Rapid pulsatile corticosterone secretion in the rat is not confirmed

We attempted to confirm and extend a previous suggestion by other workers that, in the rat, corticosterone may be released as a series of very short pulses with a period of one minute. We measured the corticosterone concentration in the blood of chronically cannulated, unanaesthetised male rats, repeatedly, at ten second intervals, for periods of up to 25 minutes while the rats were engaged in normal activity or sleep or were subject to acute or chronic stress. We could find $\text{no}$ evidence of the proposed rapid pulsatile secretion and suggest that the earlier finding may have been artifactual.     

The effect of partial noradrenergic denervation on corticosterone secretion in the rat

DSP₄ (N-(-2-chloroethyl)-N-ethyl-2-bromobenzylamine) treatment significantly decreased the noradrenaline content in the hippocampus, frontal cortex and hypothalamus of the rat brain. DSP₄ treatment did not affect plasma corticosterone levels. Clonidine, an ₂-adrenoceptor agonist, had no effect on corticosterone secretion in either DSP₄- or saline-treated rats. Isoproterenol, a -adrenoceptor agonist, significantly stimulated corticosterone secretion. This effect was inhibited by the prior administration of the -adrenoceptor antagonist propranalol. DSP₄ treatment did not alter the isoproterenol-induced stimulation of corticosterone secretion. The administration of a high dose of dexamethasone (100 g/kg, i.p.) significantly decreased the plasma corticosterone concentration of saline-treated controls, while an intermediate dose (25 g/kg, i.p.) did not suppress corticosterone release significantly. DSP₄-treatment did not influence dexamethasone-induced suppression of corticosterone secretion. These results show that significant decreases in noradrenaline content in the hippocampus, frontal cortex and hypothalamus appear to have no effect on the regulation of corticosterone secretion and that corticosterone secretion may be stimulated by catecholamines via -adrenoceptors.     

海马内NA能神经损毁对抗急性低氧诱发皮质酮分泌

本工作观察了６羟多巴胺（６ｈｙｄｒｏｘｙｄｏｐａｍｉｎｅ,６ＯＨＤＡ）损毁大鼠腹侧海马去甲肾上腺素能神经对急性低氧诱发皮质酮分泌的影响。结果显示,吸入１０４％Ｏ２３０ｍｉｎ后血浆皮质酮水平显著升高,６ＯＨＤＡ注入腹侧海马致使海马内去甲肾上腺素（ＮＡ）含量降低（－３８５％）;血浆皮质酮水平也较未损毁组为低（－３３２％）。吸入１０４％Ｏ２后,皮质酮对低氧刺激的反应性升高现象消失。结果提示：海马内ＮＡ可能参与急性低氧应激引发血浆皮质酮分泌的调节活动。     

Episodic memory signals in the rat hippocampus

How does the hippocampus signal memory for episodes? In this issue of Neuron, Ferbinteanu and Shapiro show that classic place cell activity in the rat hippocampus together with robust retrospective and prospective memory signals reflects the sequence of past, present, and future events that make up an episode.     

Direct effects of IL-15 on corticosterone secretion by rat adrenocortical cells

Cytokines might regulate the function of the hypothalamic-pituitary-adrenal axis. IL-15 is a potent non-T-cell-derived cytokine with IL-2-like activities. It has been shown that IL-15 can reverse the inhibition of glucocorticoids on PBMC. In vitro experiments were designed to assess the direct effect of IL-15 on corticosterone (CORT) secretion in the adrenal zona fasciculata-reticularis (ZFR) cells of male rats. Administration of IL-15 dose dependently decreased the basal and adrenocorticotropin-stimulated release of CORT and production of cAMP in ZFR cells. The stimulatory effect of forskolin (an adenylate cyclase activator) on CORT secretion and accumulation of cAMP in ZFR cells was attenuated by the administration of IL-15. However, 8-Br-cAMP (a cAMP analogue)-stimulated release of CORT was not affected by IL-15. Exogenous administration of IL-15 (10(-7) mol/L) significantly attenuated the pregnenolone (the substrate of 3beta-hydroxysteroid dehydrogenase)- or deoxycorticosterone (the substrate of 11beta-hydroxylase)-induced release of CORT. The results indicate that decrease of CORT secretion by IL-15 is in part because of (i) the decrease of adenylate cyclase activity and cAMP production and (ii) the inhibition of 3beta-hydroxysteroid dehydrogenase and 11beta-hydroxylase activities in rat ZFR cells.     

Episodic LH secretion patterns in the mare during the oestrous cycle.

Jugular blood samples were obtained from 8 mares at 5- and/or 20-min intervals for 2 to 5 days during various phases of the oestrous cycle for plasma LH determination. An episodic release pattern was observed in 1 of 3 mares sampled during the ovulatory period. One mare had one secretory burst and the other mare had several periods of fluctuating plasma LH concentration. During dioestrus, episodic secretions were observed in 2 mares sampled 11 to 13 days before and, in 1 mare, 9 days after ovulation. During the 2 to 5-day period before ovulation, episodic secretion was not observed (3 mares) but plasma LH concentrations fluctuated as much as 6 ng/ml during a period of 3--4 h. Daily plasma samples were obtained form 10 mares (1--8 oestrous cycles/mare) during which 22 single, 18 double and 2 luteal-phase ovulations occurred. Dioestrous ovulations were accompanied by small increases in plasma LH (1--4 ng/ml), but many similar increases in LH were not accompanied by ovulation. No significant differences in secretory patterns were observed between single and multiple ovulations. In one mare, 4 ovulations occurred in the presence of a prolonged luteal phase; 3 were accompanied by increasing LH concentrations and the other occurred when LH was at a low concentration.     

Plasma corticosterone concentrations in the perinatal rat

1. Plasma corticosterone concentrations were determined in the foetal rat during the gestational period from day 18·5 to term and in postnatal rats over the first few hours after delivery. 2. The plasma corticosterone concentrations in foetal rats are as high as six times maternal values at day 19 of gestation and are approximately equal to maternal values from day 20 to term. 3. In postnatal rats the plasma corticosterone concentrations rise 3·5-fold on average within 5hr. of delivery. 4. The results are discussed in relation to the function of adrenal steroids in postnatal liver development.     

The effects of adrenalectomy and corticosterone replacement on induction of maternal behavior in the virgin female rat

Maternal behavior of the sensitized virgin rat is affected by approach-avoidance systems as well as by hypothalamic-pituitary-adrenal (HPA) axis, which is also activated during stress. The present experiments investigated the effects of adrenalectomy and of varying corticosterone concentrations on the onset and expression of maternal behavior in sensitized virgin rats. In the first experiment, latency to onset of maternal behavior and time spent licking once maternal were positively related to endogenous levels of corticosterone. However, few rats showed licking. In the second experiment, virgin rats were adrenalectomized or given sham surgeries before being sensitized and being given 0, 25, 100, 300, or 500 microg/mL of corticosterone in their drinking water. In the third experiment, virgin rats were adrenalectomized or given sham surgeries and given either control or corticosterone time-release pellets after being sensitized. Maternal behavior was then tested. Adrenalectomy increased licking in the second experiment and time over pups in the third experiment. Corticosterone replacement reduced licking in the second experiment and both licking and time over pups in the third experiment. In conclusion, exogenous corticosterone had an inhibitory effect on the expression of maternal behavior in the sensitized virgin rat, unlike the facilitatory effect previously found in the postpartum rat.     

The involvement of coated vesicles in the secretion of corticosterone by the zona fasciculata of the rat adrenal cortex

Following exposure of rats to unpredictable stress there was a marked increase in the number of ‘coated’ vesicles in contact with or close to the cell membrane of the zona fasciculata cells. The close correlation between the vesicle numbers and the plasma levels of corticosterone led to the hypothesis that the coated vesicles were intimately involved in the secretory process. The use of horseradish peroxidase as a tracer protein confirmed that the coated vesicles were not involved in pinocytosis and the inward movement of materials, this function being performed by a much larger uncoated vesicle. The presence of microtubules associated with the coated vesicles and radiating through the Golgi body region, the site of formation of the vesicles, suggested that they may be involved in the transport of the secretory product to the cell membrane. The use of microtubule inhibitors, colchicine and vinblastine, were found to significantly reduce the plasma steroid response to stress. On the basis of these findings a new secretory mechanism was postulated.     

Effects of chronic hypogonadism on corticosterone secretion and cyclic AMP production in male rat adrenocortical cells

AIM: To determine the secretion of corticosterone (CCS) both in vivo and in vitro during different intervals after orchidectomy in male rats. METHODS: Three- and 12-month-old rats had been orchidectomized 0, 3, 6, or 9 months before decapitation. RESULTS: Orchidectomy increased the concentrations of plasma CCS, the basal release of CCS, and the adenosine 3', 5'-cyclic monophosphate (cAMP) production in rat zona fasciculata reticularis (ZFR) cells. The forskolin/3-isobutyl-l-methylxanthine-stimulated releases of CCS and cAMP production by ZFR cells were higher in rats with chronic hypogonadism. The CCS release from ZFR cells of orchidectomized rat was not altered by 8-bromo-cAMP treatment. Orchidectomy enhanced the stimulatory effect of deoxycorticosterone on CCS release in ZFR cells. CONCLUSION: These results suggest that orchidectomy-related increases of CCS secretion in rats are associated with an increase of adenylate cyclase activity, cAMP generation, and 11-beta-hydroxylase activity in ZFR cells.     

Triiodothyronine (T3) modulation of gonadotropin secretion in the female rat.

The effect of T3 upon gonadotropin secretion was examined in ovariectomized (Ovarx), Ovarx thyro-parathyroidectomized (Ovarx-TxPx), or proestrus rats. T3 (50 microgram/-100 gBW), administered late diestrus-2, abolished the LH surge during the critical period of proestrus in 7 out of 9 rats; the rise in sera FSH was not inhibited, although a distinct peak was absent. Administration of 5 or 50 microgram T3/100gBW 2.5h before the critical period resulted in either a suppression or an alteration of the timing of LH release. In the 5 microgram T3/100gBW treated animals the sera FSH peak was delayed in timing, whereas in the 50 microgram T3/100gBW treated rats sera FSH demonstrated two separate peaks during the critical period. Treatment with various dosages of T3 of Ovarx-TxPx rats resulted in significant suppressions (p less than 0.05) of sera LH and FSH. Despite depressed concentrations of sera LH and FSH in T3-treated rats pituitary sensitivity to a challenge of 3LHRH was enhanced. Hence, the pituitary was not the site of T3 inhibition of gonadotropin secretion. Additionally, T3 did not modify pituitary LH content or hypothalamic LH3 releasing activity (LHRH). Since T3 did not inhibit gonadotropin secretion at the pituitary level, a neural site of T3 action is suggested.     

Features of ginseng saponin-induced corticosterone secretion.

Ginseng saponin administered intraperitoneally to rats induced a significant rise in plasma corticosterone, while it tended to increase plasma glucose and to decrease plasma immunoreactive insulin. Oral or intraperitoneal administration of ginseng saponin increased plasma corticosterone in unanesthetized, pentobarbital-anesthetized or alloxan-diabetes rats. The histamine-induced rise in plasma corticosterone was suppressed by pretreatment with diphenhydramine, whereas the ginseng-induced rise was not. Ginseng saponin decreased rectal temperature while it increased plasma corticosterone. Ginseng-induced corticosterone secretion was superimposed on the basal levels of plasma corticosterone due to fasting and circadian rhythm. Thus ginseng saponin would be a kind of stressful agent and have different features associated with the stimulation of the pituitary-adrenocortical system from several other chemical agents.     

Antioxidant ionol suppresses ACTH-dependent secretion of corticosterone

It has been shown that the preliminary administration of a synthetic antioxidant ionol (dibunol, BHT) prevented to a considerable extent the increase in the concentration of corticosterone in the adrenal glands and blood plasma induced by ACTH administration or emotional-painful stress.