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PubMed1992

Characterization of glutamate efflux from preoptic area synaptosomes.

Treatment of ovariectomized rats in vivo with ovarian steroids has been found to influence the efflux of glutamate and gamma-aminobutyric acid from preoptic area synaptosomes incubated in vitro. Since these studies indicated a possible role of the glutamate carrier in steroid-modulated release of amino acids, the present studies examined the characteristics of efflux of glutamate and of the carrier system for glutamate in synaptosomes of the preoptic area derived from ovariectomized hormone-treated rats. The efflux of [3H]glutamate from preoptic area synaptosomes, was induced by glutamate and by the glutamate carrier agonist, D-aspartate; the putative glutamate carrier antagonist dihydrokainate failed to block this efflux. Dihydrokainate inhibited the uptake of glutamate but it was less effective than D-aspartate. The excitatory amino acid receptor agonists, N-methyl-D-aspartate and kainate were without effect while quisqualate modestly stimulated the efflux of [3H]glutamate. Efflux of [3H]glutamate, induced by glutamate itself or by D-aspartate was not blocked by the excitatory amino acid receptor antagonists, D-2-amino-5-phosphonovaleric acid, 6,7-dinitroquinoxaline-2,3-dione or kynurenate. Glutamate-induced efflux of [3H]glutamate did not require external Ca2+. Glutamate altered neither the basal nor the potassium-induced increases in the intrasynaptosomal concentration of Ca2+ as measured by the fura-2 method. Glutamate-induced efflux of [3H]glutamate was blocked by the putative chloride channel antagonist, 4,4'-diisothiocyanatostilbene-2,2'-disulfonic acid. It is concluded that the glutamate-induced efflux of [3H]glutamate in synaptosomes of the preoptic area is a carrier-mediated process that does not require activation of receptors.(ABSTRACT TRUNCATED AT 250 WORDS)

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMed1975

Sterility and delayed vaginal opening following electrolytic lesions placed neonatally in medial preoptic area in female rats.

Electrolytic lesions were placed in the preoptic area or in the middle and posterior hypothalamus of female rats within 48 hrs after birth. Vaginal opening was delayed significantly in rats having the medial preoptic area (mPOA) destructed as compared to sham-operated animals and those given lesions in the other parts of the hypothalamus. Only rats with the mPOA completely destructed developed the anovulatory syndrome. In these animals, unilateral ovariectomy was not followed by enlargement of its fellow. The present results are not in agreement with those of previous workers that electrolytic destructions of the diencephalon induced precocious puberty. The difference may be ascribable to difference in size and locus of lesions.

Animals↗
PubMed1975

Prolactin release induced by electrical stimulation of the hypothalamic preoptic area in unanesthetized sheep.

The hypothalamic preoptic area (POA) was electrically stimulated through permanently implanted electrodes in 4 unanesthetized sheep. Initiation of POA stimulation was followed witin 10-20 min by large increases in plasma levels of prolactin (PRL). The stimulation-induced discharges of PRL were consistently observed in both untreated and estradiol-treated castrated animals using 0.1 to 0.7 mA of applied current. Since behavioral modifications were only sometimes associated with electrical stimulation of the POA, the response appears unrelated to the stress-induced release of PRL.

Animals↗
PubMed1987

Steroid autoradiography of the sexually dimorphic nucleus of the preoptic area.

Autoradiography was performed to determine if the neurons of the sexually dimorphic nucleus of the preoptic area (SDN-POA) in the adult rat accumulate estradiol (E2), testosterone (T), and/or dihydrotestosterone (DHT). Three days prior to steroid administration, adult male and female Sprague-Dawley rats were gonadectomized and adrenalectomized. Animals were then given either [3H]T, [3H]E2, or [3H]DHT through an indwelling jugular cannula. One hour later, animals were decapitated and brain sections processed for thaw mount autoradiography. The autoradiograms which contained the SDN-POA and an adjacent area of the medial preoptic area (MPOA) were quantitatively analyzed using the 3 times background, 5 times background, and Poisson criteria for labeled cells. In general, cells in the SDN-POA and the MPOA accumulate T, E2, or DHT. For both sexes, there is a greater percentage of labeled cells in the SDN-POA than in the MPOA, and a greater percentage of labeled cells following E2 exposure than following T or DHT exposure. In addition, there is a sex difference (male greater than female) in the percentage of labeled cells following T exposure. In summary, these data indicate that adult SDN-POA neurons do accumulate gonadal steroids.

Animals↗
PubMed1987

Effects of castration or testosterone implants upon pituitary function in hypogonadal mice bearing normal foetal preoptic area grafts.

Grafts of normal mouse preoptic area (POA) tissue into the third ventricle of gonadotrophin-releasing hormone (GnRH)-deficient hypogonadal (hpg) mice resulted in an elevation of pituitary GnRH receptors, an increased synthesis of luteinizing hormone (LH) and follicle-stimulating hormone (FSH) by the pituitary gland, an elevation of gonadal LH receptors and in the stimulation of steroidogenesis and spermatogenesis in the testis. In normal mice both castration or the subcutaneous implantation of testosterone capsules for 10 days reduced GnRH receptors, pituitary LH and FSH content, and the latter treatment also caused a 50% reduction in testicular LH receptors. In hpg mice bearing POA grafts testosterone implants failed to affect any of the above parameters, and castration failed to affect pituitary gonadotrophin hormone content, although there was a slight reduction in pituitary GnRH receptors after castration. These experiments suggest that neither the pituitary gonadotroph, nor the GnRH neurone represent major sites for the direct negative feedback of testosterone upon gonadotrophic hormone secretion in male mice.

Animals↗
PubMed1995

Neuromodulation of transplanted gonadotropin-releasing hormone neurons in male and female hypogonadal mice with preoptic area brain grafts.

Implantation of normal preoptic area (POA) tissue into the third ventricle of adult hypogonadal (HPG) mice provides a source of GnRH neurons that innervate the host median eminence and stimulate reproductive development in the sterile mutants. To further evaluate graft-host integration, the effects of N-methyl-D,L-aspartic acid (NMA) and opiate antagonists on LH secretion in HPG mice with POA transplants (HPG/POA) were tested. NMA challenges significantly stimulated LH secretion in 10 of 11 HPG/POA females. Only 5 of 12 HPG/POA males responded to the same treatment. Administration of the opiate antagonists naloxone or naloxone methiodide was ineffective in stimulating LH release in any mice, but opiate antagonist pretreatment significantly potentiated the LH secretory response to NMA in female, but not male, HPG/POA mice. A potential anatomical substrate for this facilitation may be the beta-endorphin-immunoreactive innervation of the POA grafts in all HPG/POA brains examined. beta-Endorphin fibers were also present in the median eminence in the vicinity of GnRH outgrowth from the grafts. However, similar innervation patterns in HPG/POA males that did not respond to opioid antagonism suggests that this is not sufficient. We tested whether the sex difference in HPG/POA responsivity to neuromodulation is related to the steroid milieu in the hosts. 17 beta-Estradiol (E2) treatment facilitated the LH secretory response of male HPG/POA to NMA challenges whether animals were castrated and given an E2 capsule prior to graft implantation or one week before testing two months after graft surgery. Intact or vehicle (sesame oil)-treated, castrated HPG/POA males rarely responded to NMA challenges, yet graft-derived GnRH innervation of the hosts' median eminence was comparable in all treatment groups. GnRH challenge testing indicated that pituitary sensitivity of the HPG/POA males was not significantly altered by E2 treatment, suggesting that estrogen acted centrally. These results indicate that the activity of grafted GnRH neurons may be modulated by endogenous opioids of host origin as well as by the hormonal milieu.

Animals↗
PubMed1985

Enhanced triiodothyronine production in crested newts bearing permanent lesions to the anterior preoptic area.

In the crested newt, permanent lesions to the anterior preoptic area brought about an enhancement of triiodothyronine (T3) production. This was not mediated by prolactin, since the effect was demonstrable also in ergocryptine (CB 154)-treated animals. The observed rise in circulating T3 levels in the ergocryptine-treated surgical animals confirms that lesions to the anterior preoptic area stimulate pituitary thyrotrophic activity, resulting in the activation of the thyroid gland.

Animals↗
PubMed1987

Preoptic area opioids and opiate receptors increase during pregnancy and decrease during lactation.

Opiate receptor and endogenous opioid content were determined in pregnant, lactating, ovariectomized, and ovariectomized and subsequently estradiol- and progesterone-treated adult female rats. Levels of estradiol and progesterone produced by Silastic capsules implanted in animals of the ovariectomized, hormone-treated group were similar to natural levels of those hormones induced during pregnancy. Quantitative receptor autoradiography and radioimmunoassay were used to determine [3H]naloxone binding density and immunoreactive beta-endorphin content, respectively, in the preoptic area of the hypothalamus. Both opiate receptor binding density and beta-endorphin content in the preoptic area varied in the same direction in all experimental groups. The highest levels of both were observed during pregnancy and the lowest levels during lactation. Ovariectomy without subsequent hormone treatment produced intermediate levels of both opiate receptor and beta-endorphin. Ovariectomy with experimentally-induced estradiol and progesterone levels similar to those of pregnancy produced opiate receptor density and beta-endorphin content similar to those observed in pregnant animals. These data suggest that gonadal steroids are capable of altering function of the endogenous opiate system in the preoptic area. Moreover, preoptic area levels of opioids and opiate receptors are normally elevated during pregnancy and reduced during lactation. Since opiates are known to disrupt ongoing maternal behavior, a reduction of preoptic opiate function during lactation may be required to promote normal maternal behavior. The specific preoptic region involved in opiate regulation of maternal behavior may be illustrated by the zone of opiate receptor alteration observed herein.

Animals↗
PubMed1985

The sex hormone-dependent development of opiate receptors in the rat medial preoptic area.

The opiate receptor content of the sexually dimorphic medial preoptic area (MPOA) was examined in newborn and 5-day old (D6) male and female rats. A significant increase of [3H]naloxone binding was observed in and around the sexually dimorphic nucleus of the preoptic area (SDN-POA) in D6 female rats, relative to newborn females. Opiate receptor labeling did not increase over this period in males, nor was labeling different between males and females at birth. This dramatic alteration of MPOA opiate receptor content was observed to occur in either sex in the absence of testosterone postnatally; that is, neonatally-castrated males exhibited the same increase of labeling by D6 as did normal females. Conversely, daily postnatal testosterone treatment of females from birth to D6 resulted in the development of male-like MPOA opiate receptor pattern. The sex hormone-dependence of MPOA opiate receptor development is discussed in relation to the sex hormone-dependent ontogeny of SDN-POA structure. The overlap of critical periods for the development of these structural and chemical sexual dimorphisms suggests a role for endogenous opioids in modulating MPOA development.

Animals↗
PubMed1989

Simultaneous catecholamine histofluorescence and thymidine autoradiography of the sexually dimorphic nucleus of the preoptic area in the rat.

The sexually dimorphic nucleus of the preoptic area (SDN-POA) in the rat represents a morphological substrate in which the influence of gonadal hormones on the process of sexual differentiation of the brain can be seen. Since the medial preoptic area (MPO) is a region rich in catecholamine (CA) terminals, it is possible that catecholamines may play a role either in the differentiation of the perinatal SDN-POA or in the function of this nucleus in the adult. It is not known whether catecholamine terminals exist within the SDN-POA or whether they can directly influence the activity of SDN-POA neurons. The present study was conducted to determine the extent to which catecholamines innervate this nucleus and further to elucidate the possibility of a potential sexual dimorphism in the innervation pattern. In order to determine which of the neurons in the MPO are within the SDN-POA we have utilized the fact that the SDN-POA has a prolonged period of neurogenesis in comparison to other neurons of the MPO. Thus, tritiated thymidine-labeled neurons can be used as a detection criterion for the SDN-POA. To conduct this experiment, timed pregnant Sprague-Dawley females were given a single injection of [3H]thymidine on Day 18 of gestation. Pups were killed as adults and prepared for fluorescence histochemistry of monoamines. Sections adjacent to those examined for catecholamine fluorescence were treated for autoradiographic localization of [3H]thymidine. Fluorescence innervation patterns were plotted within the boundaries of the nucleus following its identification from Nissl sections as well as from adjacent autoradiograms simultaneously viewed in a comparator bridge microscope with dark-field illumination.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMedDate not supplied

Potentiation of the antidipsogenic action of alpha-human atrial natriuretic polypeptide at the preoptic area in spontaneously hypertensive rats.

The effect of alpha-human atrial natriuretic polypeptides on fluid intake following administration of angiotensin II and 48 hr water deprivation was assessed at the preoptic area in spontaneously hypertensive and normotensive Wistar-Kyoto rats. Angiotensin II (100 ng), injected into the preoptic area, and water deprivation increased the intake of water and of a 2.7% NaCl solution in spontaneously hypertensive as well as in Wistar-Kyoto rats. These intakes were potentiated in the spontaneously hypertensive rats. The fluid intakes evoked by angiotensin II were dose-dependently antagonized by alpha-human atrial natriuretic polypeptide and angiotensin II, administered into the preoptic area, in spontaneously hypertensive but not in Wistar-Kyoto rats. In 48 hr water-deprived rats, alpha-human atrial natriuretic polypeptide also inhibited the fluid intake in spontaneously hypertensive but not in Wistar-Kyoto rats. The results suggest that atrial natriuretic polypeptide and angiotensin II may play an important role in controlling fluid intake at the preoptic area level and that these peptides might be involved in the pathogenesis of spontaneously hypertensive rats.

Angiotensin II↗
PubMed1985

Evidence for a role of the preoptic area in lateral hypothalamic self-stimulation.

We examined the effects of unilateral radiofrequency lesions in the preoptic area on lateral hypothalamic self-stimulation in 15 rats. The animals were tested for self-stimulation in the lateral hypothalamus at 3 different current intensities from electrodes placed in both hemispheres, and then received a unilateral lesion in the preoptic area. Four hours later they were again tested for self-stimulation at the 3 current intensities and then daily over the following 14 days, or until they recovered their presurgical rates of self-stimulation. Rate of self-stimulation decreased in the damaged hemisphere, and recovered to prelesion levels within 2 weeks in 6 of 9 rats. In the intact hemisphere rate of self-stimulation increased above the prelesion level during a period from 1 to 2 weeks after the lesion. These results suggest that the preoptic area is involved in lateral hypothalamic self-stimulation. The effects of D-amphetamine (1 mg/kg) and apomorphine (2 mg/kg) injections on turning behavior were also studied in an open field and in a rotometer. Apomorphine induced contraversive turning to the lesion side in the open field and D-amphetamine induced ipsiversive turning in the rotometer.

Animals↗
PubMed2004

The role of the medial preoptic area of the hypothalamus in organizing the paradoxical phase of sleep.

Chronic experiments were performed on cats to study the effects of electrical stimulation of the medial preoptic area of the hypothalamus on the latent period, duration, and structure of paradoxical sleep, as well as the dynamics of neuron activity in this structure during the sleep-waking cycle. These investigations showed that low-frequency stimulation of the medial preoptic area during slow-wave sleep led to short-latency development of desynchronization of bioelectrical activity in the neocortex and initiated the development of paradoxical sleep or a similar state. Stimulation of this structure during paradoxical sleep led to a decrease in its duration, to the virtually complete disappearance of the tonic stage of paradoxical sleep, and to an increase in the frequency of rapid eye movements in the phasic stage. Rearrangement of neuron activity in the medial preoptic area during the sleep-waking cycle was similar to that seen in cells of the lower brainstem "executive" centers of paradoxical sleep. It is suggested that neurons in the medial preoptic area of the hypothalamus are actively involved in the mechanisms of paradoxical sleep and, in particular, in the desynchronization of neocortical bioelectrical activity which develops during this stage.

Action Potentials↗
PubMed1981

Neurogenesis of the sexually dimorphic nucleus of the preoptic area in the rat.

The sexually dimorphic nucleus of the preoptic area (SDN-POA) of Sprague-Dawley rats is larger in volume in the male and hormone-dependent early in postnatal life. In the present study, we compared for each sex the time course of neuroblast proliferation which study, we compared for each sex the time course of neuroblast proliferation which forms SDN-POA or adjacent medial preoptic area (MPOA) neurons. Additionally, we investigated whether there is a temporal gradient of production of neurons in relation to their final position within the SDN-POA. On day 15, 15, 16, 17, or 18 postfertilization (pf) pregnant rats were given a single injection of 3H-thymidine (thy). At 30 postnatally days of age the pups were sacrificed and brain sections were prepared and processed for autoradiography. Three sections of the SDN-POA and an adjacent area just lateral to it in the MPOA were also analyzed. In the MPOA and the SDN-POA the percentage (%) of labeled neurons decreases as the day of injection of thy approaches the end of gestation, but the time period in which neuroblast divisions occurred is markedly different for the SDN-POA as compared to that for the MPOA. DNA synthesis occurs as late as day 18pf for neurons which form the SDN-POA but ceases on day 16pf for those destined for the MPOA. There is a sex difference in neuronal production on both day 14 and 17pf for neurons destined for the SDN-POA. After injection on day 14pf the % labeled neurons is larger in the female than in the male but after injection on day 17pf this is reversed. There are also significant sex differences as well as a temporal gradient associated with the % labeled neurons in the SDN-POA in relation to their final anterior-posterior position. In addition, this study confirms our previous results which justify labeling the SDN-POA a nucleus, since neuronal density in this region in the male and female is significantly greater that that in the surrounding MPOA. These data illustrate that the specific neurons which comprise the SDN-POA in both the male and female are being produced as late as day 18pf, whereas neurons located in the MPOA but not in the SDN-POA have all been born by day 16pf. Neuroblast division which produces the neurons of the SDN-POA may begin earlier and terminate sooner in the female than in the male. These differences in neuronal production may partially account for the sexual dimorphism seen in the volume and neuronal number of the SDN-POA of the adult rat.

Animals↗
PubMed2003

Differential colocalization of Islet-1 and estrogen receptor alpha in the murine preoptic area and hypothalamus during development.

Estrogen receptor (ER) expression and regulation is vital to the correct functioning of the neuroendocrine brain. Islet-1 (Isl-1) is a LIM homeodomain-containing transcription factor that has been implicated in neuronal differentiation, is located in the hypothalamus, and can alter ER function in vitro. We have determined that Isl-1 is localized in several regions of the hypothalamus, including the ER rich areas of the ventromedial nucleus (VMH), the preoptic area, and the anterior hypothalamus. Using double-label immunocytochemistry, we examined the overlap between immunoreactive ERalpha and Isl-1 in these different hypothalamic brain regions. In the developing brain, almost 100% of VMH cells that contain immunoreactive ERalpha also contain Isl-1. However, in older animals, the percentage of double-label cells decreased below 70%. This change is due to a decrease in the number of cells containing Isl-1, because there was no difference in the number of ERalpha-containing cells. By contrast, in more anterior regions of the hypothalamus, cells containing both Isl-1 and ERalpha were less common, with the two populations adjacent to each other, rather than overlapping. These data suggest that, although Isl-1 and ERalpha can interact, they are not always found in the same cells and that regulation of ERalpha function is not under the same control in the VMH, preoptic area, and the anterior hypothalamus.

Age Factors↗
PubMed2000

The preoptic area in the hypothalamus is the source of the additional respiratory drive at raised body temperature in anaesthetised rats.

In mammals that use the ventilatory system as the principal means of increasing heat loss, raising body temperature causes the adoption of a specialised breathing pattern known as panting and this is mediated by the thermoregulatory system in the preoptic area of the hypothalamus. In these species an additional respiratory drive is also present at raised body temperature, since breathing can reappear at low Pa,CO2 levels, when stimulation of chemoreceptors is minimal. It is not known whether the preoptic area is also the source of this additional drive. Rats do not pant but do possess this additional respiratory drive at raised body temperatures. We have therefore tested whether the preoptic area of the hypothalamus is the source of this additional respiratory drive in rats. Urethane anaesthesia and hyperoxia were used in eleven rats to minimise behavioural and chemical drives to breathe. The presence of the additional respiratory drive was indicated if rhythmic diaphragmatic EMG activity reappeared during hypocapnia (a mean Pa,CO2 level of 21+/-2 mm Hg, n = 11), induced by mechanical ventilation. The additional respiratory drive was absent at normal body temperature (37¿C). When the temperature of the whole body was raised using an external source of radiant heat, the additional respiratory drive appeared at 40.6+/-0.5 degrees C (n = 3). In two further rats this drive was induced at normal body temperature by localised warming in the preoptic area of the intact hypothalamus. The additional respiratory drive appeared at similar temperatures to those in control rats in three rats following isolation of the hypothalamus from more rostral areas of the brain. In contrast, the additional respiratory drive failed to appear at these temperatures in three rats after isolating the hypothalamus from the caudal brainstem, by sectioning pathways medial to the medial forebrain bundle. Since the preoptic area is known to contain thermoreceptors and to receive afferents from peripheral thermoreceptors, the results show that this area is also the source of the additional respiratory drive at raised body temperature in anaesthetised rats.

Anesthesia, Intravenous↗
PubMed2002

A progestin antagonist blocks vaginocervical stimulation-induced fos expression in neurones containing progestin receptors in the rostral medial preoptic area.

Vaginocervical stimulation (VCS) has a variety of effects on the brain, physiology and behaviour. Previous work demonstrated that a progestin antagonist blocked neuronal response to VCS (i.e. Fos expression) in the absence of progesterone in some neurones, and suggested that some of the effects of VCS on the brain are mediated by ligand-independent activation of progestin receptors (PRs). Although it had been reported previously that some of the cells in which VCS induces Fos expression also contain PRs, it had not been determined if a progestin antagonist blocked Fos expression in these particular neurones. The purpose of this experiment was to determine if a progestin antagonist decreases Fos expression specifically in cells that also express PRs in the preoptic area and ventromedial hypothalamus. As has been shown previously, VCS increased Fos-immunoreactive (ir) expression in the particular areas studied. In the rostral medial preoptic area, VCS increased Fos expression in cells that coexpressed PRs, as well as in cells that do not. However, in the caudal medial preoptic area, VCS only increased Fos expression in cells that did not coexpress PRs. Injection of the progestin antagonist, RU 486, decreased Fos expression in the rostral, but not caudal medial preoptic area, and it decreased Fos expression only in cells that coexpressed PR-ir. In contrast to a previous report, in the present study, the progestin antagonist did not inhibit VCS-induced Fos expression in the ventromedial hypothalamic area. The results of this experiment suggest that the progestin antagonist inhibits VCS-induced Fos expression in some neurones by blocking PRs, and they provide further support for the idea that VCS influences neuronal response in some cells by ligand-independent activation of PRs in those cells.

Animals↗
PubMed1993

Ontogeny of Leu-enkephalin and beta-endorphin innervation of the preoptic area in male and female rats.

The distribution of endogenous opioid peptide-containing fibers in the medial preoptic area of developing male and female rats was examined using immunohistochemical methods. In particular, the ontogeny of leucine-enkephalin (leu-enk) and beta-endorphin (beta-endo) innervation was studied using antisera directed against these compounds. The distribution of Leu-enk and beta-endo differed at each age examined from birth to postnatal day 12 (P12). Furthermore, the patterns of fiber innervation differed across development. Leu-enk-like immunoreactivity was initially densest in the lateral preoptic region of both sexes, ultimately expanding into the medial preoptic region to become densest in the lateral portion of the medial preoptic nucleus by P12. This latter pattern was observed only in males, however, as females continued to exhibit diffuse medial preoptic Leu-enk-like immunoreactivity at P12. In contrast, the distribution and developmental pattern of beta-endo-like immunoreactivity was similar in both sexes; diffuse staining was observed in the medial preoptic region at birth, later becoming dense only in the periventricular and parastrial nuclei. The time course of development of Leu-enk and beta-endo innervation of the medial preoptic area suggests that the sexually dimorphic expression of opioid immunoreactivity occurs after preoptic neurons appear in their sexually dimorphic configuration. Therefore, although the development of opioid-containing pathways could be influenced by the perinatal gonadal steroid hormone environment, medial preoptic Leu-enk and beta-endo innervation might not contribute directly to the sexually dimorphic neuronal organization of the preoptic area.

Animals↗