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Exposure of the preoptic-tuberoinfundibular system to iron ions causes ovulation in the pro-oestrous rat. This electrochemical treatment has been used frequently to study the way that the hypothalamus triggers secretion of gonadotrophic hormone and most investigators have assumed that the effect is mediated by the direct excitation of those neurones exposed to the cation. The present paper reports experiments designed to confirm that iron directly excites hypothalamic neurones to the firing frequencies essential for ovulation.

Because of the difficulty of measuring input–output relationships in the diffuse preoptic-tuberoinfundibular system the experiments were performed on the anatomically distinct oxytocinergic neurones of the paraventricular-hypophysial tract in lactating rats. These neurones were stimulated electrically (from 10 to 50 Hz for between 1 and 300 s) and subjected to the electrochemical treatment by depositing iron ions from the tip of the stimulating electrode (up to 250 μA anodal current for between 60 and 180 s). Changes in intramammary pressure were used to indicate oxytocin release and mammary glands were calibrated for sensitivity by intravenous injection of oxytocin.

Electrical stimulation in excess of about 15 Hz invariably caused release of sufficient oxytocin to cause a rise in intramammary pressure. In contrast, no changes in pressure were observed during or after the electrochemical deposition of iron. The results suggest that the response of hypothalamic neurones to electrochemical treatment is not the same as their response to electrical stimulation.

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R. G. Dyer

Every physiology student is taught that oxytocin is released from the neurohypophysis and acts on the myoepithelial cells to effect milk ejection and on the myometrium to elicit uterine contractions. Milk ejection requires the bolus release of oxytocin, by the (approximately) synchronous discharge of the magnocellular oxytocin containing neurones in the hypothalamus, and this is initiated reflexly by the suckling stimulus applied to the nipple. During parturition also, oxytocin can be released as part of a neuroendocrine reflex when the fetus stimulates sensory nerve endings during its passage through the cervix. The reflex release of oxytocin at this time greatly aids the rapid completion of the delivery process.

All of the foregoing has been known for years and some of it for decades. During this time little progress was made in identifying any clearly defined physiological role for oxytocin during the earlier stages of parturition. Indeed maturational processes in the

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R. G. Dyer and S. Mansfield


Blood samples were collected from oestrogen-primed gonadectomized adult rats before and after electrical stimulation of the preoptic part of the hypothalamus. Six groups of rats were used for the experiments. These were (a) males castrated on the first day of life, (b) males castrated after puberty, (c) females ovariectomized after puberty and (d), (e) and (f) females given testosterone propionate at birth (1·25, 0·125 and 0·0125 mg/rat respectively). Neonatal exposure of the female rats to testosterone caused a dose-dependent increase in the amounts of prolactin released to levels significantly (P<0·01) higher than those observed in male animals and in untreated females. The results indicate that although neonatal testosterone inhibits oestrogen-stimulated prolactin secretion in adult rats, the neuroendocrine apparatus controlling secretion of the hormone is capable of being activated to greater effect after exposure to androgens at the time of birth.

J. Endocr. (1986) 109, 57–60

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R. G. Dyer and S. Mansfield


Two experiments were undertaken to assess further the action of the steroid anaesthetic alphaxalone upon LH secretion in chronically ovariectomized female rats.

For the first experiment, 31 rats were given two injections of oestradiol benzoate (20 μg/100 g body weight), each 72 h apart, to stimulate an LH surge 6 h after the second injection. However, one group of seven rats was anaesthetized with alphaxalone throughout the 6-h period and a second group of eight was similarly anaesthetized only for the last 2 h of the 6-h period. The steroid-stimulated LH surge was blocked in both groups of rats anaesthetized with alphaxalone.

The second experiment involved a comparison of pulsatile LH secretion in animals which were either unanaesthetized (n = 8) or anaesthetized with alphaxalone (n = 9). In six out of nine rats the anaesthetic did not affect the maximum or minimum plasma LH concentrations but significantly slowed the frequency at which LH pulses were measured. In the remaining three anaesthetized rats the drug blocked pulsatile LH secretion.

The experiments confirm that some secretion of LH continues during alphaxalone anaesthesia but indicate also that the drug has a more deleterious action upon the oestrogen-stimulated LH surge than believed hitherto.

J. Endocr. (1984) 102, 27-31

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Ferrous ions (Fe2+) were applied by microiontophoresis to 29 neurones recorded from the forebrain of ten pro-oestrous rats. The spontaneous activity of 24 cells was reduced by Fe2+ and five units did not respond. No excitations were observed. Reproducible responses could not be obtained with ferric ions (Fe3+).

Microinjection of 1 μl 200 mm-Fe2+ into the preoptic area of eight pro-oestrous rats produced a sharp increase in plasma LH levels. Similar treatment with saline was without effect. Rats anaesthetized with sodium pentobarbitone during the early afternoon of pro-oestrus ovulated overnight when injected with both Fe2+ and Fe3+.

The experiments do not confirm the widely held belief that raised plasma LH levels following deposition of iron in the rostral hypothalamus result from increased firing of nerve cells.

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R. G. Dyer and J. E. Robinson

The importance of pulsatility in Endocrinology requires no emphasis; it is an ubiquitous mode of secretion reflecting fundamental principles about the organization of hormone release mechanisms. Pulsatility is clearly exhibited in the output of hormone from the anterior pituitary gland (for recent review see Robinson & Dyer, 1988) and this is particularly striking in the case of luteinizing hormone (LH). Today, two decades after the discovery of the pulsatile nature of LH secretion, an enormous literature details variations in the characteristics of gonadotrophin release with change in physiological state in many different species. For example, we know that dramatic changes in both the frequency and amplitude of LH episodes occur at puberty, during female sexual cycles, in seasonal breeders and in a range of pathological states. Despite this we are still surprisingly ignorant of the mechanisms which cause LH to be released as a discrete bolus.

Recently, scientific weight has

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B. A. CROSS and R. G. DYER

There is now good evidence that hormones can affect the activity or responsiveness of hypothalamic neurones in the intact brain (Cross & Silver, 1966; Beyer & Sawyer, 1969) and in diencephalic islands (Cross & Dyer, 1970). The latter authors used the technique of Cross & Kitay (1967), which ensures complete neural isolation and constant anatomical contents of the islands. This paper reports the effect of removal of endogenous pituitary hormones on spontaneous activity of hypothalamic neurones in such islands.

Forty Wistar rats weighing 200–240 g and showing regular 4-day oestrous cycles were used. Thirty rats were anaesthetized with ether and placed in a Hoffman—Reiter Hypophysectomy Instrument (Model H-200, H. Neumann and Co., Illinois). Twenty of the animals had their pituitaries removed by suction via a needle inserted through the hollow ear-bar into the sellae turcicae. The remaining ten rats served as sham-operated controls and in these the needle was

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Action potentials were recorded from 174 neurones in the mediobasal hypothalamus of ovariectomized adult female rats exposed neonatally to monosodium glutamate (MSG) and from 145 neurones in control rats. All of the animals, which were anaesthetized with urethane, had been ovariectomized for at least 3 weeks and received two injections of oestradiol benzoate (20 μg/100 g body weight, i.m.) 72 h and immediately before the recording experiments. The response of each neurone to electrical stimulation of the median eminence and rostral hypothalamus (preoptic and anterior hypothalamic areas; PO/AH) was analysed. The most striking feature of the results obtained was the significant (P < 0·001) loss of inhibitory responses in those neurones remaining in the adult rats after neonatal treatment with MSG. The loss of inhibitory responses applied to both stimulation sites.

In each rat the response of one neurone, which was antidromically identified as projecting to the median eminence, was recorded before and during stimulation of the PO/AH at 50 Hz for 30 s in every min for 15 min. Before and after this stimulation blood was collected from a jugular vein for estimation by radioimmunoassay of concentrations of prolactin and TSH. In the MSG-treated rats significantly (P < 0·05) fewer neurones were inhibited by the 50 Hz stimulation than in control rats. In control rats the plasma concentrations of prolactin nearly quadrupled as an immediate consequence of this treatment, whereas in MSG-treated rats plasma concentrations barely doubled. However, in the MSG-treated rats plasma concentrations of prolactin continued to rise after stimulation ceased, possibly as a consequence of enhanced secretion of thyrotrophin releasing hormone.

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Extracellular activity was recorded from tuberoinfundibular neurones in 28 urethane-anaesthetized pro-oestrous rats. In each rat the electrical activity of one antidromically identified neurone was analysed before and during electrical stimulation in the preoptic/anterior hypothalamic areas (PO/AH). This stimulation (50 Hz, 30 s on and 30 s off for 15 min) resulted in significant increases in plasma concentrations of prolactin (from 46±11 (s.e.m.) ng/ml before stimulation to 86 ±17 ng/ml 20 min later; P<0·02) and LH (27 ± 6 to 48±11 ng/ml; P<0·01). A substantial proportion (11 out of 28) of the tuberoinfundibular neurones was inhibited by PO/AH stimulation. If such cells are directly involved with the secretion of anterior pituitary hormones it is probable that they synthesize and secrete inhibitory factors. We have suggested that cells inhibited by stimulation of the PO/AH are possibly the neurones which secrete prolactin inhibitory factor. The excited cells (eight out of 28) gave complex and variable responses to hypothalamic stimulation and were unable to follow applied stimuli at a ratio of more than one extra action potential for every ten stimulus pulses. We propose that this may explain why it is necessary to stimulate the PO/AH at ten times the frequency required for ovulation to occur following stimulation in the median eminence in anaesthetized pro-oestrous rats.

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We have studied the possible effects of monosodium glutamate (MSG) on LH secretion in ovariectomized rats.

In experiment 1 MSG-treated and control rats were given oestradiol benzoate at noon and 72 h later half the rats in each group were given a second injection of oestradiol benzoate or progesterone. Blood samples were taken immediately before and 6 h after these i.m. injections. At 78 h there were no significant differences in plasma LH concentration measured in the two groups of rats given progesterone or in the two groups given a second injection of oestradiol benzoate although for both MSG-treated and control rats progesterone produced a significantly (P < 0·01) greater LH surge than did oestradiol benzoate.

In experiment 2 100 μl blood samples were collected at 5-min intervals for up to 3 h from MSG-treated and control rats. For rats showing more than one pulsatile discharge of LH, peak and trough values for plasma LH concentrations were not significantly influenced by MSG treatment. However the mean pulse height was significantly (P < 0·001) greater in the MSG-treated group than in control rats. Pulsatile release stopped more quickly in the MSG-treated rats and their mean plasma LH concentration after 120 min of blood sampling was significantly (P < 0·05) lower than that obtained in the control animals.

Thus, although some aspects of LH secretion seem to be significantly different in MSG-treated rats, these effects may result from the greater sensitivity of the MSG-treated animals to experimental manipulation.