Steroid priming promotes oxytocin-induced norepinephrine release in the ventromedial hypothalamus of female rats

In vivo microdialysis was used to detect norepinephrine (NE) release in the ventromedial hypothalamus of estradiol (E₂)- or E₂ plus progesterone (P)-treated female rats injected with 1.0 IU of oxytocin (OXY). Dialysates were collected before and after OXY administration on 3 consecutive days and analyzed for NE content by high performance liquid chromatography with electrochemical detection. After the last sample was collected on day 1, animals were injected with 3 μg E₂ benzoate or oil. On day 3, E₂-primed animals received 200 μg of P and control females received oil prior to OXY administration. OXY administration did not induce NE release on day 1. When OXY was administered to animals that received E₂ approximately 20 h earlier, increased release of NE was not consistently seen. In contrast, E₂-primed animals that received P on day 3 displayed significant increases in the release of NE after OXY administration compared to their own basal levels and to NE levels in control animals. To distinguish whether E₂ priming is sufficient to promote OXY-induced release of NE without the addition of P, NE content of VMH dialysates in a second group of animals was examined following exposure to vehicle or E₂ alone. When OXY was administered 24 or 48 h after estrogen priming, only 1 of 4 E₂-primed females had modestly elevated dialysate NE levels. To evaluate the interactions between OXY and NE in the regulation of reproductive behavior, lordosis responses were observed in hormone-primed female rats receiving systemic injections of OXY, the ₁-adrenoceptor antagonist prazosin, or both OXY and prazosin. OXY enhanced lordosis behavior in females primed with subthreshold doses of E₂ and P. Prazosin abolished lordosis behavior in rats primed with behaviorally effective doses of E₂ and P and significantly inhibited lordosis in steroid-primed females given OXY. These data suggest that after priming with both E₂ and P together, but not with E₂ alone, OXY may facilitate lordosis behavior through activation of NE transmission.     

Oxytocin but not vasopressin facilities social recognition following injection into the medial preoptic area of the rat brain

Social recognition of juvenile rats by adult male residents has been shown to be modulated by peripheral administration of neurohypophyseal hormones vasopressin and oxytocin. In the present study, the effects of these peptides on social recognition were investigated after local injection into the medial preoptic area of the hypothalamus. It was found that oxytocin given in a wide range of doses (0.3–1000 pg) facilitated social recognition. This effect was not blocked by pretreatment with oxytocin receptor antagonist desGly(NH₂)⁹-d(CH₂)₅[Tyr(Me)²Thr⁴]OVT. Oxytocin injected into the septum in doses of 0.03–3 pg was not effective. Administration of vasopressin (100 or 1000 pg), [pGlu⁴,Cyt⁶]AVP-(4-8) (200 pg) or [pGlu⁴,Cyt⁶]AVP-(4-9) (200 pg) into the medial preoptic area did not influence social recognition. It is concluded that the medial preoptic area is a sensitive brain site for the oxytocin-induced facilitation of social recognition in rats.     

Regulation of transmitter release by high-affinity group III mGluRs in the supraoptic nucleus of the rat hypothalamus

We analyzed the subtypes of group III metabotropic glutamate receptors (mGluRs) modulating inhibitory and excitatory transmission in the rat supraoptic nucleus. Bath application of the agonist l-AP4 at 200 microM, a concentration that activates all group III mGluR subtypes, inhibited the frequency but not the amplitude of miniature inhibitory and excitatory postsynaptic currents, indicating a presynaptic site of action. l-AP4 at low concentrations (10 microM), as well as ACPT-1 (50 microM), a specific mGluR III agonist, inhibited transmission at GABAergic and glutamatergic synapses to the same extent as 200 microM l-AP4. Because the potency of l-AP4 and ACPT-1 is much higher on mGluR4 and mGluR8 than on mGluR7, these results are consistent with the presence of high-affinity group III mGluRs regulating transmitter release in this nucleus. In agreement with these findings, DCPG (30 microM), a selective mGluR8 agonist, induced a significant depression of inhibitory and excitatory synaptic currents. Group III mGluRs such as mGluR8, because of their high affinity for glutamate, are particularly well suited to detect small changes in the concentration of this excitatory amino acid in the extracellular space. Their presence, therefore, may favor the negative feedback control exerted by glutamate on its own release as well as the intersynaptic crosstalk mediated by glutamate spillover on adjacent synapses.     

5alpha-Reduced androgens block estradiol-BSA-stimulated release of oxytocin

In this study we test the postulate that estradiol conjugated to bovine serum albumin (E-BSA) acts via receptors for the steroid-binding protein sex hormone binding globulin (SHBG) by attempting to block E-BSA-stimulated release of oxytocin with two antagonists of SHBG receptor actions: the 5alpha-reduced androgens dihydrotestosterone (DHT) and 3alpha-diol. Simultaneous superfusion with either DHT or 3alpha-diol significantly blocked E-BSA-stimulated release of oxytocin. We also found that a wide range of free 17beta-estradiol was unable to stimulate oxytocin release, suggesting that E-BSA stimulates receptors other than those for free estradiol to release oxytocin, perhaps SHBG receptors.     

Taurine and the control of basal hormone release from rat neurohypophysis

Pituicytes of pituitary neural lobe are rich in the amino acid taurine, which they release upon hypoosmotic stimulation. As a generally inhibitory amino acid, taurine is thought to activate receptors on neural lobe nerve terminals and exert some control over hormone release. Previous work has shown the presence of glycine and GABA(A) receptors in neural lobe, both of which have affinity for taurine. Using a perifused explant system, we studied the effects of taurine activation of glycine and GABA(A) receptors on basal hormone release. Somewhat surprisingly, taurine induced increases in basal release of both vasopressin and oxytocin. Taurine-induced increases in oxytocin release were blocked by bicuculline, suggesting involvement of GABA(A) receptors. Increases in vasopressin release were not blocked by bicuculline, indicating involvement of receptors other than GABA(A). Although combined bicuculline and strychnine, an antagonist at most glycine receptors, also did not block increased vasopressin release, picrotoxin (a Cl(-) channel blocker) was effective in blocking increases in both vasopressin and oxytocin release. The other receptor(s) involved in taurine actions is postulated to be strychnine-insensitive glycine receptors. Thus, taurine in neural lobe may act via both a GABA(A) receptor and one or more types of glycine receptors to depolarize nerve terminal membranes under basal conditions. Taurine-induced partial depolarization resulting in Na(+) channel inactivation is probably responsible for its previously observed inhibition of stimulated hormone release from neural lobe.     

Neuropeptide specificity of prostaglandin E2-induced activation of splenic and renal sympathetic nerves in the rat

Sympathetic activation occurs rapidly following intracerebroventricular (icv) injection of prostaglandin E2(PGE2). This study examined whether neuropeptides mediate PGE2-induced sympathetic nerve activation in urethane/chloralose-anesthetized Sprague-Dawley rats. Animals were pretreated (20.0 microg, icv) with the following receptor antagonists; CRF ([D-Phe12,Nle21,38,Calpha-MeLeu37]CRF12-41), AVP-V1 (Des-Gly-[Phaa1, D-Tyr(Et)2,Lys6,Arg8]-vasopressin), or OT (OT+V1, [d(CH2)5,Tyr(Me)2,Orn8]-vasotocin) followed 20 min later by PGE2 (2.0 microg, icv). Pretreatment with the CRF antagonist attenuated the increase in renal nerve activity induced by PGE2 when measured 10 and 30 min post-injection. PGE2-induced renal nerve activity was also inhibited at both time points by the AVP antagonist and, to a similar extent, the OT antagonist. The AVP antagonist did not effect splenic nerve responses to PGE2 whereas the CRF antagonist produced an incomplete and transient reduction in PGE2-induced activation of the splenic nerve. However, the OT antagonist completely blocked the activation of the splenic nerve after central injection of PGE2. ICV injections of AVP and OT produced immediate changes in splenic and renal nerve activity whereas CRF failed to alter the activity of either nerve in anesthetized or conscious animals. Thus, PGE2 acts through neuropeptide-specific pathways to initiate sympathetic outflow and OT is a specific component of the sympathetic pathway innervating the spleen.     

Conversion between configurational states of the muscarinic receptor in rat brain

Reductive alkylation of neural membranes by N-ethyl maleimide (NEM) converts muscarinic acetylcholine receptors from a state of low to high affinity for receptor agonists. Interactions of muscarinic antagonists with the receptor are unaffected by this treatment. Muscarinic receptors from the rat telencephalon in the high agonist affinity state are increased from 34.2 to 53.4% of the total receptor population and the Ki for carbamylcholine inhibition of 3-quinuclidinyl benzilate binding is decreased from 1.2 X 10(-4) to 6.9 X 10(-5) M by NEM treatment.     

Differential effects of naloxone on neuroendocrine responses to fear-related emotional stress

Summary The effects of an opioid receptor antagonist, naloxone (NAL), were studied on the changes in pituitary hormone secretion induced by emotional stress. Male Wistar rats were trained with tone stimuli paired with electric footshocks and tested with the tone and environmental cue signals for emotional stress of fear acquired by learning as described previously (Onaka et al. 1988). Rats received s.c. injected NAL 30 min before testing at doses of 0, 0.2, 1.0, 5.0 and 25.0 mg/kg b.w. Half the rats were injected with 0.5 M NaCl (20 ml/kg b.w.) together with NAL. In these hypertonic rats plasma vasopressin level was slightly increased after NAL. The increment was statistically significant in control groups but not in experimental groups. However the suppression of vasopressin secretion by emotional stimuli was not changed by NAL. Plasma oxytocin levels were extremely high and not significantly different among experimental, unshocked control and untested control groups. NAL further increased the oxytocin level dose-dependently. NAL did not significantly change plasma adrenocorticotrophic hormone (ACTH) levels and hence did not modify the augmentative response in ACTH secretion to emotional stimuli. Plasma prolactin level was significantly elevated after emotional stimuli and NAL depressed the prolactin level in each of experimental and control groups. After NAL, the magnitude of the facilitatory response in prolactin secretion to emotional stimuli was decreased. Motor activity and its suppressive response to emotional stimuli were not influenced by NAL. In another half of rats under a normal osmotic condition the vasopressin response to emotional stimuli was not affected by NAL. NAL further augmented potentiation of oxytocin secretion after emotional stimuli dose-dependently. Effects of NAL on ACTH level, prolactin level and motor activity were similar to those in rats under hypertonic conditions. These results demonstrate that endogenous opioids are selectively and differentially involved in hypothalamo-hypophysial responses to fear-related emotional stress.     

产时催产素静脉滴注对脐动脉血血气分析影响的初步研究

本文以１０２例静脉滴注催产素的产妇和６０例正常分娩的产妇分别作为观察组和对照组，于胎儿娩出时即刻取脐动脉血进行血气分析测定。结果经统计学处理，发现：（１）观察组中碱剩余（ＢＥ）和细胞外液碱超（ＳＢＥ）两项负值增加，与对照组相比有明显差异（Ｐ〈０．０５）；（２）脐动脉血气各项指标与静滴时间（８ｈ内）无明显相关性（Ｐ〉０．０５）；（４）随第二产程的延长，两组ＰＨ、ＢＥ及ＳＢＥ均呈下降趋势，对照组下降极     

产程中使用催产素与新生儿高胆红素血症的关系

本研究采用经皮脸红素测定仪跟踪监测了1993年4月～1993年6月间在本院出生的96名足月健康新生儿生后一周内黄疸的动态变化，按其母亲产程中是否使用催产素分两组，进行统计对比分析，结果发现使用催产素后出生的新生儿黄疸发生率高，程度重。黄疸的程度与催产素的使用剂量和使用时间有关，催产素使用剂量越大，使用时间越长，黄疸的程度越重，说明催产素对新生儿高胆红素血症的发生有影响。