GABA-noradrenergic interaction: Evidence for differential sites of action for GABA-A and GABA-B receptors

Abstract

Treatment of mice with DSP₄ (a neurotoxin that abolishes the presynaptic noradrenergic neuron;Dooley et al., 1983) resulted in: (A) a decrease in the B_max for the low affinity GABA-B receptor site in the cerebral cortex and hippocampus, whereas the B_max 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 B_max 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.