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Regulation of prolactin secretion during suckling: involvement of the hypothalamo-pituitary GABAergic system

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Abstract

Previous results demonstrated that GABA exerts a dual control on PRL secretion, one excitatory mediated in part by the impairment of the tubero-infundibular dopaminergic (TIDA) system function, the other inhibitory occurring at the level of the anterior pituitary (AP), where 3H-GABA and 3H-Muscimol (3H-M) recognition sites have been described. This report provides evidence for a physiological role of the tubero-infundibular GABAergic system (TI-GABA) on PRL secretion in the rat. In lactating rats separated for 4 h from their pups reinstitution of suckling for different periods resulted in an increase either in glutamic acid decarboxylase (GAD) activity in the mediobasal hypothalamus (MBH) or in AP-GABA content. Dynamic changes of the GABAergic function in the MBH-AP system seemed to have a certain degree of specificity because suckling did not affect GAD activity in the caudate nucleus. In lactating rats 2, 4, 8 and 24 h after removal of the offsprings AP-GABA concentrations and plasma PRL titers significantly decreased with respect to values present in rats never separated from their pups. Since it has been demonstrated that the PRL lowering effect of GABA is a receptor-mediated event, we have investigated the plasticity of AP-GABA receptors during suckling. The inhibitory action of GABA seems to be mediated mainly by the activation of the high affinity binding sites. This proposition is supported by the fact that in lactating rats, where only the high affinity receptor population is present, M was still able to decrease significantly plasma PRL concentrations. These results indicate that the MBH-AP GABAergic system could play a role on PRL secretion, being involved in mechanisms which dampens PRL output during continuous suckling stimulation.

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Racagni, G., Apud, J.A., Cocchi, D. et al. Regulation of prolactin secretion during suckling: involvement of the hypothalamo-pituitary GABAergic system. J Endocrinol Invest 7, 481–487 (1984). https://doi.org/10.1007/BF03348454

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