TY - JOUR T1 - Plasticity of Hypothalamic Dopamine Neurons during Lactation Results in Dissociation of Electrical Activity and Release JF - The Journal of Neuroscience JO - J. Neurosci. SP - 4424 LP - 4433 DO - 10.1523/JNEUROSCI.4415-12.2013 VL - 33 IS - 10 AU - Nicola Romanò AU - Siew H. Yip AU - David J. Hodson AU - Anne Guillou AU - Sébastien Parnaudeau AU - Siobhan Kirk AU - François Tronche AU - Xavier Bonnefont AU - Paul Le Tissier AU - Stephen J. Bunn AU - Dave R. Grattan AU - Patrice Mollard AU - Agnès O. Martin Y1 - 2013/03/06 UR - http://www.jneurosci.org/content/33/10/4424.abstract N2 - Tuberoinfundibular dopamine (TIDA) neurons are the central regulators of prolactin (PRL) secretion. Their extensive functional plasticity allows a change from low PRL secretion in the non-pregnant state to the condition of hyperprolactinemia that characterizes lactation. To allow this rise in PRL, TIDA neurons are thought to become unresponsive to PRL at lactation and functionally silenced. Here we show that, contrary to expectations, the electrical properties of the system were not modified during lactation and that the neurons remained electrically responsive to a PRL stimulus, with PRL inducing an acute increase in their firing rate during lactation that was identical to that seen in non-pregnant mice. Furthermore, we show a long-term organization of TIDA neuron electrical activity with an harmonization of their firing rates, which remains intact during lactation. However, PRL-induced secretion of dopamine (DA) at the median eminence was strongly blunted during lactation, at least in part attributable to lack of phosphorylation of tyrosine hydroxylase, the key enzyme involved in DA synthesis. We therefore conclude that lactation, rather than involving electrical silencing of TIDA neurons, represents a condition of decoupling between electrical activity at the cell body and DA secretion at the median eminence. ER -