Enhanced neurotransmitter release at glutamatergic synapses on oxytocin neurones during lactation in the rat

Javier E. Stern, Shaul Hestrin, William Armstrong

Research output: Contribution to journalArticle

51 Citations (Scopus)

Abstract

1. The increased release of oxytocin during lactation has been shown to be dependent upon glutamatergic transmission and is associated with an increased synaptic innervation of the supraoptic nucleus (SON). 2. To determine whether the glutamatergic synaptic properties of oxytocin neurones are changed during lactation, we recorded excitatory postsynaptic currents (EPSCs) from identified oxytocin neurones in the SON of slices taken from adult virgin and lactating rats. 3. The frequency of AMPA-mediated miniature EPSCs (mEPSCs) more than doubled during lactation. In addition, the decay time constant, but not the amplitude of the mEPSCs was significantly increased in both vasopressin and oxytocin neurones. 4. Paired-pulse facilitation (PPF) was significantly reduced in oxytocin neurones during lactation, whereas no change was observed in vasopressin neurones. Elevating Ca2+ reduced PPF in oxytocin neurones in virgin rats but did not alter PPF in oxytocin neurones from lactating rats. 5. Collectively, our results suggest that excitatory glutamatergic transmission is strengthened in oxytocin neurones during lactation, probably by a combination of an increased number of terminals, slower decay kinetics, and an increase in the probability of release.

Original languageEnglish (US)
Pages (from-to)109-114
Number of pages6
JournalJournal of Physiology
Volume526
Issue number1
DOIs
StatePublished - Jul 1 2000

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Oxytocin
Lactation
Synapses
Neurotransmitter Agents
Neurons
Supraoptic Nucleus
Excitatory Postsynaptic Potentials
Vasopressins
alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid

All Science Journal Classification (ASJC) codes

  • Physiology

Cite this

Enhanced neurotransmitter release at glutamatergic synapses on oxytocin neurones during lactation in the rat. / Stern, Javier E.; Hestrin, Shaul; Armstrong, William.

In: Journal of Physiology, Vol. 526, No. 1, 01.07.2000, p. 109-114.

Research output: Contribution to journalArticle

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