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F Ellendorff

Publications and source records attributed to F Ellendorff.

At least 55 records · Page 3Linked to original sources

A means to assess nursing efficiency in the pig: the study of the milk ejection reflex.

We have recently devised a method for recording the intramammary pressure in conscious lactating sows. This technique allows for unambiguous detection of milk ejection, and permits correlation with hormone release and the behaviour of the sows and their piglets. Each milk ejection is characterized by an abrupt rise in intramammary pressure lasting 8-40 sec only. This is preceded 15-30 before by a rise in plasma concentrations of the hormone oxytocin. Milk ejections only occurred when the sow was nursing her litter, lying on her side and making her teats available. She usually grunted in a rhythmic manner, with a sharp increase in the frequency of grunts about 23 sec before milk ejection. Grunting ceased within 1 min thereafter. The whole litter had to be suckling to obtain a milk ejection, which occurred about 2-4 min after the onset of the initial phase of massage of the udders, and was coincident with a brief period of quiet suckling. Milk ejections occurred about every 45 min, i.e. only once per suckling period, eventhough the period could last over 15 min. They never occurred if the mother was not nursing, or if the piglets attempted to suckle too soon after a milk ejection. Out of 144 periods of suckling, over 20% of failures to eject milk were observed, in which case there was no oxytocin release in blood. Some "incomplete" sucklings happened with no apparent reasons, but their incidence was very high when the sow appeared to be disturbed.

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Electrical properties of paraventricular neurosecretory neurons with and without recurrent inhibition.

Twelve out of 32 neurosecretory neurons in the paraventricular nucleus of rats showed a silent phase following subthreshold stimulation to the posterior pituitary gland. After suprathreshold stimulation, the duration of the silent phase was significantly longer than that of the remaining 20 neurons, which did not show the silent phase at subthreshold stimulation. The latency and threshold in the former neurons were significantly longer and higher than those of the latter neurons. These data indicate a relationship between the recurrent inhibitory system and other electrical properties in the paraventricular neurons.

Animals↗

Catecholestrogens in the brain: neuroendocrine integration.

In a series of experiments it has been shown that 4-hydroxyestradiol (4-OHE2) as well as 2-hydroxyestradiol (2-OHE2) are involved in regulatory mechanisms of LH secretion in the miniature pig. Two-hydroxyestrone (2-OHE1) and 1-hydroxyestradiol-benzoate (1-OHE2B), however, have no significant effects on LH secretion. Moreover the studies indicate a regional specificity in the action of 4-OHE2, 2-OHE2 and estradiol (E2). 4-OHE2 and 2-OHE2 decrease plasma LH when given into the ventromedial nucleus of the hypothalamus and increase plasma LH levels when microinjected into the dorsomedial nucleus of the hypothalamus. Whereas E2 affects LH secretion when it is given into the area dorsalis of the hypothalamus and fornix. In addition the experiments performed on female and male rats to measure the effects of 2-OHE2 and 2-OHE1 on turnover rates of dopamine, norepinephrine and epinephrine in the anterior mediobasal hypothalamus and medial preoptic area show that the effects of catecholestrogens may partly be mediated by catecholamines.

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An electrophysiological study of the accessory olfactory bulb in the rabbit--II. Input-output relations as assessed from analysis of intra- and extracellular unit recordings.

The input-output relations of the rabbit accessory olfactory bulb were studied by intra- and extracellular single unit recordings following electrical stimulation of the vomeronasal nerves, the lateral olfactory tract and the corticomedial amygdala. Cellular activity of accessory bulb mitral cells evoked by stimulation of the vomeronasal nerves consisted of a brief excitation with a latency of 16 ms. This initial response was followed by a period of reduced firing probability which was due to an inhibitory postsynaptic potential. In many cases this secondary response was followed by a second excitatory postsynaptic potential on which action potentials were generated at higher stimulus intensities. Deeper cells in the granule cell layer responded with a long latency, long duration, excitation, often consisting of bursts of 2-3 spikes. The majority of mitral cells were antidromically invaded by amygdala stimulation. The latencies of the antidromic spikes showed a wide range of variation (12-80 ms). Due to this great variation in antidromic latency the inhibitory postsynaptic potential following the antidromic action potential was rather modest but prolonged in duration. In many cases the onset of the inhibitory postsynaptic potential preceded the antidromic response. The majority of cells did not respond to lateral olfactory tract stimulation. Only 10% of the tested cells were invaded antidromically by stimulation at this site. These neurons were also driven antidromically by amygdala stimulation. We conclude that, although the physiological characteristics of mitral cells of the main and accessory olfactory bulb are very similar, there are important differences. The efferent fibres of the accessory bulb conduct at very slow and variable rates and project directly to the corticomedial amygdala.

Amygdala↗

The appearance and characteristics of early pregnancy factor in the pig.

The occurrence of early pregnancy factor in the pig has been established by the rosette inhibition test and by the criteria that gel filtration of serum resulted in a number of peaks of activity similar to those observed in other species. In the pig EPF is present virtually to the end of pregnancy, with a biphasic production in which the titres of EPF decline markedly in mid-pregnancy. Free EPF-A appears concurrently with EPF in the first 3 weeks of pregnancy in some but not all pigs. The presence of excess EPF-A has an inhibitory effect in the rosette inhibition test and modifications, including an initial serum dialysis step, have been introduced into the test to take account of this inhibitory effect.

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Prostaglandin E (Sulproston) is neither luteolytic nor luteotrophic during the estrous cycle in the pig.

Prostaglandin E2 (Sulproston, S) can induce parturition and luteolysis during late pregnancy in the pig. We now tested whether Sulproston is able to interfere with the duration of the pig's estrous cycle. Sulproston was given i.m. in two injections (0.008 mg/kg each) at 12-hour-intervals to ten gilts day 10, to five gilts day 14 and to five gilts day 16 of the estrous cycle. Blood was collected shortly before and up to 48 hrs after the onset of treatment; further daily blood samples were taken from day 0 (1st day of standing heat) to the end of the cycle. Sulproston-administration did not shorten or lengthen the duration of the estrous cycle, nor were plasma-progesterone levels altered when compared to controls. In a second study five gilts received the tenfold amount of S on day 10 of the cycle. A significant decrease in plasma-progesterone (8.52 +/- 2.8 SEM ng, treatment vs. 32.95 +/- 1.86 SEM ng/ml, control) occurred on day 11, which had returned by day 16 to the level of controls (19.22 +/- 6.28 ng/ml vs. 26.75 +/- 2.10 SEM ng/ml, respectively). No alteration in cycle length occurred. Therefore the PGE2-analogue Sulproston - though luteolytic in late pregnancy - is neither luteolytic nor luteotrophic during the estrous cycle of the pig.

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The milk ejection reflex in the pig.

1. The milk ejection reflex in response to suckling was studied in conscious sows by continuous recording of intramammary pressure, radioimmunoassay of plasma concentrations of neurohypophysial hormones, and observation of the behaviour of the sows and piglets.2. A regular pattern of nursing, suckling and milk ejection was observed. The mean duration of the suckling period was 6.3 min. Over 144 suckling periods, 113 milk ejections were recorded. Each milk ejection was characterized by a sudden rise in intramammary pressure reaching 20-49 mmHg, and lasting 8-41 sec. Milk ejections occurred only once per suckling period, at a mean interval of 44.3 min.3. Each milk ejection occurred with a mean latency of 2.4 min from the onset of a period of initial massage of the udders by the piglets, and was coincident with a period of quiet suckling when the piglets were consuming milk. The onset of nursing was signalled by the sows grunting in a rhythmic manner. In most cases, the frequency of grunts, at first low, increased suddenly 23 sec before milk ejection.4. During eighteen suckling periods leading to milk ejection, neurohypophysial hormone assays performed on serial blood samples showed an increase in plasma concentration of oxytocin up to 30 sec before milk ejection. The concentration of lysine-vasopressin did not rise above basal levels.5. In 21.4% of the suckling periods, no rise in intramammary pressure was observed. In these ;incomplete sucklings', the sow usually failed to grunt rapidly, and the piglets obtained no milk. For three of these periods, hormone assay showed no increase in oxytocin or vasopressin concentrations in blood.6. Oxytocin given intravenously produced variations in intramammary pressure which depended on the dose and the rate of injection. Rapid injections of 25-50 m-u. oxytocin, caused milk ejections similar to those induced by suckling. When oxytocin was administered at different rates, the faster the injection, the shorter the latency and the higher the amplitude of the response. Plasma concentrations of oxytocin after injection of 25 m-u. were similar to those observed during reflex milk ejection.7. Trains of electrical pulses were applied to the posterior pituitary of four anaesthetized sows. At frequencies of stimulation above 10 Hz, a rise in intramammary pressure and an increase in plasma oxytocin and vasopressin concentrations were observed. At frequencies of stimulation of 30-50 Hz, the response of the mammary gland and the time course of the variations in oxytocin plasma concentrations were similar to those observed during natural reflex milk ejection.8. It is concluded that reflex milk ejections during suckling in the pig are caused by the intermittent and spurt-like release of about 25 m-u. oxytocin, without concomitant vasopressin release. It is postulated that the release of oxytocin is probably precipitated by a brief and massive activation of oxytocin-secreting neurones in the hypothalamus. Central mechanisms controlling the intermittent release of oxytocin are discussed.

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Further evidence on dual effects of norepinephrine on LH secretion.

To investigate the effects of norepinephrine (NE) on LH secretion, when given into different hypothalamic and extrahypothalamic brain regions, we microinjected 1 microliter of NE in dosages of 10(-4) M concentrations, 10(-6), 10(-8) and 10(-10) M into nine different brain areas in ovariectomized miniature pigs. Microinjections into the dorsal hypothalamus (ADH) and dorsomedial nucleus (DM) had dose-dependent effects. The higher dose of NE (10(-6) M) inhibited and the lower dose of NE (10(-10) M) stimulated LH secretion, when NE was microinjected into the ADH (n = 4 - number of animals). Microinjections into the DM (n = 6) had the opposite effect. Here the lower dose had inhibitory and the higher dose stimulatory effects on plasma LH levels. Microinjections into the ventromedial nucleus of the hypothalamus (n = 4) had no significant effect. Microinjections into the stria terminalis (n = 3) and zona incerta (n = 4) were also ineffective. The effect of NE microinjections into the subthalamic nucleus (n = 4) resembled responses to microinjections into the ADH. NE effects in the amygdala were not dose dependent. Microinjections into the basolateral amygdala (n = 5) decreased and microinjections into the corticomedial part of the amygdala (n = 5) increased plasma LH levels in all four doses of NE. The effects of NE microinjected into the hippocampus (n = 3) were not clear cut. These results indicate a dualism of NE on LH secretion. Thus, the predominant notion that NE is largely or even exclusively stimulatory to LH release should be revised. According to the previous findings and the results of the present study it has been concluded that the effects of NE on LH secretion are not only dependent on the hormonal status of the animal, but also to the dose and site of action of NE.

Animals↗

Prolactin in the circulation of chronically catheterised piglet foetuses and pregnant sows, and the effect of thyrotrophin-releasing hormone.

We chronically catheterised 12 piglet foetuses and 11 sows to determine the changes in circulating concentrations of prolactin during the last 2 weeks of gestation. Prolactin levels were measured by homologous radioimmunoassay and were found to average 2.12 +/- 0.23 ng . ml-1 in the foetuses and 4.19 +/- 0.84 ng . ml-1 in the sows. Foetal concentrations of prolactin increased significantly during the time period of the study. There was no change in maternal concentrations over the corresponding time. Injection of 5 micrograms TRH into 7 foetuses increased the plasma concentrations of prolactin in 6 animals, produced no apparent change in the seventh foetus and did not affect maternal concentrations of prolactin. The magnitude of the maximum response of TRH of the younger foetuses (less than 107 days delta = 0.7, 1.3, 4.2 ng . ml-1) was substantially less than that of the foetuses prior to term (greater than 107 days delta = 6.4, 21.7, 27.5 ng . ml-1). Injection of saline and the haemorrhage of blood sampling produced no significant change in the initial concentration of prolactin. We conclude that prolactin is present in the circulation of the pig foetus, that it is produced endogenously in lower concentrations than in the pregnant sow and that the foetal responsiveness to TRH stimulation increases towards the end of gestation.

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Electrophysiology of olfacto-limbic-hypothalamic connections in the pig.

To analyse fibre connections between the olfactory bulb (OB) and limbic-hypothalamic structures, the lateral olfactory tract (LOT) was stimulated electrically and extracellular action potentials were recorded from single units in the OB, the cortico-medial portion of the amygdala (AMY) and the mediobasal hypothalamus (MBH). More than 29% of the antidromically identified mitral cells in the OB showed a spontaneous episodic firing pattern consisting of alternating periods of activity and inactivity. Nearly 14% of the orthodromically excited non-mitral cells showed the same phasic firing pattern. 2.9% of AMY neurons were antidromically activated by LOT stimulation, whereas more than 52% showed orthodromic responses. In contrast to the AMY no neuron in the MBH could be antidromically invaded by electrical stimulation. The incidence of orthodromic responses was much less in the MBH when compared to the AMY (13.5%). It is concluded that the firing pattern of OB cells in the pig is complex, often phasic and unrelated to respiration or sniffing. The main OB is more closely related to the AMY than to the MBH. It is suggested that olfactory information is probably transmitted to the MBH via the AMY. The AMY may play a role in the regulation of OB activity.

Amygdala↗

Sleep is not a prerequisite for the milk ejection reflex in the pig.

Electroencephalographic and electromyographic activities were recorded together with variations in intramammary pressure in unanaesthetized lactating sows during suckling. During each suckling period, milk ejection resulted in a sudden and brief rise in intramammary pressure. From the onset of suckling to the beginning of milk ejection, polygraphic recordings as well as observations of behaviour revealed that the sow was invariably in a state of arousal. This suggests that, unlike what has been proposed for the rat, sleep is not a necessary component of the milk ejection reflex in the pig.

Animals↗

beta-Endorphin alters luteinizing hormone secretion via the amygdala but not the hypothalamus.

Morphine and enkephalins are able to alter pituitary hormone secretion. It has been postulated that they do not act directly at the pituitary, but rather that the hypothalamus is the site at which inhibition or stimulation of pituitary hormone secretion is initiated. On the other hand, endogenous opiates have been located in distinctly different neuronal regions, including areas outside the hypothalamus. The effects of beta-endorphin on plasma luteinizing hormone (LH) levels have not been explored, and the present experiments attempt to elucidate the contribution and the possible site of action of beta-endorphin in the control of LH secretion. The results show that beta-endorphin inhibits pituitary LH secretion if applied into the amygdala but not when given into the hypothalamus.

Amygdala↗

Gonadal steroids in the amygdala--differential effects on LH.

The direct participation of sexual steroids in the amygdala (AMY)-dependent modulation of LH secretion was investigated by means of a combination of microinjectons into the AMY and electrical stimulation of the AMY. Adult castrated male miniature pigs provided with bilateral 'electro-tubes' into the AMY were used. Electrical stimulation of the AMY without any prior steroid microinjection or with solvent microinjection decreased plasma LH levels. In contrast, electrical stimulation, 3.5 h after microinjection of 60 ng testosterone, resulted in an increase in LH levels. However, prior microinjection of estradiol-17 beta (6 ng) or 5 alpha-dihydrotestosterone (60 ng) abolished the effects of electrical stimulation. Four out of 7 of the animals responded to microinjection of 2-hydroxyestradiol-17 beta (60 ng) with a fall in plasma LH levels. Electrical stimulation increased the LH levels up to those before microinjection in these animals. In the other half of the animals, with no response to catecholestradiol microinjection, the response to electrical stimulation was depression. The results suggest a direct and differentiated effect of steroids on the AMY; the action of testosterone is independent of its aromatization or reduction and steroids could act on the AMY to inhibit or stimulate the inhibitory role of the amygdala in the control of pituitary LH secretion.

Amygdala↗