Effects of raised extracellular potassium on the excitability of, and hormone release from, the isolated rat neurohypophysis.

Abstract

1. Single neurohypophyses from male rats were maintained in an in vitro perifusion chamber. Ion-sensitive microelectrodes were introduced into the tissue to measure changes in [K+]o and [Ca2+]o during electrical stimulation. 2. Electrical stimulation at 6 Hz for 1 min and 30 Hz for 12 s raised [K+]o by 5.4 +/- 0.4 and 13.5 +/- 0.5 mM (mean +/- S.E.M., n = 8) respectively. To investigate the effects of raised [K+]o on the excitability of the neurosecretory terminals, stimulations were repeated in media of altered K+ concentration. The increase in [K+]o evoked by 6 Hz stimulation was elevated in 10 mM-K+ medium (133% of that in 5 mM-K+ medium) and reduced in 0 mM-K+ medium and in 25 mM-K+ medium. Thus it appeared that stimulus-induced changes in [K+]o might enhance the excitability of the tissue during electrical activation. 3. To test this hypothesis, we measured the field potential responses evoked by 0.5 Hz stimulation in media of different K+ concentrations. The size of the field potential was enhanced in 10 mM-K+ medium and depressed in 0 mM-K+ medium and in 25 mM-K+ medium. 4. Electrical stimulation (6 Hz, 1 min) decreased [Ca2+]o by 10.9 +/- 1.8% (n = 6). This decrease was absent in the presence of 1 microM-tetrodotoxin or 1 mM-cadmium. Again, the [Ca2+] response to stimulation was enhanced in 10 mM-K+ medium and depressed in 0 mM-K+ medium or 25 mM-K+ medium. 5. The release of vasopressin and oxytocin evoked by stimulation at 6 or 30 Hz from isolated neurohypophyses was measured by radioimmunoassay in a separate series of experiments. Stimulation at 30 Hz for 1 min released 5- to 6-fold more hormone than stimulation at 6 Hz for 5 min. Release evoked by 6 Hz stimulation was enhanced in 15 mM-K+ medium and depressed in 25 mM-K+ medium. 6. We conclude that the rise in [K+]o that accompanies high-frequency activation of axons and terminals in the neurohypophysis contributes to the facilitation of hormone release with increasing frequencies of stimulation, and in particular to the efficiency of the milk-ejection burst discharge of oxytocin neurones for evoking oxytocin release.

Model Roles of the Hypothalamo-Neurohypophysial System in Neuroscience Study

“…Among them, burst firing activity of OXT neurons specifically depends on suckling stimulation [62], intranuclear release of OXT [63], and a neuromodulation of the "burst synchronization center" in the mammillary body complex [64]. Relative to the regulation [44] and AQP4-coupled inwardly rectifying K + channel 4.1 [39], as a result of burst-evoked increase in extracellular K + levels [45,46]. The activation of these ion transporters decreases extracellular K + levels and could also lead to the post-burst inhibition [47] in OXT neurons.…”

Type 1 ryanodine receptor knock-in mutation causing central core disease of skeletal muscle also displays a neuronal phenotype

“…The nerve terminals were stimulated either by a prolonged depolarization to mimic the depolarization caused by K + accumulation outside the nerve terminals ( Fig. 4A) (24) or a train of short depolarizations to mimic a burst of action potentials (NS80 in Fig. 4C) (24,25).…”

“…4A) (24) or a train of short depolarizations to mimic a burst of action potentials (NS80 in Fig. 4C) (24,25). Global Ca 2+ transients were measured with fluo-3, which is sufficiently rapid to give an indication of the rate of rise of the transients (26).…”

Extracellular K+ in the supraoptic nucleus of the rat during reflex bursting activity by oxytocin neurones.

“…to rise by up to about 5-3 mm and that such an increase facilitates oxytocin release (Leng, Shibuki & Way, 1988). We have now addressed the question of whether increases in [K+].…”