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gamma-Aminobutyric acid (GABA) autoreceptors in rat cerebral cortex and spinal cord represent pharmacologically distinct subtypes of the GABAB receptor.

gamma-Aminobutyric acid (GABA) autoreceptors regulating release of [3H]GABA have been characterized pharmacologically by using rat cerebral cortex and spinal cord synaptosomes exposed in superfusion to mild depolarization (9 mM KCl). In both regions GABA inhibited the K(+)-evoked overflow of [3H]GABA. The EC50 values amounted to 1.23 microM (cortex) and to 1.01 microM (spinal cord). Also the GABAB receptor agonist 3-aminopropylphosphonous acid (3-APPA) decreased the [3H]GABA overflow: EC50 values = 0.095 microM (cortex) and 0.078 microM (spinal cord). The classical GABAB receptor agonist (-)-baclofen was equipotent to GABA at the cortical autoreceptor (EC50 = 1.37 microM), whereas it was almost ineffective in the spinal cord (EC50 = 425 microM). (+)-Baclofen was extremely weak in both brain areas. Two GABAB receptor antagonists, phaclofen and (CGP 35348) [3-aminopropyl(diethoxymethyl)phosphinic acid] provided opposite results at the two autoreceptors examined. The IC50 values for phaclofen amounted to 47.9 microM (cortex) and to > 1000 microM (spinal cord), respectively. In contrast, CGP 35348 was almost ineffective at the cortex autoreceptors (IC50 > 300 microM), but was rather potent in the spinal cord (IC50 = 1.07 microM). To conclude, GABA autoreceptors in the cerebral cortex are classically sensitive to (-)-baclofen and to 3-APPA; they are also sensitive to phaclofen, but resistant to CGP 35348. Surprisingly, GABA autoreceptors in the spinal cord are poorly sensitive to (-)-baclofen, although they are as sensitive as the cortical autoreceptors to 3-APPA; moreover they are resistant to phaclofen, but highly sensitive to CGP 35348. The data show that pharmacologically distinct release-regulating GABAB autoreceptors exist in the central nervous system of a same animal species.