Reproductive experience increases striatal and hypothalamic dopamine levels in pregnant rats

The effects of parity on the dopaminergic function of rats were studied. Striatal and hypothalamic levels of dopamine (DA), 3,4-dihydroxyphenylacetic acid (DOPAC), homovanillic acid (HVA), norepinephrine (NE), serotonin (5-HT), and 5-hydroxyindoleacetic acid (5-HIAA) as well as serum prolactin (PRL) levels of 7-days primigravid and multigravid rats were compared. Brains and trunk blood were collected from 1200–1400 h on day 7 of pregnancy and assayed for monoamines and their metabolites, and prolactin, respectively. Multigravid rats showed a significant increase in striatal and hypothalamic dopamine levels. A tendency to increase in striatal DOPAC levels was also observed in multigravid rats. Levels of other neurotransmitters and metabolites were not statistically different. Haloperidol (1 mg/kg) treatment induced a significant increase in multigravid 5-HT striatal levels. There was no statistical difference among primigravid and multigravid serum PRL levels after either saline or haloperidol treatment. These data suggest that prior parity produces a shift in dopaminergic activity in multigravid rats.     

The effect of intraventricular gamma aminobutyric acid (GABA) on hypothalamic catecholamines and LHRH and on pituitary hormone release

The present experiments were designed to evaluate the role of catecholamines in mediating the actions of GABA on pituitary hormone release following its intraventricular injection. GABA was administered intraventricularly, at doses of 0.1 and 4 μMol, to chronically ovariectomized rats. Five and 15 min after intraventricular injection, the animals were sacrificed by decapitation. Blood was collected for LH and PRL determination by RIA, and brains were frozen for subsequent determination of LHRH by RIA, and dopamine (DA) and norepinephrine (NE) by radioenzymatic assay. Brain areas analyzed included the median eminence (ME), medial basal hypothalamus (MBH) and suprachiasmatic-medial preoptic area (Sch-PO). Controls received an equal volume (2 μl) of saline. As previously observed, GABA had opposite effects on prolactin (PRL) release depending on the dose employed. A decline in serum PRL was induced by a low (0.1 μMol) dose, whereas a larger (4 μMol) dose induced an increase in PRL levels. LH levels were increased only with the 4 μMol dose. The elevated LH values were paralleled by an increase in LHRH levels in the Sch-PO region 15 min after GABA. Marked changes in catecholamines, particularly in DA, were seen after GABA injection. Significant increments in DA levels in the ME were seen 5 and 15 min after the 0.1 μMol dose of GABA. Similarly, this low dose of GABA induced a marked increase in DA levels in the anterior-pituitary (AP) gland at 15 min. No changes in DA were seen in either MBH or Sch-PO areas. The 4 μMol dose of GABA induced only a small increase in AP levels of DA, without altering the amine levels in any of the brain areas examined. NE levels in the ME were elevated 5 min after the administration of either dose of GABA. No changes in NE were seen in either the MBH or Sch-PO areas. These results indicate that intraventricular GABA injection not only alters pituitary hormone release but also release of DA and NE from terminals in the ME. The released catecholamines may be important in mediating the effects of GABA on releasing factor discharge. In addition, the DA released may have acted directly on the AP to inhibit release of PRL.     

Presence of tyrosine-hydroxylase activity in interior pituitary adenomas and ectopic anterior pituitaries in male rats

There is evidence for local regulatory effects of dopamine (DA) and norepinephrine (NE) on the release of prolactin (PRL) and other hormones from the anterior pituitaries transplanted to an ectopic site. In order to further explore these suspected regulatory mechanisms and to determine if they may exist also in pituitary tumors, we have examined the activity of tyrosine-hydroxylase (TH) in ectopic pituitaries and in hyperplastic pituitaries of estrogen-treated rats. Adult male rats with a pituitary graft in each kidney and sham-operated controls were examined 5 weeks after surgery. Rats implanted for 3 months with Silastic capsules containing diethylstilbestrol (DES) or with empty capsules were used 10 weeks after the capsules were removed. TH activity in ectopic anterior pituitaries of grafted rats was significantly higher than that measured in the eutopic anterior pituitaries of control animals. Similarly, TH activity was significantly higher in DES-induced pituitary tumors than in control pituitaries. These data support the possible existence of local catecholaminergic mechanism(s) that could be modulating PRL secretion from pituitary tumors and from ectopic pituitaries.     

锁孔手术切除鞍区肿瘤及垂体柄的保护

目的 探讨锁孔手术切除鞍区肿瘤的效果,以及术中垂体柄的保护方法。方法 回顾性分析2014年6月至2017年3月采用锁孔手术切除的36例鞍区肿瘤临床资料,采用眶上锁孔入路和翼点锁孔入路。结果 术后病理证实,垂体腺瘤13例,脑膜瘤14例,颅咽管瘤9例。肿瘤全切除33例,近全切除3例。垂体柄全保留32例,部分保留3例,术中未发现垂体柄1例。近全切除3例术后行伽玛刀治疗。所有病例术后随访3个月~2年,均未见肿瘤复发。结论 锁孔手术治疗鞍区肿瘤,既安全、便捷、微创,又能达到切除肿瘤、保护垂体柄等重要结构的目的。     

Changes in the local metabolism of dopamine in the anterior and neural lobes but not in the intermediate lobe of the pituitary gland during nursing

Dopamine (DA), produced by tubero-infundibular dopaminergic (TIDA) neurons of the arcuate nucleus (ARN) is the established inhibitor of the secretion of prolactin (PRL). Changes in dopaminergic (DAergic) neuronal activity in the median eminence–long portal vessels (ME–LPV) and/or the concentration of DA in the anterior lobe (AL) are inversely related to the secretion of PRL. However, conflicting reports concerning DAergic neuronal activity during the suckling-induced release of PRL persist. In addition to TIDA neurons, PeVN-hypophysial DAergic (PHDA) and tubero-hypophysial DAergic (THDA) neurons which, respectively, innervate the intermediate lobe (IL) and the IL/neural lobe (NL) also have a significant role. We measured the concentrations of DA and its main metabolite, 3,4-dihydroxyphenylacetic acid (DOPAC), in the median eminence and the three pituitary lobes of lactating mothers. Concentrations of DA and DOPAC from tissues and the concentration of PRL in plasma were measured by HPLC-EC and RIA, respectively. There were no changes in the concentration of DA and DOPAC of the IL due to the suckling stimulus. In the NL, a decrease in the concentration of DOPAC was detected due to the suckling stimulus. In addition, there were no changes of DA or DOPAC in the outer zone of the AL (AL-OZ) due to suckling. However, a decrease in the concentrations of DA and DOPAC was detected in the inner zone of the AL (AL-IZ). These data suggest lactotrophs from the AL-IZ are responsible for the changes in the concentration of plasma PRL in response to the suckling stimulus. In addition TIDA and THDA neurons, but not PHDA neurons, regulate the control of the secretion of PRL in response to suckling.     

Effects of estrogen upon dopamine release from the corpus striatum of young and aged female rats

In vitro superfusion was used to examine the effects of estrogen administration upon striatal dopamine release in ovariectomized young and aged female Fischer 344 rats in response to 10 μM amphetamine or 30 mM potassium stimulation. Estrogen treatment increased basal dopamine and decreased DOPAC release in young and aged females (10 μg estradiol benzoate given subcutaneously 24 and 48 h prior to superfusion). Amphetamine-stimulated dopamine release was significantly decreased in aged estrogen-treated females, but did not differ in young females as a function of estrogen treatment. Conversely, young females treated with estrogen showed significantly decreased striatal dopamine release in response to potassium stimulation, while aged females showed no differences as a function of hormone treatment. Striatal dopamine content was siginificantly decreased in all estrogen-treated young and aged females. It appears that estrogen is altering dopamine uptake mechanisms in both age groups, since basal DOPAC release is decreased and dopamine is increased. This estrogen effect depletes the readily releasable dopamine storage pool to a greater extent in the aged female as evidenced by reduced amphetamine-stimulated dopamine release. By contrast, estrogen does not alter vesicular dopamine storage pools in aged females, which are mobilized by potassium. These results may have important implications regarding sex differences in expression and treatment of age-related movement disorders.     

Age related signal changes of the pituitary stalk on thin-slice magnetic resonance imaging in infants

Purpose

Signals of some brain regions change along with development in T1-weighted imaging (T1WI) in infants. This study aimed to assess the association of the signal intensity of the pituitary stalk on thin-slice T1WI with infant age.

Effect of exogenous dopamine on hypothalamic dopamine and norepinephrine concentrations in the neonatal brain in rats

Hypothalamic dopamine (DA) and norepinephrine (NE) concentrations were studied in the neonatal rats after acute (postnatal day 4) or chronic (postnatal days 1-10) DA injections (0.5 mg in 5% dextrose in 0.45% saline). Acute injection of DA twice on postnatal day 4 resulted in an increase of hypothalamic DA and NE concentrations 16 hr later. Chronic treatment with the DA (twice in a day) for 10 days resulted in a reduction of NE concentration in the hypothalamus. The results of these studies suggest that the amount and duration of exposure to exogenous DA during postnatal development may result in divergent effects on hypothalamic catecholamine concentration.     

Prolactin increases the activity of tuberoinfundibular and nigroneostriatal dopamine neurons: Prolactin antiserum inhibits the haloperidol-induced increases in dopamine synthesis rates in median eminence and striatum of rats

The role of PRL in mediating the haloperidol-induced increase in tuberoinfundibular dopamine synthesis rate was assessed by studying the effects of administration of PRL antiserum. Antiserum to PRL generated in rabbits and not cross-reacting with other anterior pituitary hormones was administered IV to adult, male rats which received haloperidol 2.5 mg/kg or tartaric acid vehicle SC 22 hr and 12 hr before measurement of dopamine turnover. Comparable groups of haloperidol or vehicle-treated animals received normal rabbit serum as control. Dopamine synthesis or turnover rate was estimated by measurement of accumulation of L-dihydroxyphenylalanine following inhibition of L-aromatic amino acid decarboxylase with m-hydroxybenzylhydrazine. Haloperidol increased median eminence dopamine synthesis rate, and PRL antiserum completely prevented this effect, supporting the thesis that the haloperidol-induced increase in tuberoinfundibular dopamine turnover is mediated by PRL. PRL antiserum did not alter basal median eminence dopamine synthesis rate in male rats. In addition to its effect in median eminence, PRL antiserum blunted the haloperidol-induced increase in striatal dopamine synthesis rate, suggesting that the haloperidol-induced increase in nigroneostriatal dopamine turnover is mediated in part by PRL. Neither haloperidol nor PRL antiserum altered serotonin synthesis rate in mediobasal hypothalamus or striatum. The data provide further support for a mechanism by which PRL can regulate its own secretion. They also suggest that prolactin alters the activity not only of tuberoinfundibular but also of nigroneostriatal neurons.     

Inhibitory effect of diazepam on the activity of the hypothalamic-pituitary-adrenal axis in female rats

Summary The acute intraperitoneal administration of anxiolytic diazepam (2 mg/kg) inhibits the activity of the hypothalamic-pituitary-adrenal (HPA) axis, i.e., it decreases the concentration of adrenocorticotropic hormone (ACTH) and corticosterone in female rats. This fall of ACTH and corticosterone levels was reversed by an antagonist of central benzodiazepine receptors — flumazenil. The antagonist of peripheral benzodiazepine receptors — PK 11195, failed to affect diazepam-induced decrement of plasma ACTH and corticosterone levels. The suppressed HPA function obtained after diazepam administration was also antagonized by bicuculline, an antagonist of GABA recognition sites, and by picrotoxin, a drug that blocks the GABA-A receptor associated chloride channel. These results suggest that central benzodiazepine receptors, the part of GABA-A macromolecular complex, are involved in diazepam-induced inhibition of the activity of the HPA axis.     

Regulation of luteinizing hormone secretion by neuropeptide Y in rats: hypothalamic and pituitary actions

Previous studies have suggested that the stimulatory effect of neuropeptide Y (NPY) on the release of luteinizing hormone (LH) in rats may be due to a central action of the peptide that promotes the release of LH-releasing hormone (LHRH) from the hypothalamus, and to an action in the pituitary gland, to potentiate the release of LH induced by LHRH. The objectives of the present experiments were to test 1) whether NPY stimulation of LHRH release requires extracellular Ca++, and 2) whether NPY can exert direct stimulatory effects on the release of LH from anterior pituitary cells. The in vitro release of LHRH from medial basal hypothalamic fragments induced by KCl depolarization (56 mM), but not the basal release, was blocked by omission of Ca++ and addition of 0.1 mM EGTA to the incubation medium and also by cobalt (1 mM). Depolarization-induced release of the peptide was unaffected by nifedipine, diltiazem, or lanthanum. However, the stimulation of LHRH release by NPY (1 microM) still occurred in Ca++ free/EGTA medium. In a second set of experiments, 10 min pulses of NPY (1-100 nM) alone were ineffective in stimulating the release of LH from dispersed, perifused anterior pituitary cells obtained from ovariectomized, untreated or ovariectomized, estrogen-treated rats, under conditions where pulses of LHRH (0.1-10 nM) were consistently effective. A brief increase in LH release was observed during a 30 min exposure to 100 nM NPY in estrogen-pretreated cells, but not from untreated cells, and the effect was not as marked as that produced by LHRH.(ABSTRACT TRUNCATED AT 250 WORDS)     

Behavioural actions of prolactin locally applied into the hippocampus of adult female rats

Summary The probable behavioural effects of rat prolactin (rPRL) locally applied into the ventral hippocampus (HPC) were studied in cycling female rats. Three experiments were performed examining the behavioural responses of rats subjected to three different situations: (i) Exploratory activity in an enriched holeboard (ii) exploratory activity under conflicting situation and (iii) escape behaviours in a forced swimming test. Behavioural parameters studied were: underground and object-directed exploration and locomotion (Experiment 1); latency time and exploration behaviours (Experiment 2); swimming time and escape behaviours (Experiment 3). In Experiment 1 results showed that rPRL decreased the underground exploration and also locomotion but increased the object-directed exploration and had no effect on non-ambulatory activity. In Experiment 2 results showed that treatment of rPRL increased the latency time but did not modify the exploratory activity. In Experiment 3 results showed that rPRL augmented the swimming time and one of two parameters (frequency of immersions intents) of the escape behaviour. Results are interpreted as local actions of PRL on hippocampal neuron affecting expression of behaviours of rats depending on the stressful conditions of the environment.     

模拟失重雌性大鼠L5椎骨的应力松弛特点

背景：航天医学有必要了解模拟失重对雌性大鼠承重骨应力与时间的变化规律。 目的：观察模拟失重对雌性大鼠承重骨应力松弛的影响,为航天医学提供模拟失重动物椎骨应力松弛数据。 设计、时间及地点：随机对照动物实验,于2005-07/09在吉林大学力学实验中心完成。 材料：6月龄雌性大鼠30只,体质量275~296 g,随机分为正常对照组、失重组各15只。 方法：大鼠复制失重骨质疏松动物模型。在日本岛津电子万能试验机上对正常和失重组各10个试样进行应力松弛实验,应力松弛实验的应变增加速度为50%/min,设定时间为7 200 s,采集100个数据以一元线性回归分析的方法处理实验数据。 主要观察指标：①应力松弛实验数据和曲线。②归一化应力松弛函数计算。 结果：正常和失重组应力松弛最初600 s变化较快,之后应力缓慢下降,对照组7 200 s应力松弛量为0.88 MPa,失重组7 200 s应力松弛量为0.62 MPa。 结论：应力松弛曲线是以对数关系变化的,失重骨质疏松对应力松弛具有一定影响。     

Progesterone decreases the concentration of hypothalamic and anterior pituitary estrogen receptors in ovariectomized rats

In a study of cellular mechanisms of progesterone's antiestrogenic action on behavior and neuroendocrine responses, we investigated the influence of progesterone on the concentration of estrogen receptors in the hypothalamus-preoptic area (HP), anterior pituitary gland (AP), and uterus of chronically estradiol-treated ovariectomized rats. Ovariectomized (OVX) rats were implanted s.c. with 15 mm silastic capsules of estradiol. One week later, they were injected with progesterone or oil vehicle and killed 6 h or 24 h later. Confirming previous reports, progesterone caused a decrease in the concentration of uterine cytosol and nuclear estrogen receptors at both times. Less consistent results were obtained in HP and AP; a decrease in the concentration of HP cytosol estrogen receptors was detected at 6 h, as was a small decrease in the concentration of HP nuclear estrogen receptors at 24 h. More consistent results were seen when a low priming dose of estradiol was used. Although progesterone was without effect on the concentration of nuclear estrogen receptors in HP and AP at 6 h, cytosol receptor levels were depressed by 25% in HP and 14% in AP. At 24 h after progesterone injection, nuclear estrogen receptor levels were decreased in all tissues, while cytosol estrogen receptor levels remained depressed. A study of the time course of progesterone's suppression of cytosol estrogen receptor concentration revealed that the effect is transient, occurring by 6 h after progesterone injection, but returning to baseline by 48 h after injection. Scatchard analysis confirmed that the decreased concentration of cytosol binding in HP was due to a decrease in the concentration of binding sites. As with nearly all of progesterone's neuroendocrine effects, the suppression of estrogen receptor levels requires estrogen priming. HP and AP cytosol from progesterone-treated rats did not seem to contain an estrogen receptor-regulatory factor as do uterine cell nuclei; loss of binding sites at 37 degrees C was no faster in cytosol from progesterone-treated rats. These results demonstrate that, under some conditions, progesterone decreases HP and AP estrogen receptor concentrations. Unlike progesterone's action in the uterus, the primary effect in the brain and pituitary gland seems to be on the cytosol receptor.     

Progesterone decrease the concentration of hypothalamic and anterior pituitary estrogen receptors in ovariectomized rats

In a study of cellular mechanisms of progesterone's antiestrogenic action on behavior and neuroendocrine responses, we investigated the influence of progesterone on the concentration of estrogen receptors in the hypothalamus-preoptic area (HP), anterior pituitary gland (AP), and uterus of chronically estradiol-treated ovariectomized rats. Ovariectomized (OVX) rats were implanted s.c. with 15 mm silastic capsules of estradiol. One week later, they were injected with progesterone or oil vehicle and killed 6 h or 24 h later. Confirming previous reports, progesterone caused a decrease in the concentration of uterine cytosol and nuclear estrogen receptors at both times. Less consistent results were obtained in HP and AP; a decrease in the concentration of HP cytosol estrogen receptors was detected at 6 h, as was a small decrease in the concentration of HP nuclear estrogen receptors at 24 h.More consistent results were seen when a low priming dose of estradiol was used. Although progesterone was without effect on the concentration of nuclear estrogen receptors in HP and AP at 6 h, cytosol receptor levels were depressed by 25% in HP and 14% in AP. At 24 h after progesterone injection, nuclear estrogen receptor levels were decreased in all tissues, while cytosol estrogen receptor levels remained depressed. A study of the time course of progesterone's suppression of cytosol estrogen receptor concentration revealed that the effect is transient, occuring by 6 h after progesterone injection, but returning to baseline by 48 h after injection. Scatchard analysis confirmed that the decreased concentration of cytosol binding in HP was due to a decrease in the concentration of binding sites. As with nearly all of progesterone's neuroendocrine effects, the suppression of estrogen receptor levels requires estrogen priming. HP and AP cytosol from progesterone-treated rats did not seem to contain an estrogen receptor-regulatory factor as do uterine cell nuclei; loss of binding sites at 37 °C was no faster in cytosol from progesterone-treated rats.These results demonstrate that, under some conditions, progesterone decreases HP and AP estrogen receptor concentrations. Unlike progesterone's action in the uterus, the primary effect in the brain and pituitary gland seems to be on the cytosol receptor.     

Dopaminergic neuronal function, anterior pituitary dopamine content, and serum concentrations of prolactin, luteinizing hormone and progesterone in the aged female rat

The serum concentrations of prolactin (PRL), progesterone and luteinizing hormone (LH), and the content and rate of synthesis of dopamine (DA) in selected brain regions were determined in young (3–6 months), intermediate (13–15 months) and aged (24–25 months) female Long-Evans rats. Young rats were examined on the days of diestrus 2 and estrus. Intermediate rats were divided into 2 groups, a group which was cycling regularly (examined on the day of estrus) and a group which exhibited constant estrus. Aged rats were divided into 3 groups one which cycled regularly (examined on day of estrus), one which exhibited constant estrus, and one which exhibited repetitive pseudopregnancies.Serum PRL was increased in all intermediate and aged rats when compared to values in young animals. Serum LH was increased and progesterone decreased in those intermediate and aged rats which exhibited constant estrous reproductive patterns. The DA content was generally decreased in the median eminence, posterior pituitary, striatum, nucleus accumbens and olfactory tubercle of all aged rats, while the rate of DA synthesis was decreased only in the median eminence of aged, non-cycling rats. This suggests that all DA neuronal systems except those in the tuberoinfundibular system are able to compensate for the age-related loss. Despite the apparent reduction of tuberinfundibular DA neuronal function the concentration of DA in the anterior pituitary, which is believed to represent amine released from the neurons, is dramatically increased in intermediate age rats in constant estrus, and in all groups of aged rats. The maintenance of high PRL secretion despite the elevated content of DA in the anterior pituitary suggests in age-related defect in the dynamics of DA in this gland; this defect may contribute to the loss of reproductive function in the aging rat.     

The effects of chronic naloxone on pituitary hormone secretion in female rats

The effects of a sustained-release implant for naloxone (NAL) on serum concentrations of prolactin (PRL), immunoreactive beta-endorphin (IR-beta-ENDO), growth hormone (GH) and thyroid stimulating hormone (TSH) were evaluated in ovariectomized female rats. After 9 days of exposure to NAL, serum levels of none of these 4 pituitary hormones were altered. However, the NAL implant antagonized the stimulatory effects of morphine (15 and 30 mg/kg body weight) on PRL and IR-beta-ENDO secretion, enhanced the stimulatory effects of morphine on GH secretion, and had no effect on morphine-induced suppression of TSH secretion. These results indicate that while chronic NAL exposure does not, by itself, persistently alter pituitary hormone secretion, it differentially effects the response of these hormones to morphine exposure. These data suggest that chronic treatment with narcotic antagonists may invoke differential compensatory mechanisms to maintain normal hormone secretion.     

The effect of long-term treatment with deprenyl on basal and L-DOPA evoked dopamine release in vitro from the corpus striatum of aged rats

Summary In the present experiment, male rats (15–17 months) were injected with deprenyl (0.25 mg/kg) three times per week for six months. At 21–23 months of age the male rats were sacrificed, the corpus striatum removed and superfused in vitro. Basal and evoked dopamine and DOPAC levels, as obtained with either two infusions of L-DOPA (L-DOPA/L-DOPA) or L-DOPA followed by amphetamine (L-DOPA/AMPH), were measured from effluent superfusion samples and compared with values obtained from similarly aged animals treated identically with saline and from that obtained with young (2–4 months) animals. Treatment with deprenyl resulted in significantly greater basal dopamine and significantly lower basal DOPAC output compared with basal release levels from saline-treated aged rats and young animals. Responses to L-DOPA/LDOPA or L-DOPA/AMPH evoked dopamine and DOPAC release did not differ between deprenyl and saline-treated aged rats, however, both groups showed a significantly reduced response profile to these stimulations (L-DOPA/ L-DOPA or L-DOPA/AMPH) compared to that of young rats. These results indicate that the selective Type-B monoamine oxidase inhibitor, deprenyl, exerts a basic change in dopamine metabolism within the corpus striatum of aged rats resulting in an increase of endogenous dopamine and a decrease in endogenous DOPAC output.