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Biomedical subjects

H Jarry

Publications and source records attributed to H Jarry.

103 records · Page 6Linked to original sources
PubMed1988

Pituitary-dependent effects of estradiol-17-beta on catecholamine turnover rates, gamma-aminobutyric acid and glutamate concentrations in various hypothalamic and limbic brain structures.

Estrogens exert many effects in a variety of hypothalamic and mesolimbic structures. Whether the actions of the estrogens are direct or indirect, possibly involving anterior pituitary hormones, is largely unknown. We therefore studied catecholamine turnover rates, gamma-aminobutyric acid and glutamate concentrations in various hypothalamic and mesolimbic structures in estrogen-treated hypophysectomized (hypox) rats and compared the measured parameters with those in sham hypophysectomized (sham) animals. Results clearly demonstrate that many of the effects of estrogen require an intact pituitary. Dopamine turnover rates in hypox rats were significantly reduced in the hypothalamus and the striatum, whereas they increased in the medial septum and medial preoptic area in comparison with sham rats. Norepinephrine turnover rates were reduced in the anterior mediobasal hypothalamus, somatosensory cortex and the nucleus accumbens of hypox animals in comparison with the sham-operated animals. In contrast, norepinephrine turnover was accelerated in the mediocortical amygdala and posterior medial basal hypothalamus of hypox rats. A significant reduction of epinephrine turnover was evident in the nucleus accumbens of hypox rats. Gamma-aminobutyric acid concentrations increased in the medial septum, anterior and posterior part of the mediobasal hypothalamus, but decreased in the mediocortical amygdala of hypox animals. Concentrations of glutamate were also decreased in the mediocortical amygdala in hypox animals. These results indicate that many direct effects of estrogens in the brain are accompanied by indirect effects which require an intact pituitary.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Further evidence that preoptic anterior hypothalamic GABAergic neurons are part of the GnRH pulse and surge generator.

The in vivo release rates of GABA from the preoptic/anterior hypothalamic area (PO/AH) of ovariectomized rats were assessed by means of a focal perfusion cannula system. Seven days after surgery all animals received a sc silastic capsule implant containing either estradiol-17 beta (E2) or corn oil, and they were perfused 3 days later. Perfusate fractions were sampled at 5-min intervals and blood was collected every 10 min over a period of 5 h. In ovariectomized animals PO/AH GABA release was pulsatile without any diurnal rhythm. Prior to frequency analysis by means of the pulsar-programme, LH and GABA values were z-transformed. Significant LH peaks of all examined ovariectomized rats were superimposed and GABA data were arranged accordingly. It became evident that LH episodes are preceded by a significant reduction of preoptic anterior hypothalamic GABA release. The secretion patterns of GABA and LH were profoundly affected by E2 replacement. During early noon when LH levels were low, constantly elevated hypothalamic GABA release rates were observed in E2-substituted rats in comparison to ovariectomized rats. GABA release rates fell significantly during the E2-induced LH surge. Our previous demonstration of the existence of a large number of estrogen-respective GABAergic neurons in the PO/AH is suggestive of these neurons changing their activity in response to estrogen treatment. We conclude that these estrogen-respective GABAergic neurons are involved in the generation of GnRH pulses as well as in the generation of the so-called positive feedback effect of E2 on LH release.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Angiotensin II/III and substance P in human follicular fluid obtained during IVF: relation of the peptide content with follicular size.

Ovarian follicular fluid (FF) of a number of species contain regulatory peptides secreted by granulosa cells or by autonomic nerve terminals. In this report we demonstrate the presence of authentic (HPLC-verification) angiotensin II and III as well as of substance P (SP) in human FF obtained from hMG stimulated infertile patients undergoing in vitro fertilization. Angiotensin II/III (AII/III), estradiol (E2) and progesterone concentrations increase with the size of the follicles. SP concentrations did not vary significantly in FF of various sizes. These peptide concentrations in FF are about 10-fold higher than those measured in the serum of the same patients. Attempts to correlate SP, AII/III, E2 and progesterone concentrations in the individual FF with the ability of an oocyte to be fertilized, failed. Neither AII/III, SP, E2 nor progesterone concentrations were different in these subclasses of FF. Follicles of patients punctured under general anesthesia contained significantly more SP than follicles of patients which had lumbar analgesia. AII/III concentrations were the same in FF of both treatment groups. The presence of angiotensin II and III in FF in increasing concentrations depending on the maturity of the follicle and the inability of general anesthesia to affect the AII/III concentrations suggests that this peptide is produced within the ovary.

Anesthesia, General↗
PubMed1987

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↗
PubMed1986

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↗
PubMed1986

Neurochemical characterization of the actions of 5-amino-2,4- dihydroxy-alpha-methylphenylethylamine (5-ADMP): a selective neurotoxin to central noradrenergic neurons.

The concentrations of amine neurotransmitters [dopamine (DA), norepinephrine (NE) and 5-hydroxytryptamine] and some of their deaminated metabolites [dihydroxyphenylacetic acid and 5-hydroxyindoleacetic acid] were determined in selected regions of the rat brain, including several hypothalamic nuclei, at various times after the i.c.v. injection of various doses of 5-amino-2,4-dihydroxy-alpha-methylphenylethylamine (5-ADMP). Seven days after a single i.c.v. injection of 100 micrograms of 5-ADMP the concentration of NE in all brain regions examined was reduced markedly, as was the concentration of DA in the median eminence. The concentrations of DA and dihydroxyphenylacetic acid in regions other than the median eminence, and the concentrations of 5-hydroxytryptamine and 5-hydroxyindoleacetic acid in all regions analyzed were unaltered. Multiple injections of 5-ADMP (100 micrograms i.c.v. every 48 hr X 3) did not increase the NE depletion, but caused slight decreases in DA and 5-hydroxytryptamine in some regions. The NE concentrations in hypothalamic nuclei were reduced significantly 4 hr after 100 micrograms i.c.v. administration of 5-ADMP and this depletion was maintained for at least 28 days. The 5-ADMP-induced decline of NE in all brain region, but not the decline of DA in the median eminence, was prevented partially by pretreatment with desipramine. These results indicate that 5-ADMP is a relatively specific neurotoxin for NE neurons, being particularly effective in destroying NE nerve terminals in the hypothalamus.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1985

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↗
PubMedDate not supplied

[Cranial irradiation induces premature activation of the gonadotropin-releasing-hormone].

BACKGROUND: CNS-irradiation in prepubertal children with leukemia or brain tumors can lead to precocious or in high doses to delayed puberty. The underlying mechanisms of these disorders are unknown. METHODS: A new animal model of experimentally induced pubertal disorders by cranial irradiation has been developed. In infantile or juvenile (12 - 23 days old) female rats precocious or delayed puberty have been induced by selective cranial Co60-irradiation (4 - 18 Gy). At age of 32 - 38 days or 3 months relevant hormone parameters have been studied basal and after stimulated conditions. RESULTS: Low radiation doses (5 or 6 Gy) led to accelerated onset of puberty as well as elevated LH- and estradiol levels. High radiation doses (9 - 18 Gy) caused retardation of sexual development, lower gonadotropin levels and growth retardation associated with growth hormone deficiency. After cranial irradiation with 5 Gy the release rates of the inhibitory neurotransmitter gamma-aminobutyric-acid (GABA) from hypothalamic explants were significantly lower (p < 0,05). The gonadotropin-releasing-hormone (GnRH) expression in the hypothalamic preoptic area of irradiated animals (5 Gy) was significantly higher than in controls (p < 0,05). CONCLUSION: The GnRH-pulse generator is very radiosensitive as low dose irradiation causes precocious puberty, whereas high dose irradiation is associated with delayed sexual maturation. Radiation induced precocious puberty might be caused by damage to inhibitory GABAergic neurons leading to desinhibition and premature activation of GnRH neurons. Our animal model of cranial irradiation seems to be suitable to study neurotransmitter disorders, molecular mechanisms and potential preventive intervention of radiation induced pubertal changes.

Abnormalities, Radiation-Induced↗
PubMedDate not supplied

Effects of endotoxin on in vitro release of LHRH and amino acid neurotransmitters by preoptic mediobasal hypothalamic fragments.

Alterations in the immune system are often accompanied by reproductive disorders. The bacterial endotoxin lipopolysaccharide (LPS) has central inflammatory effects, and activates the release of cytokines (immune system mediatory factors) in the hypothalamus, where the LHRH neurons are located. Therefore, these studies were designed to investigate a possible effect of the LPS and LHRH secretion and the possible interaction with excitatory and inhibitory amino acids. Animals were decapitated at 09.00 h, and the preoptic mediobasal hypothalamic area (PO/MBH) dissected and superfused. Superfusate fractions were collected at 15-min intervals. After a stabilization superfusion period of 60 min four fractions were collected; LPS (100 ng/ml) was then added to the superfusion medium for the duration of 1 h. This was followed by a washout period of 60 min. The PO/MBH fragments were then subjected to a 56 mM K+ stimulus. Control PO/MBH fragments were continuously superfused with Earle's balanced salt solution. LHRH release was significantly (p < 0.05) reduced during and following exposure to LPS. At this time GABA and taurine concentrations increased in the superfusion medium, while glutamate decreased significantly compared with the control group. These observations indicate that LPS inhibits LHRH and glutamate release, but stimulates taurine and GABA secretion. These effects may be explained by the stimulation of cytokines of neuronal and/or glial source which may interact with the excitatory and inhibitory amino acids.

Animals↗
PubMedDate not supplied

Bacterial endotoxin inhibits LHRH secretion following the increased release of hypothalamic GABA levels. Different effects on amino acid neurotransmitter release.

Immune system disorders are often accompanied by alterations in the reproductive axis. The bacterial endotoxin (lipopolysaccharide, LPS) has inflammatory effects and activates cytokine release in the pituitary and hypothalamus. LPS inhibition of luteinizing-hormone-releasing hormone (LHRH) release at the hypothalamic level appears to be associated with modifications in the inhibitory GABAergic neurotransmitter system. Then, knowing that gamma-aminobutyric acid (GABA) mediates other neurotransmitter effects in the central nervous system, the possibility arises that this amino acid might mediate the effect of LPS on LHRH release by modifying amino acid neurotransmitter release at the hypothalamic level. Therefore, the present study was designed to investigate a possible mediatory function of the GABAergic system in the LPS-induced inhibition of LHRH secretion. To this end, the modifications in the excitatory (glutamate, Glu) and inhibitory (taurine, Tau, and GABA) amino acid neurotransmitter release after the application of GABA-A and GABA-B antagonists, respectively, were studied and the effects of LPS on their release determined. Male rats were decapitated at 9.00 h, and the preoptic/mediobasal hypothalamic area (POA/MBH) was dissected and superfused with Earle's balanced salt solution. Superfusate fractions were collected at 15-min intervals after a 60-min stabilization superfusion period. LPS (100 ng/ml) was then added to the superfusion medium over 1 h in three different experimental designs: (1) LPS only (2) LPS simultaneously with bicuculline (GABA-A antagonist) or with phaclofen (GABA-B antagonist), and (3) LPS and subsequently bicuculline or phaclofen, performed in different experiments. This was followed by a wash-out period. The POA/MBH fragments were then subjected to a 56-mM K+ stimulus. Control POA/MBH fragments were continuously superfused with Earle's solution. As expected, LHRH release was significantly reduced (p < 0.05) during and following exposure to LPS. At the same time, GABA and Tau concentrations increased in the superfusion medium, while Glu decreased significantly compared with the control group. The GABA antagonists blocked and reversed the LPS effect on LHRH secretion. No significant differences were found between the effect of GABA-A and-B receptor antagonists. Meanwhile, GABA levels measured in the control group did not increase since they were the same as when LPS was added alone. Furthermore, LPS was without effect on Glu and Tau release in the presence of the GABA blockers. Therefore, the effect of the bacterial endotoxin was blocked. These observations indicate that there is an increase in GABA release that becomes significant at the same time when LHRH release is decreased. This effect can be blocked by GABA-specific receptor blockers. The effect of LPS is thus exerted by increasing GABA. The elevated GABA levels may also reduce Glu release and enhance Tau release. These modifications in neurotransmitter release may also contribute to LHRH suppression. These effects may be explained by the stimulation of cytokines of neuronal and/or glial origin that interact with the excitatory and inhibitory amino acids.

Animals↗