Plasticity in the electrophysiological properties of oxytocin neurons

In mammals, the neurohypophysial hormone oxytocin (OT) is released into the bloodstream during labor and lactation to promote uterine contraction and milk ejection, respectively. Electrophysiological studies have established that OT neurons fire in brief, synchronized bursts during this release. During pregnancy and lactation, the intrinsic membrane and synaptic properties of OT, and to a lesser extent vasopressin (VP) neurons, are altered as a part of the adaptation to these specialized states. During lactation OT neurons specifically exhibit an enhanced rebound depolarization which could assist in instigating bursts and an increased gating of firing frequency which is correlated with an enhanced Ca²⁺-dependent after hyperpolarization. Spike broadening occurs in both VP and OT neurons, but in OT neurons this and other changes are present during late pregnancy, suggesting involvement of steroidal hormones in programming neuronal adaptations. Excitatory and inhibitory synaptic activity also are altered by reproductive state. There is a doubling of glutamatergic activity specific to OT neurons which is consistent with an increase in terminal numbers, but this is accompanied by an increase in paired-pulse facilitation, 1 suggesting an increase in the probability of glutamate release during lactation as well. Together with profound changes in both pre- and postsynaptic GABAergic synaptic activity, these data suggest that neurosecretory, and particularly OT neuronal, properties are state-dependent. These modifications may adjust the responsiveness of these neurons to afferent stimulation during periods of increased hormone demand and thereby enhance stimulus-secretion coupling.