergic interaction: evidence for differential sites of action for GABA-A and GABA-B receptors.
Treatment of mice with DSP4 (a neurotoxin that abolishes the presynaptic noradrenergic neuron; Dooley et al., 1983) resulted in: (A) a decrease in the Bmax for the low affinity GABA-B receptor site in the cerebral cortex and hippocampus, whereas the Bmax for the high affinity GABA-B receptor site was unaffected; (B) a greater potentiation of norepinephrine stimulated adenylate cyclase by baclofen in cerebral cortex slices; and (C) a decrease in the Bmax for both the high and low affinity GABA-A receptor sites in the cerebral cortex and hippocampus. These data, coupled with previous work from our laboratory, suggest that the GABA-B receptor may be associated with both the noradrenergic nerve terminal and the post-synaptic neuron receiving noradrenergic input, whereas the GABA-A receptor may be associated with the noradrenergic nerve terminal. These data further suggest a functional coupling between the noradrenergic and GABA-ergic systems.
D000320:Adrenergic Fibers / Q000502:physiology; D000818:Animals; D001418:Baclofen / Q000494:pharmacology; D001596:Benzylamines / Q000494:pharmacology; D002540:Cerebral Cortex / Q000502:physiology*; D000242:Cyclic AMP / Q000378:metabolism; D006624:Hippocampus / Q000502:physiology*; D008297:Male; D051379:Mice; D009638:Norepinephrine / Q000502:physiology*; D011963:Receptors, GABA-A / Q000502:physiology*; D005680:gamma-Aminobutyric Acid / Q000502:physiology*
D001596:Benzylamines; D011963:Receptors, GABA-A; D005680:gamma-Aminobutyric Acid; D000242:Cyclic AMP; D001418:Baclofen; C012102:DSP 4; D009638:Norepinephrine