Activation of neurosecretory cells by osmotic stimulation of anteroventral third ventricle

Honda, Kazumasa; Negoro, Hideo; Higuchi, Takashi; Tadokoro, Yoshikatsu

doi:10.1152/ajpregu.1987.252.6.r1039

Cited by 17 publications

(16 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Many studies have shown that ablation of the AV3V which includes the OVLT (one of the CVOs) results in the reduction or abolishment of osmoreception for vasopressin release or antidiuresis in dogs (THRASHER et a!., 1982) and in rats (JOHNSON et a!., 1978;SLADEK and JOHNSON, 1983;GRUBER et a!., 1986). Furthermore, we have observed that microinjection of hypertonic NaCI solution into the AV3V excited not only putative vasopressin neurones but also putative oxytocin neurones (HONDA et a!., 1987). We therefore attempted to determine the effect of the AV3V lesion on the plasma oxytocin concentration and found that the lesion abolished the response of oxytocin release to the osmotic stimuli.…”

Section: Discussionmentioning

confidence: 48%

“…And it is now widely accepted that there are cranial osmoreceptors for vasopressin release, which are excited when the receptor cells are dehydrated due to withdrawal of water from the cells by osmotic agents which hardly permeate the cell membrane, such as NaCI, sucrose and mannitol (SLADEK and KNIGGE, 1977;THRASHER et al, 1980a, b) although the precise location of the osmoreceptors is somewhat controversial (LENG et al, 1982;THRASHER et al, 1982;SLADEK and JOHNSON, 1983;HONDA et al, 1987). Recently it has been shown that oxytocin, the other neurohypophysial hormone, is also secreted in response to hypertonlc NaCI In rats (JONES and PICKERING,1969;BRIMBLE et al, 1978;BALMENT et al, 1980).…”

mentioning

confidence: 99%

See 1 more Smart Citation

Osmoreceptor mechanism for oxytocin release in the rat.

et al. 1988

View full text Add to dashboard Cite

In order to determine whether oxytocin release is controlled by an osmoreceptor mechanism identical with that for vasopressin release, the plasma oxytocin concentration and plasma osmolality were measured during intraatrial infusion and after intraventricular injection of various osmotic solutions in unanesthetized rats. Intraatrial infusion of 0.6 M NaCI Locke solution (LS.) or 1.2 M mannitol L.S. elevated plasma oxytocin significantly, while 1.2 M urea L.S. caused only a small increase and isotonic L.S. did not change in plasma oxytocin. All hypertonic solutions produced significant and similar increases in the plasma osmolality. Plasma oxytocin was positively correlated with plasma osmolality in the animals infused with hypertonic NaCI or mannitol but not in the animals infused with hypertonic urea. The injection of 2 tl of 0.6 M NaCI artificial cerebrospinal fluid (CSF) or 1.2 M mannitol CSF into the third ventricle caused a significant increase in plasma oxytocin immediately (5 min after injection) without changing plasma osmolality, while the intraventricular injection of 1.2 M urea CSF or isotonic CSF produced no significant change in plasma oxytocin. These results indicate that oxytocin release is controlled by osmoreceptors rather than Na receptors, that the adequate stimulus for the osmoreceptors is one which produces cellular dehydration and that the osmoreceptors are located in the brain region which is accessible to osmotic agents from both the outside and inside of the bloodbrain barrier. Since the organum vasculosum of the lamina terminalis (OVLT) lacks a blood-brain barrier and is known to be involved in osmotic control of vasopressin release, a lesion was made in the anteroventral region of the third ventricle which encompasses the OVLT and the effect of hypertonic NaCI infusion on oxytocin release was examined. No significant increase in plasma oxytocin was observed after intraatrial infusion of 0.6 M NaCI L.S. in the lesioned rats. All of these findings lead to the conclusion that oxytocin release is under the control of osomoreceptors identical to those for vasopressin release.

show abstract

Section: Discussionmentioning

confidence: 48%

mentioning

confidence: 99%

Osmoreceptor mechanism for oxytocin release in the rat.

et al. 1988

View full text Add to dashboard Cite

show abstract

“…Furthermore, intracellular recordings in hypothalamic explants have indicated that OVLT neurones projecting to the supraoptic nucleus can be excited by hypertonic stimuli (Nissen, Bourque & Renaud, 1993), suggesting that these cells may relay osmotic information to hypothalamic MNCs. In agreement with this hypothesis, local osmotic stimulation of the anteroventral region of the third ventricle has been shown to modulate the frequency of firing of hypothalamic MNCs in vivo (Honda, Negoro, Higuchi & Tadokoro, 1987) and in vitro (Richard & Bourque, 1992). In this study, we have examined the processes underlying the effects of local osmotic stimulation of the OVLT during intracellular recordings obtained from supraoptic nucleus MNCs in superfused explants of rat hypothalamus.…”

mentioning

confidence: 76%

Synaptic control of rat supraoptic neurones during osmotic stimulation of the organum vasculosum lamina terminalis in vitro.

Richard

Bourque

1995

The Journal of Physiology

153

145

View full text Add to dashboard Cite

1. The effects of osmotic or electrical stimulation of the organum vasculosum lamina terminalis (OVLT) were examined during intracellular recordings (32°C) obtained from ninety-five supraoptic nucleus magnocellular neurosecretory cells (MNCs) in superfused explants of rat hypothalamus. 2. Brief (10-20 s) applications of hypertonic and hypotonic solutions to the area of the OVLT caused prolonged (> 1 min) increases and decreases, respectively, in electrical activity in seventy of seventy-four trials performed on neurones with membrane potentials near spike threshold (~-55 mV). Changes in firing frequency were related to changes in external osmolality in a dose-dependent manner between 275 and 355 mosmol kg-'.3. When 30 s periods recorded immediately before, and 30 s following, the application of an osmotic stimulus were examined, the frequency of spontaneous EPSPs (sEPSPs) was related in a dose-dependent manner to the osmolality of the solution superfusing the OVLT region. The increased EPSP frequency was maintained and did not adapt if the osmolality of the medium was raised for periods of > 10 min. In contrast, the frequency of spontaneous IPSPs (sIPSPs) was virtually unaffected by changes in external osmotic pressure. 4. Osmotically evoked changes in MNC firing were strongly correlated with accompanying changes in the frequency of sEPSPs (slope, 0 9; correlation coefficient (r) = 0 7), but not sIPSPs (r = 0 2), suggesting that changes in firing rate following osmotic stimulation of the OVLT are selectively mediated by changes in synaptic excitation.5. In the presence of bicuculline (5-10 /M), electrical stimulation of the OVLT evoked fast EPSPs in forty-seven of forty-eight MNCs tested. These responses were reversibly reduced by application of 20-40 /M kynurenic acid (n = 3) or 20-40 uM 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX; n = 11). Similarly, bath application of CNQX (n = 3) or kynurenic acid (n = 4) reversibly abolished the excitatory response of supraoptic neurones following hypertonic stimulation of the OVLT. 6. Brief (10-15 s) applications of y-aminobutyric acid (GABA) over the OVLT reversibly abolished increases in sEPSP frequency and action potential firing rate evoked by hyperosmotic stimulation of the OVLT. In the presence of GABA, the rates of sEPSP and sIPSP frequency were reduced to 37 + 10 and 44 + 13% (means + S.E.M.), respectively, of those observed under isotonic conditions (295 mosmol kg-1). 7. These results suggest that inhibitory and excitatory pathways originating from neurones located within the OVLT are tonically active under resting osmotic conditions in rat hypothalamic explants. Osmotically evoked changes in MNC firing, however, are selectively mediated through increases or decreases in the intensity of the excitatory component of OVLT-derived inputs.

show abstract

“…Only a small number of these cells were tested for osmosensitivity but two of the four OD + cells were excited by the osmotic stimulus and two of the three OD-cells were inhibited. (Thrasher, Keil & Ramsay, 1982), cells in the region are osmosensitive (Sayer et al 1984) magnocellular neurosecretory cells (Honda et al 1987), it is reasonable to suggest that osmosensitive elements in the AV3V region provide osmotic drive to the supraoptic nucleus. The present investigation was undertaken to provide electrophysiological evidence for such a direct connection between the two regions.…”

Section: Recordings From Cells In the A V3v Regionmentioning

confidence: 99%

The role of interconnection between supraoptic nucleus and anterior third ventricular region in osmoregulation in the rat.

Chaudhry¹,

Dyball²,

Honda³

et al. 1989

The Journal of Physiology

View full text Add to dashboard Cite

SUMMARY1. To determine the importance of the region of the hypothalamus anterior and ventral to the third ventricle (AV3V) in the osmotic regulation of neurohypophysial hormone release, extracellular recordings were made in the urethane-anaesthetized rat from neurones in the supraoptic nucleus (SON) and in the AV3V using a ventral surgical approach.2. In the first series of experiments, recordings were made from SON cells (n = 41) which could be antidromically activated from the neural stalk in control rats and rats 2 weeks after electrolytic destruction of the AV3V (n = 74). Destruction of AV3V significantly (P < 0-01) reduced the responsiveness of SON cells to an osmotic challenge (1 ml of 1-5 M-NaCl i.P.).3. In the second series of experiments recordings were made in the AV3V region while stimulus pulses were applied to the region of the SON. The cells recorded could be divided into five groups; those which were inhibited (presumably synaptically; OD -; n = 97), those which were excited (also presumably synaptically; OD +; n = 73), those which could be antidromically activated (AD; n = 50), those which showed a complex cycle of excitation and inhibition after the stimulus (n = 40) and those which did not respond to the stimulus (n = 47).4. The characteristic response of OD -cells to an osmotic challenge was inhibition (six out of ten cells) and that of OD + cells was excitation (thirteen out of seventeen cells). No AD cells showed excitation following i.P. NaCl injection (nine out of nine).5. Our experiments provide clear evidence that the AV3V region is important for the normal responsiveness of the cells of the SON to raised plasma osmolality and for an interaction between the SON and the AV3V region.6. Our results also suggest, contrary to our expectation, that the SON exerts both excitatory and inhibitory influences on the AV3V. Since the cells which project from the AV3V to the SON region are not osmoresponsive, the importance of the direct projection from the AV3V to SON may be to maintain the responsiveness of SON neurones rather than to provide osmotic drive.

show abstract

Activation of neurosecretory cells by osmotic stimulation of anteroventral third ventricle

Cited by 17 publications

References 0 publications

Osmoreceptor mechanism for oxytocin release in the rat.

Osmoreceptor mechanism for oxytocin release in the rat.

Synaptic control of rat supraoptic neurones during osmotic stimulation of the organum vasculosum lamina terminalis in vitro.

The role of interconnection between supraoptic nucleus and anterior third ventricular region in osmoregulation in the rat.

Contact Info

Product

Resources

About