Lesions of Hypothalamic Mammillary Body Desynchronise Milk‐Ejection Bursts of Rat Bilateral Supraoptic Oxytocin Neurones

Abstract

Successful milk ejection depends on a bolus release of oxytocin, which results from the synchronised burst firing of magnocellular oxytocin neurones in several hypothalamic nuclei. Despite extensive studies of the mechanism underlying the burst synchrony of oxytocin neurones in the same nucleus, brain regions controlling burst synchronisation among different nuclei remain elusive. We hypothesised that some structures in the ventroposterior hypothalamus may function as the major component of neural circuits controlling burst synchronisation of bilateral oxytocin neurones. To test this hypothesis, we recorded burst firing of bilateral oxytocin neurones in the two supraoptic nuclei after microsurgical disconnection of different hypothalamic regions in anaesthetised lactating rats. The results obtained showed that the interhemispheric section of the caudal part of the hypothalamus but not the rostral hypothalamus resulted in burst desynchronisation. The difference in burst onset time between paired bursts of bilateral oxytocin neurones was 129.2 ± 34.7 s, which is significantly (P < 0.01) longer than that of sham-lesioned controls (0.24 ± 0.02 s). Hypothalamic lesions leading to the desynchronisation involved the mammillary body, supramammillary nucleus and tuberomammillary nucleus in the ventroposterior hypothalamus. Consistently, electrolytic lesion of the median part of this mammillary body region also desynchronised the burst of bilateral oxytocin neurones and disrupted milk ejections. These results indicate that the mammillary body region is critically involved in the burst synchronisation of bilateral oxytocin neurones during suckling and possibly functions as the major component of a putative synchronisation centre.