[Correlations of psychological, physical and endocrine factors in the menstrual cycle].
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Adaptation, Psychological↗
Biomedical subjects
W Wuttke
Publications and source records attributed to W Wuttke.
Endocrinological changes following etomidate, midazolam, or methohexital for minor surgery.
Etomidate is known to inhibit adrenocorticosteroid synthesis. The extent and duration of the effects of etomidate (63 +/- 6.4 mg) on spontaneous and stimulated corticosteroid levels, as well as on plasma concentrations of ACTH, beta-endorphin, and catecholamines were examined and compared to those following administration of the new benzodiazepine, midazolam, or of methohexital. Twenty-nine healthy, young, male orthopedic patients were randomized into three groups receiving either etomidate/fentanyl (n = 12), midazolam/fentanyl (n = 8), or methohexital/fentanyl (n = 9). Etomidate caused cortisol levels to decrease from 12.5 +/- 1.2 micrograms/dl preoperatively to 5.9 +/- 0.8 micrograms/dl after operation (P less than 0.001), compared to an increase from 12.0 +/- 1.9 micrograms/dl to 18.5 +/- 2.9 micrograms/dl in the group receiving methohexital. At 6 and 20 h postoperatively, all cortisol levels were normal. The cortisol decrease from 12.5 +/- 1.7 to 7.6 +/- 1.5 caused by midazolam was similar to that following etomidate, but the response to exogenous ACTH was significantly impaired in patients receiving etomidate as compared to those receiving midazolam. ACTH and beta-endorphin levels increased in patients receiving etomidate, presumably as a result of the interruption of negative feedback due to cortisol synthesis inhibition. Midazolam on the other hand prevented the increase of ACTH and beta-endorphin levels. Etomidate completely suppressed spontaneous aldosterone levels (from 33 +/- 6.7 to 7 +/- 2.1 pg/ml), as well as the response to stimulation with exogenous ACTH without affecting serum electrolytes. Etomidate had no influence on plasma catecholamines, but midazolam attenuated the stress-related epinephrine increase.
Adrenocorticotropic Hormone↗
Stress-induced changes in cholecystokinin and substance P concentrations in discrete regions of the rat hypothalamus.
The effects of acute stress exposure upon cholecystokinin (CCK) and substance P (SP) concentrations in discrete hypothalamic regions of the adult male rat brain were studied. Animals were exposed to foot shock stress for periods of 2, 4, 10, 30 or 60 min duration; immediately afterwards they were decapitated; brains were frozen and subsequently microdissected. CCK and SP concentrations were assayed by a specific RIA, as were serum levels of ACTH, corticosterone, PRL, GH, LH and testosterone. Stress had no effect upon SP concentrations in the anterior or posterior parts of the arcuate nucleus (ARC), but led to elevated CCK levels in the posterior ARC following 60 min of exposure. In both the ventromedial and dorsomedial hypothalamic areas, stress induced depletions of both neuropeptides. In the anterior (but not the posterior) portions of the lateral hypothalamic area, CCK and SP concentrations were reduced by stress exposure. These studies demonstrate that discrete hypothalamic CCK and SP neuronal systems are responsive to stress. This suggests that endogenous hypothalamic CCK and SP participate, along with other neurotransmitters/neuromodulators, in the integrated hypothalamic stress response, and mediate stress-neuroendocrine interactions.
Animals↗
Effects of systemic and local administration of etomidate on adrenocortical steroidogenesis in male rats.
A method for focal dialysis of the adrenal cortex is introduced allowing determination of adrenal steroid local release rates in conscious, freely moving rats. Etomidate, an anaesthetic drug known to interfere with adrenal steroid synthesis, blocks not only corticosterone but also aldosterone and, to a lesser degree, progesterone release. Intra-adrenal application of the drug via the dialysis system for a defined time resulted in low release rates of corticosterone without inducing sedation of the animals or even anaesthesia. Remaining low steroid concentrations during the next 5 h after cessation of the dialysis with drug-containing medium indicate that the inhibition of steroid synthesis lasted for several hours. It is concluded that the inhibitory effect of etomidate on steroid biosynthesis can be explained on the basis of an interaction of the drug with adrenocortical enzymes without the involvement of hypothalamic or hypophyseal mechanisms.
Adrenal Cortex↗
Demonstration of mRNAs for oxytocin and prolactin in porcine granulosa and luteal cells. Effects of these hormones on progesterone secretion in vitro.
The relative levels of mRNAs for relaxin, prolactin, inhibin and oxytocin have been measured in porcine granulosa as well as luteal cells by hybridisation to single-stranded synthetic DNA. The likelihood of a paracrine function of oxytocin and prolactin in the porcine ovary was inferred from the in vitro effects of both hormones on progesterone secretion of ovarian cells. Both hormones were found to inhibit progesterone secretion of luteal cells. In contrast, only prolactin but not oxytocin stimulated progesterone secretion in granulosa cells.
Animals↗
Release rates of catecholamines, GABA and beta-endorphin in the preoptic area and the mediobasal hypothalamus of the rhesus monkey in push-pull perfusates: correlation with blood hormone levels.
Push-pull cannulae were implanted into the preoptic area and into the mediobasal hypothalamic median eminence complex of ovariectomized rhesus monkeys. After recovery, perfusion of the implanted areas was performed over a period of 56 h before and following estradiol benzoate treatment. This treatment results in a drop of LH levels followed by an increase. Catecholamine (norepinephrine, epinephrine and dopamine) concentrations in perfusates collected at 15 min intervals fluctuated tremendously prior to treatment with the estrogen. These fluctuations were largely reduced in perfusates of both structures following the estrogen treatment. They reoccurred at the time of increasing LH levels. beta-endorphin and GABA concentrations were also measured in the perfusates of both structures. Occasional secretory bursts were observed without any obvious relation to the estrogen treatment. It is concluded that catecholamine release in the preoptic area and in the mediobasal hypothalamic median eminence complex is of a pulsatile nature in ovariectomized rhesus monkeys. This pulsatility is largely reduced or abolished following estrogen treatment. The reduced pulsatility may bear a signal character for the release of LH.
Animals↗
Postnatal development of transmitter systems: sexual differentiation of the GABAergic system and effects of muscimol.
The development and sex differences of the central nervous GABAergic system were examined by measuring GABA (gamma-aminobutyric acid) in discrete brain nuclei of the hypothalamus, as well as the nigrostriatal and the limbic systems of male and female rats on the day of birth and on days 5, 10, and 15. The highest concentrations were found in the hypothalamic and nigrostriatal nuclei; the lowest in the limbic system. Sex differences were observed only on day 10 in the medial preoptic area, with GABA being higher in males than in females; and also in the substantia nigra, where female GABA levels were higher than male. These results suggested an involvement of GABA in the sexual differentiation of the brain. As a control, concentrations of the GABA precursor glutamate were determined. No sex differences in glutamate concentrations were found in any brain region during the first 15 days postnatally. Since a GABA mimetic substance applied during the critical period of brain differentiation could disturb the development of the GABAergic system, the consequences of a perinatal treatment with the GABA agonist muscimol were investigated. Significant reduction of GABA concentrations by muscimol were observed in the hypothalamic and nigrostriatal systems at specific times postnatally. On day 5, GABA concentrations were diminished only in the medial preoptic area, then on day 10, in the anterior hypothalamus and the substantia nigra, and still later, on day 15, in the caudato putamen. In contrast, the effects of muscimol on glutamate concentrations could be observed over a longer postnatal period. Glutamate was already diminished on day 5 in 7 areas of the hypothalamic, nigrostriatal, and limbic systems.
Aging↗
Intraovarian secretion of catecholamines, oxytocin, beta-endorphin, and gamma-amino-butyric-acid in freely moving rats: development of a push-pull tubing method.
We have developed and validated a push-pull technique that allows focal perfusion of the ovary in unanesthetized freely moving rats. We have used this method to investigate the intraovarian secretion of catecholamines (dopamine, norepinephrine, epinephrine), oxytocin, beta-endorphin and gamma-amino-butyric acid (GABA) during the estrous cycle. Cycling animals were implanted with ovarian push-pull catheters and jugular vein catheters under ether anaesthesia on proestrus, estrus and diestrous Day 2. This procedure did not disrupt normal preovulatory release of prolactin and luteinizing hormone (LH). Thus, perfusion of the ovary and simultaneous monitoring of hormone levels in systemic blood in freely moving rats allow correlation of the temporal relationship of ovarian events with cyclic gonadotropin secretion. The results clearly indicate that a rise in ovarian norepinephrine occurs concomitant with the preovulatory surge in prolactin and LH. Ovarian beta-endorphin concentrations exhibit cyclic changes, whereas GABA release rates remain stable throughout the cycle. Oxytocin is secreted by ovarian tissue, and the secretion rate appears to be inversely related to prolactin. In view of the proposed involvement of ovarian nerves and particularly catecholamines in the process of follicular maturation and ovulation, our findings suggest a preovulatory activation of ovarian noradrenergic sympathetic neurons.
Animals↗
Estrous cycle variations in cholecystokinin and substance P concentrations in discrete areas of the rat brain.
Cholecystokinin (CCK) and substance P (SP) were measured in discrete areas of the rat brain at different stages of the estrous cycle. Significantly higher levels of CCK were found in the lateral septum during diestrus as compared to proestrus. In the parietal cortex, CCK concentrations were significantly higher in diestrus than in proestrus. In the amygdala, estrous levels of CCK were significantly higher than proestrous levels. SP concentrations were significantly higher in diestrus than in proestrus in the medial and lateral septum, and the medial and lateral preoptic area. In the amygdala and ventral tegmental area, SP concentrations were significantly higher in estrus than in proestrus. These data suggest that certain CCK and SP neuronal systems may play a role in regulating the hypothalamo-pituitary-gonadal axis and/or be involved in steroid-dependent behavior.
Amygdala↗
Evidence for estrogen-receptive GABAergic neurons in the preoptic/anterior hypothalamic area of the rat brain.
Estrogen target neurons are numerous in the medial preoptic/anterior hypothalamic area (MPO/AH) of the female rat brain, and they are thought to play a crucial role in reproductive functions. This brain region is also known to contain high concentrations of the inhibitory transmitter gamma-aminobutyric acid (GABA) and of its synthesizing enzyme glutamate decarboxylase (GAD). Since it is known that GABA is involved in the regulation of gonadotropin release from the pituitary gland it has been proposed that estrogen feedback may be mediated by this transmitter. Here we show, by a combined method of estrogen autoradiography and GAD immunocytochemistry, that estrogen-receptive neurons of GABAergic nature exist in the MPO/AH.
Animals↗
Rates of release of GABA and catecholamines in the mediobasal hypothalamus of ovariectomized and ovariectomized estrogen-treated rats: correlation with blood prolactin levels.
Push-pull cannulae were implanted into the mediobasal hypothalamus of ovariectomized (ovx) rats. After recovery animals were treated with estradiolbenzoate (E2B) or oil and they were perfused 3 days later. Only the E2B-treated animals which exhibited prolactin surges in the afternoon without concomitant LH surges were used in this study. In ovx animals hypothalamic GABA release, measured in 5-min intervals, was pulsatile, with pulses occurring every 37 min. This pattern was profoundly affected by E2B treatment: the pulse frequency was significantly reduced to 1 pulse every 117 min in steroid-treated rats. No differences in overall mean GABA release rates and pulse amplitudes were observed in ovx vs. E2B-treated rats. Our earlier demonstration of the existence of a large number of estrogen-receptive, GABAergic neurons in the MBH of rats is suggestive that these neurons change their secretory pattern in response to estrogen treatment. Estrogen-induced prolactin surges were accompanied by increased hypothalamic NE release. Concomitant changes in DA or E release rates were not demonstrable since catecholamine concentrations were too low to be reliable. However, the daily overall release rates of these two catecholamines were lower in E2B-treated rats compared to ovx animals. It is concluded that the positive feedback action of estradiol on prolactin release involves a stimulatory noradrenergic mechanism and may also involve estrogen-receptive, GABAergic neurons.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
Cholecystokinin and substance P concentrations in discrete areas of the rat brain: sex differences.
Cholecystokinin (CCK) and substance P (SP) concentrations were measured in discrete brain areas of adult male and diestrous female rats. Significant sex differences in CCK concentration were found in the ventromedial hypothalamic area, medial and lateral preoptic area, nucleus of the diagonal band of Broca, ventral tegmental area, entorhinal and in several cortical areas. No sex differences in SP concentrations were observed in any of these areas. However, significant sex differences in SP concentration were found in the amygdala. These data indicate that the CCK and to some extent the SP systems are sexually differentiated in certain brain areas.
Animals↗
Adrenal release of catecholamines and Met-enkephalin before and after stress as measured by a novel in vivo dialysis method in the rat.
A dialysis tubing was implanted in the adrenal gland of rats. Adrenomedullary secretion products were dialysed into Ringer solution in the awake animal. Catecholamines (CAs) and methionine-enkephalin (Met-Enk) were measurable under resting conditions. Epinephrine, norepinephrine and Met-Enk-like immunoreactive material increased following application of an immobilization stress for 5 min. The results demonstrate that adrenomedullary CAs and peptides are coreleased. They also demonstrate that Met-Enk-like immunoreactive material is released under stress.
Adrenal Medulla↗
Preoptic catecholamine, GABA, and glutamate release in ovariectomized and ovariectomized estrogen-primed rats utilizing a push-pull cannula technique.
The push-pull cannula technique was used to evaluate the role of the medial preoptic/anterior hypothalamic area (MPO) in regulating pituitary luteinizing hormone (LH) and prolactin release. The concentrations of the three catecholamines--dopamine, norepinephrine (NE), epinephrine (E)--and gamma-aminobutyric acid (GABA) and glutamate could be measured in 15-min fractions at which interval blood samples for LH and prolactin determination were also collected. Comparison of neurotransmitter release rates into the MPO were made between ovariectomized and ovariectomized estradiol benzoate treated rats. Release of the neurotransmitters occurred in a pulsatile manner, the release episodes for each transmitter appeared to be independent of the others. No direct correlation between neurotransmitter release episodes and blood LH or prolactin levels could be established. The release of GABA was significantly lower and that of NE and E higher in ovariectomized animals in comparison to estrogen-primed ovariectomized animals under negative feedback conditions. In the afternoon, however, when the estrogen stimulated LH and prolactin release, preoptic GABA release was low, whereas preoptic NE and particularly E release rates were high. Conspicuously high dopamine and NE release episodes were observed in estrogen-primed animals at noon, i.e., prior to the expression of the positive feedback signal. This may reflect a biochemical correlate to the so-called critical period. No consistent differences between ovariectomized and ovariectomized estradiol-17 beta benzoate treated animals were observed for preoptic glutamate release rates. The data show that preoptic GABA release rates show generally an inverse pattern to NE and E release and therefore also to blood LH and prolactin levels. No direct mathematical correlation between any of the neurotransmitter release rates and blood hormone levels could be established.
Animals↗
Sex differences in gamma-aminobutyric acid and glutamate concentrations in discrete rat brain nuclei.
gamma-Aminobutyric acid (GABA) and glutamate concentrations were measured in discrete brain nuclei in adult male and female rats. Significant sex differences in GABA and glutamate concentrations were found in the medical preoptic area (MPA) and ventromedial hypothalamic area (VMH) as well as the lateral hypothalamus, habenula and diagonal band for glutamate. Significant differences in GABA and glutamate concentrations were also observed throughout the estrous cycle in several brain areas. These results suggest that these neuronal systems are sexually differentiated as well as involved in the expression of gonadal steroid feedback.
Animals↗
Astrocytes in primary cultures: membrane potential characteristics reveal exclusive potassium conductance and potassium accumulator properties.
Mouse astrocytes in homogenous primary cultures were used to study the membrane potential response, measured with intracellular microelectrodes, to alterations of external ion composition and to certain drugs, and the observations were correlated with radiotracer measurements of equilibrated K+ content. The membrane potential was--92 mV at 3 mM K+, and reduction of external Na+ and Cl-concentration, as well as addition of furosemide, which acts on Cl- and Na+ fluxes, had no effect, showing that there is no other ion than K+ which significantly contributes to membrane conductance. Addition of ouabain showed that there is no electrogenic component of the membrane potential at either 'resting' conditions or during stimulation. Nevertheless, the behavior of the membrane potential was found to deviate from a Nernst potential for K+ when extracellular K+ was changed (the slope was linear from 1.5 to 100 mM K+ with 51 mV/10-fold change compared with 61 mV for a Nernstian behavior at 37 degrees C). The radioisotope measurements at different external K+ showed that this was due to accumulation of intracellular K+. We conclude that these astrocytes have spatial buffer and active accumulator properties towards the K+ ion.
Animals↗
In vivo release of neurotransmitters in the medial basal hypothalamus of the monkey.
In vivo release rates of norepinephrine (NE), epinephrine (E), dopamine (DA), gamma-aminobutyric acid (GABA), glutamate (GLU) and beta-endorphin (beta E) in the medial basal hypothalamus (MBH) of unanaesthetized female macaca fascicularis monkey, and the effects thereon of estrogen (E2) treatment, have been estimated using push-pull perfusion methodology. DA, NE, E, GABA, GLU and beta E were all detectable in 30 min perfusate fractions. No direct correlation between their release rates and those of LH and PRL could be observed. E2 induced an initial decrease, then an increase, in LH and PRL secretion, and concomitant changes in the release patterns of DA, NE, E. GABA and GLU were apparent. This study demonstrates that in vivo push-pull perfusion methodology may be applied to the unanaesthetized monkey, and when combined with venous catheterization for serial blood sampling may prove to be a powerful tool in the investigation of the central molecular events governing neuroendocrine functions.
Animals↗
Involvement of catecholamines and glutamate in GABAergic mechanism regulatory to luteinizing hormone and prolactin secretion.
There is some evidence that a population of estrogen-receptive neurons exists in the preoptic/anterior hypothalamic area which uses gamma-aminobutyric acid (GABA) as neurotransmitter and which is involved in mediating the negative feedback of estrogens on pituitary luteinizing hormone (LH) secretion. These neurons are proposed to be presynaptic inhibitors to norepinephrine (NE) release thereby inhibiting the stimulatory effect of NE on LHRH neurons. Muscimol, a potent GABA agonist, inhibits pituitary LH release in ovariectomized rats after intraventricular injection of 5 nmol. This treatment significantly increased prolactin levels. Catecholamine turnover rates in micropunches of various hypothalamic and mesolimbic structures following intraventricular treatment with muscimol were determined using the method of blocking the activity of tyrosine hydroxylase by alpha-methyl-p-tyrosine. Muscimol did not affect catecholamine, GABA and glutamate concentrations. Turnover rates of NE were significantly reduced in the medial preoptic/anterior hypothalamic area. In this structure as well as in the nucleus accumbens and in the anterior mediobasal hypothalamus turnover rates of dopamine (DA) were also reduced whereas DA turnover in mediocortical amygdalae was increased by muscimol. The selective reduction of NE turnover following muscimol may be explained by a direct or indirect action of the GABA-eric drug on NE axon terminals. The reduced NE and DA turnover in the medial preoptic area may be causally related to reduced serum LH levels whereas the reduced hypothalamic DA turnover may explain increased blood prolactin levels.
Animals↗