17β‐Oestradiol modulates in vitro electrical properties and responses to kainate of oxytocin neurones in lactating rats

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Abstract
1 Intracellular current clamp recordings were performed from identified oxytocin (OT) neurones in acute hypothalamic slices taken from lactating Wistar rats at early (5th day: LD-5) and late (21st day: LD-21) lactation. 2 The basic electrophysiological properties of LD-21 OT neurones differed from those of LD-5 OT neurones: their resting membrane potential was more depolarised (-51·5 versus -54·9 mV); their action potential duration was longer (1·6 versus 1·2 ms); their hyperpolarising after-potential (HAP) following single spikes and after-hyperpolarisation (AHP) following a burst of action potentials had smaller amplitudes (-46 and -67 %, respectively); and they lacked spike frequency adaptation during a burst. 3 In LD-21 neurones bath application of 17β-oestradiol (10−7 M, 6–14 min) reversibly restored all these properties to values observed in LD-5 cells. This treatment had no effect on LD-5 neurones. 4 LD-21 neurones were less sensitive to kainate than LD-5 neurones. 17β-Oestradiol significantly potentiated the kainate-induced response in LD-21, but not in LD-5 neurones. 5 The effects of 17β-oestradiol were presumably mediated through a non-genomic mechanism since they occurred within a few minutes of administration, and disappeared within 30–40 min of washout. They were not inhibited by tamoxifen, an antagonist of the nuclear oestrogen receptor ER-α. Lastly, cholesterol, a non-active lipophilic molecule, had no effect. 6 Our observations demonstrate that, in the absence of 17β-oestradiol, the basic electrical properties and sensitivity to kainate of OT neurones become altered between early and late lactation. However, the rise in circulating levels of oestrogens during the late phase of lactation may contribute to maintain OT neurone reactivity as long as suckling continues.