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F Naftolin

Publications and source records attributed to F Naftolin.

At least 19 recordsLinked to original sources
PubMed1992

Unilateral transplantation of human fetal mesencephalic tissue into the caudate nucleus of patients with Parkinson's disease.

BACKGROUND: Parkinson's disease is characterized by the loss of midbrain dopamine neurons that innervate the caudate and the putamen. Studies in animals suggest that fetal dopaminergic neurons can survive transplantation and restore neurologic function. This report compares the clinical results in four case patients with severe Parkinson's disease who underwent stereotaxic implantation of human fetal ventral mesencephalic tissue in one caudate nucleus with the results in a control group of similar subjects assigned at random to a one-year delay in surgery. METHODS: Each case patient received cryopreserved tissue from one fetal cadaver (gestational age, 7 to 11 weeks). Before implantation, adjacent midbrain tissue underwent microbiologic, biochemical, and viability testing. Cyclosporine was administered for six months postoperatively. RESULTS: The procedure was well tolerated. Three case patients showed bilateral improvement on motor tasks, as assessed on videotape, and were more functional in the activities of daily living, as assessed by themselves and neurologists, during both optimal drug therapy and "drug holiday" periods. One case patient, who died after four months from continued disease progression, had striatonigral degeneration at autopsy. In the patients who received transplants, optimal control was achieved with a lower dose of antiparkinsonian medications, whereas the controls required more medication. Positron-emission tomography with [18F]fluorodopa before and after surgery in one patient revealed a bilateral restoration of caudate dopamine synthesis to the range of normal controls, but continued bilateral deficits in the putamen. CONCLUSIONS: Although the case patients continued to be disabled by their disease, unilateral intracaudate grafts of fetal tissue containing dopamine diminished the symptoms and signs of parkinsonism during 18 months of evaluation.

Activities of Daily Living↗
PubMed1992

Sex differences in estrogen receptor binding in the rat hypothalamus: effects of subsaturating pulses of estradiol.

The effects of subsaturating pulses of estradiol on cell nuclear retention of estrogen receptors in brain regions of male and female rats were determined. In the first experiment, age-matched adrenalectomized/gonadectomized (ADX/GDX) rats were killed 1 h after i.v. injection of a subsaturating dose of free estradiol (1.0 microgram/kg b. wt.) and cell nuclear estrogen receptor binding was measured in microdissected brain areas by an in vitro exchange assay. As we have previously reported with saturating doses of estradiol (3.6-36.0 micrograms/kg b. wt.), a greater concentration of receptors was measured in the ventromedial nucleus (VMN), periventricular preoptic area (PVPOA), and medial preoptic area (mPOA) of the female than in the same regions of the male brain. Binding levels did not differ between the sexes in the bed nucleus of the stria terminalis, arcuate nucleus, or the corticomedial amygdala. In the second experiment, GDX/ADX male and female rats received either a single or double pulse of 0.5 microgram estradiol/kg b. wt. administered 6 h apart. Rats were killed 1 h after the second pulse. In animals treated with a single pulse of estradiol 1 h before sacrifice, higher concentrations of estrogen binding were measured in the female VMN and PVPOA than in the male. Except in the mPOA, the concentration of estrogen receptor binding measured was not different from that measured in animals that had received an additional, earlier pulse of estradiol. In this area, receptor concentrations were lower in male rats treated with two pulses than in males treated with one pulse.(ABSTRACT TRUNCATED AT 250 WORDS)

Analysis of Variance↗
PubMed1992

Neuroanatomical specificity in the autoregulation of aromatase-immunoreactive neurons by androgens and estrogens: an immunocytochemical study.

Testosterone (T) increases brain aromatase activity (AA) in quail and other avian and mammalian species. It was shown both in quail and in rat that this enzymatic induction results from a synergistic action of androgens and estrogens. These studies provide little information on possible anatomical or cellular specificity of the effect. Using a polyclonal antiserum against human placental aromatase, we have previously identified aromatase-immunoreactive (ARO-ir) neurons in the quail brain and demonstrated that T increases the number of ARO-ir cells in the quail preoptic area (POA) supporting previous evidence that T increases AA in the brain. However, which T metabolites are involved, the actual mechanism of regulation and the possibility of anatomical specificity for these effects are not yet clear. In the present study, we disassociated the effects of androgens and estrogens in aromatase induction by comparing ARO-ir neurons of quail treated with T alone or T in the presence of a potent aromatase inhibitor (R76713), which has been shown to depress AA levels and to suppress T-activated copulatory behavior. T increased the number of ARO-ir cells in POA, bed nucleus striae terminalis (BNST) and tuberal hypothalamus (Tu). The T effect was inhibited by concurrent treatment with aromatase inhibitor in Tu, but not in POA and BNST. This differential effect of the aromatase inhibitor fits in very well with our previous studies of the co-localization of aromatase and estrogen receptors. The T effect was blocked by R76713 in areas where ARO-ir and estrogen receptor-ir are generally co-localized (Tu) and was not affected in areas with mainly ARO-ir positive, estrogen receptor-ir negative cells (POA, BNST). This suggests anatomical differences in the expression or clearance of aromatase which may be differentially sensitive to androgens and estrogens and dependent upon the presence of sex steroid receptors.

Animals↗
PubMed1992

Regulation of plasminogen activators and type-1 plasminogen activator inhibitor by cyclic AMP and phorbol ester in rat astrocytes.

Two plasminogen activators (PAs): tissue-type plasminogen activator (t-PA) and urokinase-type plasminogen activator (u-PA), as well as the type-1 plasminogen activator inhibitor (PAI-1) are synthesized and secreted by rat astrocytes. Preliminary studies suggest that PA activity plays a role in astrocyte development and differentiation. We have examined the regulation of the PA system by the cAMP-dependent protein kinase (PKA) and protein kinase C (PKC) in purified rat astrocyte cultures. PKA activity was increased by exposing cultured astrocytes to forskolin or dibutyryl cyclic AMP, whereas PKC activity was stimulated with phorbol-12-myristate 13-acetate (PMA). Activation of both second-messenger pathways produced a time- and dose-dependent increase in the total PA activity. However, based on SDS-PAGE/zymography we found that forskolin increased t-PA activity and reduced u-PA activity, whereas PMA treatment caused a significant increase in u-PA activity without altering t-PA activity. Reverse zymography analysis revealed that astrocyte PAI-1 activity is decreased by forskolin and increased by PMA. Together, these results demonstrate that the components of the PA system in rat astrocytes are independently and reciprocally regulated by PKA and PKC. Our findings raise the possibility that the plasminogen activator system could be involved in some of the actions of growth factors and/or neuromodulators that modulate PKC or PKA in astrocytes.

Animals↗
PubMed1992

Effects of a phytoestrogen diet on estrogen-dependent reproductive processes in immature female rats.

The study reported here examined the effects of a phytoestrogen diet on progestin receptor induction, vaginal opening, and the onset and maintenance of vaginal cycles in developing female rats. A natural dietary concentration (0.01%) of the isoflavonoid coumestrol was incorporated into the AIN semipurified diet and fed from 21 to 24 days (acute treatment) or from 22 to 60 days (chronic treatment). Progestin receptor induction was observed in the uterus, pituitary, and hypothalamus-preoptic area following acute treatment. Responses were more marked in the uterus and pituitary than in the hypothalamus-preoptic area. Vaginal opening was accelerated by 4 days during chronic coumestrol treatment and occurred at a lighter body weight. Vaginal cycles began on vaginal opening and did not differ in regularity from those of control animals. However, irregular cycles were observed in coumestrol-treated animals at 116 to 131 days, suggesting that chronic coumestrol treatment may have induced some permanent changes in reproductive function. These findings demonstrate that plant estrogens, at natural dietary levels, produce significant, agonistic actions in several estrogen-dependent tissues and processes.

Analysis of Variance↗
PubMed1992

Effects of a normal, human-concentration, phytoestrogen diet on rat uterine growth.

The estrogenic action of the prototype natural phytoestrogen coumestrol was examined in rats in in vitro and in vivo tests. To establish the binding specificity of coumestrol and its relation to biological activities, saturation analyses and uterine weight assays were performed. These assays indicated that coumestrol competitively inhibited binding to the estrogen receptor and induced increases in uterine weight in keeping with its estrogen receptor affinity constant. Most importantly, coumestrol was uterotrophic when incorporated in a semipurified diet at natural dietary concentrations. Significant increases occurred in both uterine wet weight and dry weight, indicating that coumestrol produces true uterine growth. Effects appeared to be cumulative, raising questions of time-related interactions with other estrogen-sensitive mechanisms and clearance of isoflavonoids. Coumestrol induced uterine growth over a 90-hour period at dietary concentrations of 0.01 to 0.1%. Lower doses not active over this period were active when provided over a longer period of time: a 0.005% concentration was not active over a 90-hour period, but was active when provided over a 180-hour period. Coumestrol-induced uterine growth was accompanied by the induction of cytosolic progestin receptors and increases in nuclear estrogen binding. Scatchard analyses verified that these changes were due to changes in receptor number. These studies show that the naturally occurring phytoestrogens have dramatic estrogenic effects at natural dietary levels. These actions may be expressed via traditional receptor-mediated actions and therefore may have the same implications for development, health, and disease as do the steroidal estrogens produced by the body. Because rats have no sex hormone-binding globulin, further studies must be conducted in humans. However, these findings suggest that the natural dietary phytoestrogen coumestrol is a potent estrogen that must be considered in calculating the total estrogenic load to which humans are exposed during normal life.

Animals↗
PubMed1992

GABAergic and catecholaminergic innervation of mediobasal hypothalamic beta-endorphin cells projecting to the medial preoptic area.

In the absence of cellular estrogen receptors or proven direct estrogen action in the rat, it is assumed that estrogen indirectly regulates the secretory activity of the preoptic area luteinizing hormone-releasing hormone-producing cells. We have previously shown that pro-opiomelanocortin neurons in the arcuate nucleus of the rat send axons rostrally to connect with luteinizing hormone-releasing hormone neurons of the preoptic area. An experiment combining retrograde tracing and double-immunostaining was used to test the hypothesis that rat GABAergic and/or catecholaminergic neurons can influence luteinizing hormone-releasing hormone-producing cells via mediobasal hypothalamic beta-endorphin neurons. The retrograde tracer horseradish peroxidase was injected into the medial preoptic area; two days later, arcuate nucleus Vibratome sections were double-immunostained for beta-endorphin and glutamate decarboxylase or tyrosine hydroxylase. Light and electron microscopic analysis of these triple-labeled sections demonstrated that a population of beta-endorphin-immunoreactive neurons concentrated in the ventromedial arcuate nucleus contain retrogradely transported horseradish peroxidase granules and form synaptic contacts with glutamate decarboxylase- and tyrosine hydroxylase-immunoreactive axon terminals. The present data suggest that arcuate nucleus GABA and catecholamine fibers may influence luteinizing hormone-releasing hormone-containing neurons via projective pro-opiomelanocortin cells.

Animals↗
PubMed1992

Presence of calbindin and lack of parvalbumin in progesterone receptor-containing neurons of the monkey mediobasal hypothalamus.

All of the progesterone receptor-containing cells of the monkey hypothalamus are GABAergic. The aim of this study was to further characterize these GABAergic progesterone receptor-containing neurons based on their calbindin or parvalbumin content. These calcium-binding proteins are characteristic markers of different populations of GABAergic neurons in the central nervous system. Double-immunolabeling for progesterone receptor and either calbindin or parvalbumin was performed on hypothalamic Vibratome sections of estrogen primed African green monkeys (Cercopithecus aethiops). Progesterone receptor-containing calbindin-immunoreactive neurons were observed in the ventromedial and periventricular areas of the hypothalamus. Forty-one per cent of the progesterone receptor-containing cells in this area were calbindin immunopositive. No double-immunolabeled neurons could be detected in the infundibular (arcuate) nucleus. In tissue double-immunolabeled for progesterone receptor and parvalbumin, none of the progesterone receptor-containing neurons exhibited immunoreactivity for parvalbumin. Electron microscopic double-immunostaining for progesterone receptor and calbindin confirmed the light microscopic results. Furthermore, a large number of asymmetric synaptic contacts were observed on the calbindin-immunoreactive neurons. These observations demonstrate that progesterone receptor-containing cells in the monkey mediobasal hypothalamus consist of at least two different types of GABA neurons, and indicate that progesterone receptor-containing calbindin cells may be postsynaptic targets of excitatory fibers.

Animals↗
PubMed1992

Steroid hormones and CNS sexual dimorphisms modulate symptom expression in Tourette's syndrome.

We present our hypothesis that various steroid hormones play an important role in the symptom expression of Gilles de la Tourette's syndrome (TS) and that androgenic hormones, in particular, are likely to exacerbate symptoms of the disorder. We review the clinical evidence supporting our hypothesis. Sex steroids establish brain sexual dimorphisms early in CNS development, and we suggest mechanisms whereby androgenic and other hormonal changes later in human development might act at dimorphic brain regions to influence the natural history of TS. Finally, we discuss the various ways in which neuroendocrine studies might assist in genetic and neurobiologic research programs in TS.

Adolescent↗
PubMed1992

Estrogen-like effects of the mammary carcinogen 7,12-dimethylbenz(alpha)anthracene on hypothalamic neuronal membranes.

Previous studies have shown that in Sprague-Dawley female rats, but not in Wistar females, the mammary carcinogen dimethylbenz(alpha)anthracene (DMBA) results in extended preovulatory prolactin and estradiol surges, associated with inhibition of preovulatory gonadotropin surges, and in the induction of mammary tumors. Because earlier studies of similar endocrine states have shown this to be linked to hypothalamic arcuate nucleus neuronal membrane organization, in this study freeze-fracture methodology was used to determine whether DMBA may affect the ultrastructure of the neuronal membrane in the arcuate nucleus. The effects of estradiol valerate and DMBA were studied on 55- to 60-day-old cycling females, in Sprague-Dawley and Wistar rats, 8 weeks after the treatment. DMBA alone (15 mg/rat by gastric intubation) resulted in a significant decrease in the numerical density of intramembrane protein particles (IMP) in Sprague-Dawley rats but not in Wistar rats. The SC injection of estradiol valerate (1 mg/rat) resulted in a significant decrease of IMP numbers in both strains of rats. Although the subcutaneous injection of DMBA alone (1 mg/rat) did not affect IMP numerical density in either strain, the same potentiated the effect of estradiol valerate (1 mg/rat) on IMP's in Sprague-Dawley but not in Wistar females. These results indicate that DMBA affects the organization of neuronal plasma membrane in the hypothalamus of Sprague-Dawley rats. Wistar females are insensitive to both the endocrine and neuronal membrane effects of DMBA. Estradiol affected neuronal membranes in both strains and potentiated DMBA's effect. It appears that the estrogen-sensitive mechanism of DMBA activation may be lacking in Wistar rats.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1992

Transmitter content and afferent connections of estrogen-sensitive progestin receptor-containing neurons in the primate hypothalamus.

Progestin receptor-containing cells in the hypothalamus of the adult female green monkey (Cercopithecus aethiops) were examined by double-label immunocytochemical methods to determine their anatomical location, neurotransmitter content and afferent connections. Animals were ovariectomized and administered either estradiol valerate or the oil injection vehicle, and were sacrificed after 10 days of treatment. Using a monoclonal antibody raised against rabbit uterine progestin receptor (PR), the distribution of PR-immunoreactive cells in the mediobasal hypothalamus and the effect of estrogen treatment on this distribution was determined. PR-immunoreactive cells were found throughout the ventromedial nucleus (VMN), in the area between the VMN and fornix, and in the medial portion of the infundibular nucleus. Estrogen treatment dramatically increased both the number of labeled cells and the intensity of immunoreaction product in these regions. In double-immunostained sections, boutons immunoreactive for antigens indicative of serotonin, pro-opiomelanocortin derived peptides, GABA, catecholamine, neuropeptide Y, substance P, cholecystokinin, and somatostatin were demonstrated to establish synaptic contact with the soma of PR-immunoreactive hypothalamic neurons. In colchicine-pretreated animals, all PR-containing neurons in the mediobasal hypothalamus were found to contain immunoreactivity for glutamic acid decarboxylase, the enzyme required for synthesis of GABA. No evidence of colocalization with other antigens, including LHRH, was observed. Because LHRH neurons are known to receive a rich GABAergic innervation PR-containing GABAergic cells may represent steroid-sensitive sites of integration for inputs from other neural systems involved in the control of gonadotropin secretion.

Afferent Pathways↗
PubMed1992

Beta-endorphin innervation of dopamine neurons in the rat hypothalamus: a light and electron microscopic double immunostaining study.

Pharmacological data suggest that opiates, acting indirectly via the catecholaminergic system, are involved in the inhibition of LH release and the stimulation of PRL secretion. The aim of this study was to demonstrate on the ultrastructural level whether beta-endorphin-immunoreactive fibers form synaptic contacts with hypothalamic dopaminergic neurons. Light and electron microscopic double immunostaining experiments were performed on vibratome sections prepared from the hypothalamus of acrolein-fixed female rat brains. Immunoreactivity for beta-endorphin was visualized by a dark blue to black nickel ammonium sulfate-intensified diaminobenzidine reaction, and in a consecutive immunostaining procedure, the tyrosine hydroxylase-immunoreactive dopamine cells were labeled with the brown diaminobenzidine reaction product. Under the light microscope, beta-endorphin axon terminals were found to contact dopamine cell bodies and dendrites throughout the hypothalamus. The majority of opiate target dopamine neurons were found in the periventricular area, retrochiasmatic area, and lateral part of the zona incerta. A much smaller number was observed in the dorsomedial hypothalamic nucleus and the anterior hypothalamus, and only a very few dopamine cells could be detected in contact with beta-endorphin axons in the arcuate nucleus (particularly in the posterior part where the beta-endorphin cells are located) and the medial part of the zona incerta. After light microscopic examination and color photography, the double immunostained sections were embedded for correlated electron microscopy to verify and characterize the putative synaptic connections. Electron microscopy revealed symmetric synaptic connections between beta-endorphin-immunoreactive boutons and tyrosine hydroxylase-immunopositive cell bodies and dendrites. These results together with the observation of dopamine innervation of LHRH-producing neurons and progesterone receptor-containing cells indicate that neurons of the hypothalamic dopaminergic system probably mediate opiate effects on hypophyseal hormone secretion.

Animals↗
PubMed1992

Involvement of protein kinase-C in the mitogenic effect of insulin-like growth factor-I on rat astrocytes.

Insulin-like growth factor-I (IGF-I) stimulates the proliferation of many cell types, including astrocytes. Astrocytes are a population of brain cells highly enriched in IGF-I receptors, which unlike neurons, retain the ability to proliferate in the adult brain. Although astrocyte proliferation in response to IGF-I is well documented, the intracellular mechanisms that mediate this phenomenon are poorly defined. Interestingly, activation of protein kinase-C (PKC) by IGF-I has been observed in several cell types. In this report we first characterized the mitogenic effects of IGF-I on highly purified type I rat astrocyte cultures. Next, we determined whether IGF-I activates PKC in our cultures. Finally, since astrocyte proliferation is stimulated by both IGF-I and the phorbol ester 12-O-tetradecanoyl phorbol-13-acetate (TPA), we decided to test the possible involvement of PKC in the mitogenic activity of IGF-I on astrocytes. IGF-I stimulated the DNA synthesis rate in rat astrocytes. Analysis of the time course revealed that IGF-I (10 nM) induces maximal stimulation of [3H]thymidine incorporation (a 4-fold increase) 16-18 h after exposure. TPA also stimulated mitogenesis in our cultures. The dose-response of [3H]thymidine incorporation induced by IGF-I and TPA indicated that 10 nM was the lowest concentration producing a maximal effect for both agents. Analysis of proteins by Western blot revealed that 10 nM IGF-I translocates PKC(alpha), the predominant PKC isoform in astrocyte cultures, from the cytosol to the membrane fraction within 20 min. A similar activation of PKC was achieved with 100 nM TPA. When astrocytes were exposed to IGF-I (10 nM) and TPA (10 nM) in combination, [3H]thymidine uptake was significantly higher than the uptake induced by either IGF-I (10 nM) or TPA (10 nM) alone. However, the effect of IGF-I plus TPA was not fully additive. In a second experiment, the mitogenic effect of IGF-I was partially abolished in cells depleted of PKC by preincubation with high concentrations of TPA (300 nM). Finally, incubation of astrocytes with the PKC inhibitor H-7 at 20 microM, a concentration that completely blocked the mitogenic action of TPA, only reduced the ability of IGF-I to stimulate DNA synthesis by 50%. In summary, our results demonstrate that IGF-I can rapidly activate PKC in astrocytes, and that PKC activation is involved in the mitogenic effect of IGF-I on these cells. However, we conclude that IGF-I also stimulates astrocyte proliferation through PKC-independent pathways.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed1992

Neuropeptide-Y innervation of beta-endorphin-containing cells in the rat mediobasal hypothalamus: a light and electron microscopic double immunostaining analysis.

Central administration of neuropeptide-Y (NPY) inhibits pituitary LH release in ovariectomized rats and stimulates LH release in intact and ovariectomized rats pretreated with ovarian steroids. Although the precise neural mechanism of this dual effect of NPY is not known, experimental evidence suggests an underlying interaction between hypothalamic NPY and the inhibitory beta-endorphin (beta END) systems in the neuroendocrine regulation of pituitary LH release in the rat. The present study was undertaken to examine the morphological basis of the interaction between these two peptidergic systems in the hypothalamus. Sections of the mediobasal hypothalamus of colchicine-pretreated female rats were double immunostained for NPY and beta END and examined by light and electron microscopy. The light brown diaminobenzidine reaction was used to visualize beta END cells, while NPY neurons were labeled with a dark blue nickel ammonium sulfate-intensified diaminobenzidine reaction. Under the light microscope, a dense network of NPY-immunoreactive axons and axon terminals was observed in close apposition with beta END-immunoreactive neurons throughout the medial basal hypothalamus. Electron microscopic examination revealed that NPY-immunoreactive boutons formed axosomatic and axo-dendritic synaptic connections with beta END cells. A majority of these synaptic membrane specializations appeared asymmetrical [corrected]. In light of the previous evidence of excitatory and inhibitory effects on LH release and the existence of direct synaptic connections between NPY and LHRH neurons in the hypothalamus, the current results imply that the dual effects of NPY on LH secretion may involve modulation of LHRH secretion, both by the direct route and indirectly through the hypothalamic beta END system.

3,3'-Diaminobenzidine↗
PubMed1992

The in vitro perifused rat ovary: I. Steroid secretion in response to ramp and pulsatile stimulation with luteinizing hormone and follicle stimulating hormone.

A computer-controlled perifusion apparatus has been used to investigate the effects of different patterns of hormonal stimulation on secretion of steroids by ovaries from untreated, or pregnant mare serum gonadotropin (PMSG)-pretreated, immature rats. With ovaries from untreated rats, a low rate of increasing concentration of gonadotropins (luteinizing hormone (LH) plus follicle stimulating hormone (FSH)) induced a maximum secretion of estradiol within 60 min (22.6 +/- 1.4 pg/mg/30 min). An intermediate and a high rate of increasing gonadotropin concentration stimulated maximum secretion (26.0 +/- 1.2 pg/mg/30 min) and 28.1 +/- 2.8 pg/mg/30 min), respectively) within 30 min. Peak secretion, however, was not maintained and was reduced despite continued LH/FSH pulses. Progesterone secretion increased during, and subsequent to, the decreasing estradiol output. Increasing amplitudes of LH/FSH or constant perifusion with LH/FSH did not change the profile, or the concentration of estradiol, but these measures increased progesterone release. An occasional transient increase in estradiol secretion was observed when ovaries from unstimulated rats were perifused with low LH/FSH pulse frequency. Thus, these studies support the hypothesis that in the prepubertal rat ovary, elements of pulse characteristics, such as rate of increasing LH/FSH concentration, and amplitude are important in differentially regulating steroid output. The steroid secretory pattern of ovaries from PMSG-treated prepubertal rats was different from that of untreated rats. With ovaries from PMSG-treated rats, an acute increase in secretion of progesterone, testosterone or estradiol was not observed, whether low or high rates of increasing gonadotropin concentration were used. Rather, the concentration of these steroids continued to rise following LH/FSH pulses. Thus, in contrast to the untreated ovary, the PMSG-treated ovary did not show differential regulation of steroid secretion in response to LH/FSH. In conclusion, we have shown the in vitro perifusion model to be a useful tool for studying the effects of different patterns of hormonal stimulation on ovarian steroidogenesis. In addition, differential effects of gonadotropins on steroid output were shown, depending upon prior maturation of the ovary.

Animals↗
PubMed1992

The in vitro perifused rat ovary: II. Role of oxygen tension in the whole and quartered ovary.

In vitro perifusion of whole ovaries raises questions about tissue viability and its effects on the observed ovarian steroid secretion. To assess effects of tissue degeneration, whole and quartered ovaries from pregnant mare serum gonadotropin (PMSG-) treated immature rats were perifused for 8 h, employing various levels of pO2. Histological examination of both the whole and quartered ovary showed signs of degeneration in centrally located follicles but not in follicles located near the surface. However, basal and gonadotropin-stimulated (luteinizing hormone plus follicle stimulating hormone) secretion of estradiol, testosterone and progesterone were not significantly different in the whole ovary whether in the presence of high or low pO2 (n = 8; p > 0.05). Similarly, although the quartered ovary secreted greater amounts of steroids than did the whole ovaries (p < 0.05, n = 8), pO2 levels did not affect the steroid output. We conclude that during in vitro perifusion, minimal oxygen supply is sufficient for ovarian steroidogenesis to proceed. In addition, although quartered ovaries displayed some evidence of tissue degeneration, they were more responsive in terms of steroid output per mg ovary than were whole ovaries.

Animals↗
PubMed1991

Loss of sexual dimorphism in rat arcuate nucleus neuronal membranes with reproductive aging.

Arcuate neurons of the rat hypothalamus have a sexual dimorphic membrane phenotype: quantitative analysis of freeze-fracture replicas has revealed that a population of intramembrane protein particles (IMP) of small size (less than 10 nm) is enriched in the plasma membrane of perikarya and dendritic shafts of cycling females compared to males, whereas a population of large IMPs (greater than 10 nm) is enriched in the membrane of dendritic shafts of males. This different membrane organization is associated with a sex dimorphic synaptic connectivity. To determine whether sex differences in neuronal membrane are affected by reproductive senescence, IMPs were assessed in freeze-fracture replicas of arcuate neuronal plasma membranes of male and female Sprague-Dawley rats aged 3, 15, and 18 months. Three-month-old cycling females were studied on the morning of estrus. Senescent females were in constant estrus (15 months old) or in constant diestrus (18 months old). Young females had more IMPs with diameters under 10 nm in the inner and outer leaflets of the plasma membrane of the perikarya and dendritic shafts compared to males of the same age. In addition, young males showed an increased number of large (greater than 10 nm) IMPs in the outer membrane leaflet of dendritic shafts. No sex differences were detected in the membrane of dendritic spines. In senescent females the number of small IMPs was decreased in the perikarya and dendritic shafts compared to young females while the number of large particles was increased in the outer leaflet of the membrane of dendritic shafts, reaching values similar to those observed in males. IMP counts were not modified with aging in males and in dendritic spines of females. These results indicate that reproductive aging in female rats is associated with a remodeling of neuronal plasma membranes in arcuate neurons.

Aging↗