Opioid inhibition of luteinizing hormone secretion in the postpartum lactating sow

Twelve lactating sows were used at 22.4 +/- 0.8 days postpartum to determine whether endogenous opioid peptides (EOP) are involved in the suckling-induced inhibition of luteinizing hormone (LH) secretion. Four sows each received either 1, 2, or 4 mg/kg body weight of naloxone (NAL), an opiate antagonist, in saline i.v. Blood was collected at 15-min intervals for 2 h before and 4 h after NAL treatment. All sows were then given 100 micrograms gonadotropin-releasing hormone (GnRH) in saline i.v., and blood samples were collected for an additional h. Pigs were weaned after blood sampling. At 40 h after weaning, sows were treated and blood samples collected as during suckling. Serum concentrations of LH after treatment with NAL were similar for all doses; therefore, the data were pooled across doses. During suckling, serum concentrations of LH were 0.41 +/- 0.04 ng/ml before NAL treatment, increased to 0.65 +/- 0.08 ng/ml at 30 min after NAL treatment, and remained elevated above pretreatment concentrations for 120 min (p less than 0.05). Naloxone failed to alter serum concentrations of LH after weaning. These data indicate that EOP may be involved in the suckling-induced suppression of LH secretion and that weaning may either decrease opioid inhibition of LH secretion or decrease pituitary LH responsiveness to endogenous GnRH released by NAL.     

Absence of brain opioid peptide modulation of luteinizing hormone secretion in the prepubertal gilt

Three experiments were conducted to evaluate the role of endogenous opioid peptides (EOP) in modulating luteinizing hormone (LH) secretion in the prepubertal gilt. In Experiment I, 8 prepubertal (P) gilts, 160-170 days of age (puberty = 197 +/- 10 days), received either 1 (n = 2), 3 (n = 3), or 6 (n = 3) mg/kg BW of naloxone (NAL), an opiate antagonist, in saline i.v. Blood was collected by jugular vein cannula every 15 min for 2 h before and 2 h after NAL. All doses of NAL failed to alter serum LH concentrations. In Experiment II, 21 P gilts 160-170 days of age and 21 mature (M) gilts were ovariectomized (OVX). At the time of OVX, gilts were classified as prepubertal if their ovaries were devoid of corpora albicantia and corpora lutea. Three weeks after OVX, P and M gilts were injected twice daily for 10 days with either 0.85 mg/kg BW of progesterone (P4) or oil vehicle (V), resulting in the following groups: PP4 (n = 11), PV (n = 10), MP4 (n = 11), and MV (n = 10). All gilts received 1 mg/kg BW of NAL on the last day of treatment. Blood samples were collected via a jugular cannula every 15 min for 4 h before and 2 h after NAL treatment. NAL treatment resulted in an increase (p less than 0.05) in serum LH concentrations only in the MP4 gilts. In Experiment III, 15 OVX gilts 280 days of age were used. Ten of the 15 gilts were OVX prior to puberty at 160 days of age and were classified as chronologically mature (CM) at the time of treatment. The remaining 5 gilts were OVX after puberty, and were classified as sexually mature (SM) at the time of treatment.(ABSTRACT TRUNCATED AT 250 WORDS)     

天麻素对CUS大鼠抑郁样行为和海马BDNF/GDNF水平的影响

目的:探讨天麻素对慢性不可预见应激(CUS)大鼠抑郁样行为的改善作用及对海马脑源性神经营养因子(BDNF)及胶质原纤维酸性蛋白(GDNF)表达的影响。方法:将64只SD大鼠随机分为对照组(Sham),Sham+天麻素低、中、高剂量组,模型组(CUS),模型(CUS)+天麻素低、中、高剂量组,每组8只。对照组每天腹腔注射生理盐水(1 m L/kg),连续14天;Sham+天麻素低、中、高剂量组每天腹腔注射不同剂量的天麻素(50、100或者200 mg/kg),连续14天;模型组接受CUS造模,并且在造模结束后每天腹腔注射生理盐水(1 m L/kg),连续14天;模型+天麻素低、中、高剂量组在CUS造模结束后每天腹腔注射不同剂量的天麻素(50、100或者200 mg/kg),持续14天。随后,通过糖水偏好实验和强迫游泳实验检测各组大鼠的抑郁样行为,在行为学检测结束后处死大鼠,通过Elisa检测海马GFAP和BDNF的表达情况。结果:(1)慢性不可预见应激(CUS)可以导致明显的抑郁样行为,包括糖水偏好减少(P0.05)和强迫游泳不动时间增加(P0.01),CUS组大鼠海马GFAP和BDNF水平下降(P0.01)。(2)一定剂量(100和200 mg/Kg)天麻素干预可以缓解CUS大鼠的抑郁行为,CUS与CUS+GAS(M)组(P0.05)以及CUS与CUS+GAS(H)组之间(P0.01)存在显著性差异。(3)中高剂量的天麻素可以恢复CUS大鼠海马的BDNF和GDNF水平,CUS与CUS+GAS(M)组(P0.05)以及CUS与CUS+GAS(H)组之间(P0.05)的BDNF和GDNF水平存在显著性差异。结论:天麻素可以缓解CUS模型大鼠抑郁样行为,恢复CUS模型大鼠海马的BDNF和GDNF水平。     

Opiate antagonist treatment reinstates estrous cycles in middle-aged persistent-estrous rats

Middle-aged female rats display luteinizing hormone (LH) surge deficits and cycle irregularity followed by the onset of persistent estrus (PE). The central nervous system has been identified as a primary locus of failure in PE rats, but the particular neural elements involved have not been determined. The goal of the present study was to identify a role for endogenous opioid peptides (EOP) in age-related acyclicity by evaluating the effect of opiate antagonist treatment on vaginal cytology in PE rats. PE rats were administered, s.c., saline (SAL), naloxone (NAL) or naltrexone (NTX) once daily for 20 days, or repetitively on Day 1 and on successive proestrus days if cyclicity was resumed. Single NTX (50 mg/kg), but not NAL (2 mg/kg), treatment interrupted the PE state in almost half of treated animals. Daily or repetitive proestrus NTX (10 mg/kg) treatment interrupted PE more frequently, and many animals displayed repeated estrous cycles and ovulation. Afternoon LH surges were observed after initial NTX treatment in animals displaying PE interruption. This demonstration that LH surges and ovulatory cycles can be reinitiated in PE rats with NTX suggests that dysfunction in the 'brake' on EOP secretion during proestrus may be one of the neuroendocrine impairments mediating acyclicity in aging female rats.     

Immobilization of white-tailed deer by etorphine and xylazine and its antagonism by nalmefene and yohimbine

White-tailed deer (Odocoileus virginianus) were immobilized with either 4.0 mg etorphine hydrochloride (ETOR) or 3.5 mg ETOR and 50.0 mg xylazine (XYL). Deer immobilized with ETOR only were given 4.0 mg nalmefene hydrochloride (NAL), a new opioid antagonist, 20 min after induction. Deer immobilized with ETOR and XYL received 3.5 mg NAL and 0.125 mg/kg yohimbine hydrochloride (YOH). The dose of 4.0 mg ETOR did not provide acceptable immobilization and was discontinued. A NAL:ETOR ratio of 1:1 was insufficient for complete and sustained antagonism of ETOR. Subsequently, deer were immobilized with ETOR and XYL as before which was then antagonized with 35.0 mg NAL and 0.125 mg/kg YOH. The 10:1 ratio of NAL:ETOR appeared to provide complete antagonism with no evidence of renarcotization. Although more study is required, NAL could become a useful antagonist for opioid-induced immobilizations.     

Differential effects of naloxone on basal and stress-induced release of ACTH and prolactin in the male rat

The effect of i.v. injection of various doses of naloxone (NAL) on plasma adrenocorticotropin (ACTH) and prolactin (Prl) in conscious animals bearing an indwelling intrajugular catheter was assessed. The effects were evaluated in animals which were left undisturbed and in others subjected to either restraint or ether stress. The results revealed that the dose of 3 mg/kg of NAL significantly reduced basal Prl levels, whereas a dose of 6 mg/kg of NAL was required to block completely either ether or restraint stress-induced release of Prl. The behavior of ACTH contrasted with that of Prl. There was no effect whatsoever of the 3 mg/kg dose of NAL on either resting or stress-induced ACTH levels, whereas a 6 mg/kg or 12 mg/kg dose of NAL elevated resting ACTH levels and only partially attenuated the further elevation induced by stress in these animals. The results clearly indicate a NAL sensitive step in the control of resting and stress-induced Prl release but indicate that the control of resting and stress-induced release of ACTH is different in that the predominantly millimicron receptor blocker, NAL, can elevate ACTH at high doses and can only partially block the response to stress. In contrast to Prl where opioid peptide control is solely stimulatory, this control of ACTH secretion appears to have both stimulatory and inhibitory features.     

Stimulation of prolactin secretion by morphine: role of the central serotonergic system.

Unanesthetized male rats with indwellinh right atrial cannulae were injected with morphine (MOR) i.v. which produced a dose-related increase in plasma prolactin levels (PRL). This effect was blocked partially by naloxone (NAL) at a dose of 0.06 mg/kg and totally by 0.6 mg/kg NAL. Interruption of central serotonergic neurotransmission by receptor blockade, with metergoline (MET) or cyproheptadine (Cypro), inhibition of tryptophan hydroxylase by para-chlorophenylalanine or destruction of serotonin neurons by 5, 7-dihydroxytryptamine antagonized the morphine (3 mg/kg) induced elevation in PRL release. Depression of dopaminergic activity with α-methyl-para-tyrosine elevated the basal PRL levels, but it did not prevent a further increase of prolactin levels by morphine (3 mg/kg). These data are compatible with the hypothesis that morphine stimulates PRL release by activation of the central serotonergic system.     

Endogenous opioids: Naloxone disrupts learned performance in rats

The effect of naloxone on learned performance reinforced by food was examined in 2 experiments. Male rats were trained to run down a short runway for 5 (45 mg) food pellets per trial and were then shifted either to 1 or 0 pellets. Following such an abrupt reinforcement shift, animals typically show an emotional disruption of performance (Crespi, 1942) referred to as “depression.” We examined the postshift depression-effect in groups treated either with saline (SAL) or naloxone (NAL). In experiment 1 NAL groups received a single 10 mg/kg (s.c.) injection prior to each postshift session. When compared with SAL controls, NAL animals showed an exaggerated postshift depression-effect. Furthermore, a single (0.3 mg/kg, s.c.) injection of the enkephalin analog FK 33-824 (D-Ala², MePhe⁴, Met-(0)⁵-o1) produced a dramatic recovery of performance. In the second experiment, these effects were replicated at a low NAL dose (1 mg/kg), which had no direct effect on motor performance. These findings suggest that opiate systems may modulate the incentive motivation that maintains learned performance.     

The effect of pentobarbital on the antinociceptive action of morphine in morphine-tolerant and non-tolerant rats

The interaction of sodium pentobarbital with morphine sulfate in both morphine-tolerant and non-tolerant rats was investigated using the tail-compression test for analgesia. Male Sprague-Dawley rats (300–350 g) were given pentobarbital (4, 8, or 16 mg/kg) 5 min before morphine (2, 4, 6, or 8 mg/kg). Control animals received two saline injections, or pentobarbital plus saline, or saline plus morphine. All injections were subcutaneous. Prior to the first injection, a baseline nociceptive threshold was determined for each rat by applying a modified micrometer to its tail and increasing the pressure until a squeak was elicited. Test readings were taken every half-hour for 2 hr beginning 30 min after the second injection. For the chronic studies, animals were first made tolerant to morphine by the administration of the narcotic twice a day for 3 days, increasing the dose from 10 to 50 mg/kg/injection. Identical testing procedures were then followed with these rats except that the test dose of morphine given on day 4 was in the range 8–128 mg/kg. It was found that Na pentobarbital, in the subanesthetic doses used, had neither antinociceptive nor hyperalgesic properties. Furthermore, the barbiturate had no effect on the antinociceptive action of morphine in either morphine-tolerant or non-tolerant rats.     

Mechanisms of organophosphate insecticide-induced airway hyperreactivity

It has been suggested that pesticide exposure may be a contributing factor underlying the increased incidence of asthma in the United States and other industrialized nations. To test this hypothesis, airway hyperreactivity was measured in guinea pigs exposed to chlorpyrifos, a widely used organophosphate pesticide. Electrical stimulation of the vagus nerves caused frequency-dependent bronchoconstriction that was significantly potentiated in animals 24 h or 7 days after a single subcutaneous injection of either 390 mg/kg or 70 mg/kg of chlorpyrifos, respectively. Mechanisms by which chlorpyrifos may cause airway hyperreactivity include inhibition of acetylcholinesterase (AChE) or dysfunction of M3 muscarinic receptors on airway smooth muscle or of autoinhibitory M2 muscarinic receptors on parasympathetic nerves in the lung. AChE activity in the lung was significantly inhibited 24 h after treatment with 390 mg/kg of chlorpyrifos, but not 7 days after injection of 70 mg/kg of chlorpyrifos. Acute exposure to eserine (250 microg/ml) also significantly inhibited lung AChE but did not potentiate vagally induced bronchoconstriction. Neuronal M2 receptor function was tested using the M2 agonist pilocarpine, which inhibits vagally induced bronchoconstriction in control animals. In chlorpyrifos-treated animals, pilocarpine dose-response curves were shifted significantly to the right, demonstrating decreased responsiveness of neuronal M2 receptors. In contrast, chlorpyrifos treatment did not alter methacholine-induced bronchoconstriction, suggesting that chlorpyrifos does not alter M3 muscarinic receptor function on airway smooth muscle. These data demonstrate that organophosphate insecticides can cause airway hyperreactivity in the absence of AChE inhibition by decreasing neuronal M2 receptor function.     

Effect of substance P on thyrotropin secretion from the pituitary gland in the rat

The role of substance P (SP) on thyrotropin (TSH) secretion was investigated in ovariectomized (OVX) female, estrogen-primed OVX, and normal male rats. Third ventricular administration of SP induced a significant increase in plasma TSH levels when compared to control animals in E-primed OVX rats (p less than 0.001). The plasma TSH levels increased in a dose-related manner and reached maximum levels at 10 min after injection. In contrast, intraventricularly injected SP failed to alter plasma TSH levels in both OVX rats and normal male rats. Intravenous administration of SP dramatically stimulated TSH release in E-primed OVX rats (p less than 0.001), whereas SP had no effect on the release of TSH when injected in OVX rats and normal male rats. To investigate any direct action of SP on TSH release from the anterior pituitary gland, synthetic SP was incubated with dispersed anterior pituitary cells harvested from E-primed OVX rats and normal male rats. SP, in the dose range between 10(-8) M and 10(-6) M, failed to alter the release of TSH into the culture medium in vitro. These findings indicate that SP has a stimulatory role in the control of TSH release by an action on the hypothalamus but only in estrogen-primed rats.     

Intracerebroventricular beta-endorphin increases food intake of rats

B-Endorphin (B-END), met-enkepalin (M-ENK), and DAla²NMe⁵-met-enkephalinamide were administered intracerebroventricularly to rats and effects on the ingestion of a liquid diet were examined. B-END significantly increased food intake in a half-hour test at a dose of 200 ng/rat. Lower or higher doses did not affect food intake. Neither M-ENK or the synthetic enkephalin analog affected ingestion of the liquid diet. These findings demonstrate rapid action of an endorphin on food intake administered at a lower dose than has previously been reported and suggest a specificity for B-END in the endorphinergically mediated hyperphagic response.     

Antagonism of naloxone hyperalgesia by ethanol

Male Sprague-Dawley rats (8 per group) received 1.25 g/kg ethanol (EtOH) in saline or saline alone i.p. and either saline, 0.1, or 2.0 mg/kg naloxone HC1 (NAL) s.c. five min later. Beginning 15 min after the second injection, rats received five noncontingent 0.5 sec footshocks at each of three intensities (0.6, 0.8, 1.3 mA) in a random order on a variable time 1 min schedule. The amplitude of the startle response, number of audible vocalizations, and extent of overt movements were recorded. EtoH significantly reduced startle response amplitude and overt movements at 0.8 and 1.3 mA; NAL failed to antagonize these indices of EtOH analgesia. NAL was itself without effect upon overt movements but significantly increased startle response amplitude and vocalizations at 1.3 mA. EtOH prevented these NAL-induced increases but this does not appear attributable to ethanol's analgesic or motoric effects. Possible mechanisms of ethanol's effects upon endorphin systems are considered.     

Influence of stage of the estrous cycle on endogenous opioid modulation of luteinizing hormone, prolactin, and cortisol secretion in the gilt

Fourteen gilts that had displayed one or more estrous cycles of 18-22 days (onset of estrus = Day 0) and four ovariectomized (OVX) gilts were treated with naloxone (NAL), an opiate antagonist, at 1 mg/kg body weight in saline i.v. Intact gilts were treated during either the luteal phase (L, Day 10-11; n = 7), early follicular phase (EF, Day 15-17; n = 3), or late follicular phase (LF, Day 18-19; n = 4) of the estrous cycle. Blood was collected at 15-min intervals for 2 h before and 4 h after NAL treatment. Serum luteinizing hormone (LH) concentrations for L gilts averaged 0.65 +/- 0.04 ng/ml during the pretreatment period and increased to an average of 1.3 +/- 0.1 ng/ml (p less than 0.05) during the first 60 min after NAL treatment. Serum prolactin (PRL) concentrations for L gilts averaged 4.8 +/- 0.2 ng/ml during the pretreatment period and increased to an average of 6.3 +/- 0.3 ng/ml (p less than 0.05) during the first 60 min after NAL treatment. Serum PRL concentrations averaged 8.6 +/- 0.7 ng/ml and 7.6 +/- 0.6 ng/ml in EF and LF gilts, respectively, prior to NAL treatment, and decreased (p less than 0.05) to an average of 4.1 +/- 0.2 ng/ml and 5.6 +/- 0.4 ng/ml in EF and LF gilts, respectively, during the fourth h after NAL. Naloxone treatment failed to alter serum LH concentrations in EF, LF, or OVX gilts and PRL concentrations in OVX gilts.(ABSTRACT TRUNCATED AT 250 WORDS)     

Sex-related differences in cadmium-induced lipid peroxidation in the rat

Male and female rats were dosed once a day for 2 days injection with 1.5 mg of Cd/kg as CdCl₂. 24 hr after administration of cadmium, lipid peroxidation determined by estimation of malondialdehyde (MDA) was greatly increased in male rat liver, but was not in female rats. Cadmium in a larger dose of 4.5 mg/kg, subcutaneous single injection, significantly increased content of MDA in female rat liver. These results suggest that sex-related differences exist in the ability of cadmium to induce MDA formation in rat liver, although administration of cadmium causes the enhancement of MDA formation in both male and female rats. The reason why sex-related differences exist in lipid peroxidation of rat liver is discussed.     

Physiological response of gray wolves to butorphanol-xylazine immobilization and antagonism by naloxone and yohimbine

Captive gray wolves (Canis lupus) were immobilized (loss of consciousness) with 2.0 mg/kg xylazine hydrochloride (XYL) and 0.4 mg/kg butorphanol tartrate (BUT) administered intramuscularly. Induction time was 11.8 +/- 0.8 min (mean +/- SE). Immobilization resulted in bradycardia, respiratory depression, and normotension. Fifteen min after induction, six wolves were given either 0.05 mg/kg naloxone hydrochloride (NAL) and 0.125 or 0.250 mg/kg yohimbine hydrochloride (YOH), or an equal volume of saline (control) intravenously. Antagonism resulted in shortened recovery times compared to control animals (P less than 0.03); there was no difference in recovery times between the YOH doses (P greater than 0.05). Antagonism caused increases in heart rate (HR) and respiratory rate (RR), but no changes in MABP. Eight other wolves were similarly immobilized, but given only NAL. This resulted in partial antagonism with the animals appearing to be sedated with XYL only. Three wolves given only 0.4 mg/kg BUT assumed a state described as "apathetic sedation." Three other wolves sedated with only 2.0 mg/kg XYL showed a profound sedation characterized by recumbency, bradycardia and shallow, but regular, respiration. This study demonstrated that (1) BUT and XYL together, but not separately, can completely immobilize wolves, (2) this combination can be rapidly antagonized by NAL and YOH, and (3) there appeared to be no adverse cardiopulmonary reactions to any of the drugs used.     

Effect of hypothyroidism on responsiveness to beta-adrenergic stimulation.

Chronic administration of aminotriazole (0.5 g/kg food) to rats was accompanied by a reduced responsiveness to acute administration of the beta-adrenergic agonist, l-isoproterenol (50-100 mug/kg, sc). The responses tested included water intake, change in heart rate in the anesthetized and unanesthetized rat, change in mean blood pressure, and change in blood glucose concentration. In addition, the increase in tail skin temperature accompanying administration of epinephrine (1 mg/kg, sc) was significantly reduced in the hypothyroid group. Administration of l-thyroxine (25 mug/kg per day, ip) to aminotriazole-treated rats prevented the reduction in responsiveness to beta-adrenergic stimulation. Thus, an interaction appears to exist between the level of thyroid activity and responsiveness to beta-adrenergic agonists in rats.     

Effects of progesterone on gonadotropin-releasing hormone receptor concentration in cultured estrogen-primed female rat pituitary cells

Acute (0.5–4 h) treatment of estradiol (E)-primed female rat pituitary cells with progesterone (P) augments gonadotropin-releasing hormone (GnRH)-induced LH release, whereas chronic (48 h) P-treatment reduces pituitary responsiveness to the hypothalamic decapeptide. Dispersed E-primed (48 h, 1 nM) rat pituitary cells were cultured for 4 or 48 h in the presence of 100 nM P to assess the effects of the progestagen on GnRH receptors and on gonadotrope responsiveness to the decapeptide. P-treatment (4 h) significantly augmented GnRH-receptor concentrations (4.44 ± 0.6 fmol/10⁶ cells) as compared to cells treated only with E (2.6 ± 0.5fmol/10⁶ cells). Parallel significant changes in GnRH-induced LH secretion were observed. The acute increase in GnRH-receptor number was nearly maximal (180% of receptor number in cells treated with E alone) within 30 min of P addition. Chronic P-treatment (48 h) significantly reduced pituitary responsiveness to GnRH as compared to E-treatment. The GnRH-receptor concentrations (3.9 ± 0.6 fmol/10⁶ cells), however, remained elevated above those in E-primed cells. GnRH-receptor affinity was not influenced by any of the different treatments. These results indicate that the acute facilitatory P-effect on GnRH-induced LH release is at least chronologically closely related to an increase in GnRH-receptor concentration. The chronic negative P-effect on pituitary responsiveness to GnRH, however, shows no relation to changes in available GnRH receptors.     

Paced mating behavior in female rats in response to different hormone priming regimens

A female rat will display a repertoire of behaviors during a sexual encounter with a male rat including sexually receptive (the lordosis response) and proceptive (hopping, darting) behaviors. In addition, when given the opportunity, a sexually receptive female rat will approach and withdraw from the male rat, controlling the timing of the receipt of mounts, intromissions, and ejaculations, a behavior known as paced mating behavior. The present experiments tested the hypotheses (1) that progesterone regulates paced mating behavior, and (2) that multiple hormone regimens used previously to induce sexual receptivity have the same effect on paced mating behavior. Paced mating behavior was assessed in sexually receptive ovariectomized female rats after treatment with: (1) estradiol benzoate (EB; 30.0 mg/kg) followed by a range of doses of progesterone (P; 1.0-8.0 mg/kg), (2) two pulses of unesterified estradiol (E2; 2.0 microg/rat) followed by 1.0 mg/rat of P, and (3) EB alone (5.0 microg/rat) for 6 days. No differences in sexual receptivity or in paced mating behavior were observed across doses of P (1.0-8.0 mg/kg). In contrast, the number of hops and darts per min increased with the dose of P administered. E2 + P administration resulted in slightly, but significantly, lower levels of sexual receptivity along with significantly longer contact-return latencies following an intromission in relation to the other treatment conditions. In addition, female rats exhibited fewer hops and darts per min in response to E2 + P than in response to EB + 8.0 mg/kg of P. The administration of EB alone for 6 days induced levels of receptivity and paced mating behavior indistinguishable from EB + P, while eliciting significantly fewer hops and darts per min than the EB + 8.0 mg/kg P treatment condition. Hormone priming regimen had no effect on the percentage of exits displayed during the paced mating tests in any experimental phase. Dose of P had no effect on paced mating behavior in sexually receptive rats. In addition, P does not appear to be necessary for the display of paced mating behavior following long-term treatment with EB. In contrast, the pulsatile administration of E2 + P induced a different pattern of paced mating behavior in sexually receptive rats.     

Influence of naloxone and yohimbine administration on pulsatile LH secretion in luteal phase beef cows

This study examined the effects of two specific neurotransmitter receptor antagonists, naloxone (NAL; mu-opioid) and yohimbine (YOH; alpha(2)-adrenergic), on pulsatile luteinizing hormone (LH) release during the luteal phase (Day 10; Day 0 = estrus) of beef cows. Treatments were saline i.m. (C; n = 4); 1mg/kg NAL i.m. followed 3 h later by two 0.5 mg/kg injections spaced 2.5 h apart (N; n = 4); 0.2 mg/kg YOH i.v. (Y; n = 3); or combined N and Y regimens, with Y preceding N by 30 min (NY; n = 4). Blood samples were collected for 8 h before (Period I) and after (Period II) initiation of treatment. Respiration rates of Y cows were similar to C cows during Period II. However, respiration rates of N and NY animals increased 70% within 30 min of the first NAL injection. Acute LH release was not observed in response to either NAL or YOH. Pulsatile LH secretion was unchanged in N, Y and NY cows during Period II when compared with Period I. In contrast, basal and pulsatile LH secretion was inhibited in C cows during Period II. The inhibition of LH secretion in C animals following NAL indicate that the cows were under stress during Period II. Thus, these data suggest that the inhibition of LH release in stressed animals can be overcome by pharmacologic attenuation of inhibitory (N) or accentuation of stimulatory (Y) signals to LHRH-containing neurons.