PT  - JOURNAL ARTICLE
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
TI  - Plasticity of Hypothalamic Dopamine Neurons during Lactation Results in Dissociation of Electrical Activity and Release
AID  - 10.1523/JNEUROSCI.4415-12.2013
DP  - 2013 Mar 06
TA  - The Journal of Neuroscience
PG  - 4424--4433
VI  - 33
IP  - 10
4099  - http://www.jneurosci.org/content/33/10/4424.short
4100  - http://www.jneurosci.org/content/33/10/4424.full
SO  - J. Neurosci.2013 Mar 06; 33
AB  - 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.