Health & Environmental Research Online (HERO)


Print Feedback Export to File
7615599 
Journal Article 
Plasticity of hypothalamic dopamine neurons during lactation results in dissociation of electrical activity and release 
Romanò, N; Yip, SH; Hodson, DJ; Guillou, A; Parnaudeau, S; Kirk, S; Tronche, F; Bonnefont, X; Le Tissier, P; Bunn, SJ; Grattan, DR; Mollard, P; Martin, AO; , 
2013 
Yes 
Journal of Neuroscience
ISSN: 0270-6474
EISSN: 1529-2401 
SOC NEUROSCIENCE 
WASHINGTON 
4424-4433 
English 
23467359 
WOS:000315926300021 
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.