There are currently a few methods that can be used to assess the time of impending parturition in the goat, especially if exact breeding dates are unknown. One indicator of the onset of parturition is a decrease in the doe’s blood progesterone level approximately 24–30 h prior to parturition. Laboratory serum/plasma progesterone assays commonly require 24 h or more to obtain results, as well as being expensive. This study was designed to evaluate whether semi-quantitative enzyme immunoassay (EIA) progesterone kits could be used to determine plasma progesterone levels in does during late gestation, and whether a correlation could be drawn between the test result and the time of parturition. Plasma samples were collected twice daily from 16 pregnant does starting on day 143 of pregnancy and ending 1 day following parturition. The plasma progesterone levels indicated by the three EIA kits were compared to one another and to a radioimmunoassay, and assessed for any relationship to the actual time of parturition. Test results indicating low plasma progesterone levels (<1.0–2.8 ng/ml) from the Status Pro (Synbiotics), TARGET (Biometallics), and PreMate (Camelot Farms) and tests were found to be correlated 100, 83 and 100% with the onset of parturition within 24 h. Test results indicating high plasma progesterone levels (>5.0–7.8 ng/ml) from the Status Pro, TARGET, and PreMate tests were found to be correlated 100, 100, and 82.2% with delayed parturition. The radioimmunoassay results concurred with the progesterone ranges given for Status Pro, TARGET, and PreMate tests in 75.7, 58.8 and 53.7% of the cases, respectively. The results of this study indicates that any one of the commercially produced EIA progesterone tests can be used to predict with a high degree of accuracy the likelihood of parturition occurring within the next 24–30 h. These tests are simple to perform and cost effective.

Dilated cardiomyopathy, a lethal disease characterized by left ventricular dilation and systolic dysfunction, is relatively common in humans and other mammals. Idiopathic dilated cardiomyopathy (IDCM) is a primary myocardial disease of unknown cause and can be a familial disorder. This report describes autosomal recessive IDCM in dogs. It occurs in Portuguese Water Dog (PWD) pups and is manifested by acute, vague clinical signs and sudden death. Affected pups have progressive reduction of fractional shortening that can be demonstrated by echocardiography prior to the development of clinical signs. Furthermore, these pups have low plasma taurine levels when consuming certain diets. Affected pups had dilation of the left ventricle and alterations in the sarcomere appearance, while immunohistochemical and biochemical studies demonstrate an increase in desmin, a cytoskeleton protein. The clinical and morphologic findings of IDCM in PWDs are distinct from those reported in adult IDCM. Finally, the clinical and echocardiographic manifestations were reversible in some pups following oral taurine supplementation for 2 months. These results suggest that IDCM in PWDs is correlated with low plasma taurine levels.

Regional distribution of gonadotropin-releasing hormone (GnRH)-like-, β-endorphin (β-end)-like-, and methionine-enkephalin (met-enk)-like-immunoreactivity was quantified across various regions of the central nervous system (CNS) of male and female goats by using highly specific radioimmunoassays. All the animals were sacrificed during the months of March through June (non-breeding season). Although the distribution of these three neuropeptides was similar to other mammalian species, species-specific gender differences in the levels of neuropeptides were noticed in the goat CNS. Highest levels of GnRH-like immunoreactivities were found in the hypothalamus. The hypothalamus of male goats exhibited significantly higher levels of GnRH-like immunoreactivities compared to female goats. Other regions exhibiting GnRH-like immunoreactivities included olfactory bulbs, preoptic and supraoptic regions, and mamillary bodies. Both β-end- and met-enk immunoreactivities were detected in all selected regions of goat CNS, but highest levels of these opioid peptide-like immunoreactivities were limited to the forebrain regions of the goat. The supraoptic area of the female goats contained significantly higher levels of β-end-like immunoreactivities than that of the male goats. Met-enk-peptide-like immunoreactivity also exhibited gender-specific differences in its content in some regions of the CNS. The male goats exhibited significantly higher levels of met-enk-like immunoreactivity in both the striatal and hypothalamic regions of the brain.

Effects of acute exposure (2 hr) to either 1.5% halothane or 0.5% methoxyflurane were investigated in the Sprague Dawley rat. Pituitary (PIT) and central nervous system (CNS) substance P (SP)-like and β-endorphin (β-end)-like immunoreactivities were evaluated immediately after anesthetic exposure (2 h), after righting reflex (4 h) or 24 hr postexposure (24 h). Only halothane significantly reduced SP-like immunoreactivity in olfactory bulbs in both the 2-h and 4-h groups. Halothane elevated SP-like immunoreactivity of hippocampus at all three time periods, and in the hypothalamus at 2 h. Both anesthetics significantly depleted thalamic concentrations of SP-like immunoreactivity. Methoxyflurane anesthesia resulted in a drastic decrease in SP-like immunoreactivity in PIT at all three time periods periods, while halothane elevated PIT concentrations of this peptide at 4 h. Both anesthetics significantly decreased β-end-like immunoreactivity in the olfactory bulbs and thalami at 2, 4, and 24 h. However, halothane alone significantly elevated β-end-like immunoreactivity in the spinal cord at 24 h. Halothane significantly elevated PIT β-end-like immunoreactivity at 2 and 24 h, while methoxyflurane significantly lowered it in the 4-h group, but elevated the levels of the same in the 24-h group. Brain stem β-end immunoreactivity were significantly reduced at 2 h by both anesthetics, and at 4 h by methoxyflurane. Results indicate that halothane and methoxyflurane may differ significantly in their actions on SP and β-end secreting neurons in the CNS.

The effects of nitrous oxide (N2O) on steady-state concentrations and turnover rates of catecholamines in the olfactory bulb, hypothalamus, brain stem, hippocampus, striatum, thalamus, cerebral cortex, and spinal cord were determined in rats. Animals were exposed for 2 h to either 60% N2O or air. Immediately following exposure, all animals were injected intraperitoneally with alpha-methylparatyrosine (alpha MPT), a competitive inhibitor of tyrosine hydroxylase, and sacrificed at 0, 30, or 90 min postinjection. Brain catecholamine concentrations were determined using high-performance liquid chromatography coupled with electrochemical detection (HPLCEC). Results indicate that N2O exposure significantly elevates steady-state concentrations of norepinephrine (NE) in the hypothalamus and striatum yet decreases amine levels in the brain stem region. Steady-state levels of dopamine (DA) were not significantly altered in any region of the CNS by N2O exposure. Acute exposure to N2O also resulted in significant decreases in the turnover rate of NE in the brain stem, yet it increased turnover of this amine in the olfactory bulb, hypothalamus, and striatum. Acute exposure to N2O resulted in a decreased turnover rate of DA in the hippocampus and striatum. In contrast, N2O appears to increase DA turnover in the olfactory bulb. These results indicate that acute exposure to N2O in rats causes region-specific alterations in steady-state levels and turnover rates of DA and NE within the central nervous system. (C) 1998 Elsevier Science Inc.

Effects of acute exposure (2 h) to either 1.5% halothane or 0.5% methoxyflurane on chemical mediators of the hypothalamic-pituitary-adrenal (HPA) axis were evaluated in male Sprague-Dawley rats immediately after exposure, after the righting reflex (4 h), or 24 h postexposure. Effects of these anesthetics on hippocampal corticotropin releasing factor (CRF) were also evaluated, Methoxyflurane caused significant elevations in pituitary adrenocorticotropin hormone (ACTH)-like immunoreactivities in all three of the experiment's time groups, yet halothane failed to cause the same response immediately after exposure, Serum ACTH-like immunoreactivities were significantly elevated immediately after exposure to both anesthetics, but were not elevated at 4 and 24 h postexposure. Corticosterone (CORT)-like immunoreactivities were significantly elevated by halothane in all experimental groups, and in the 2- and 24-h groups following methoxyflurane exposure. Hippocampal CRF-like immunoreactivities remained unaffected by either anesthetic, Results indicate that a 2-h exposure to either halothane or methoxyflurane results in significant activation of the rat hypothalamic-pituitary-adrenal axis, and that the activation appears to be sustained over a 24-h period, (C) 1998 Elsevier Science Inc.

The effect of exposure to nitrous oxide (N2O) on the levels of preproenkephalin mRNA in the hypothalamus of rats was examined. In the first experiment, rats were exposed to 1000 ppm N2O for 8 h a day over 4 days. Compared with controls (which were exposed to air over the same duration), the N2O exposed animals exhibited significant elevations in preproenkephalin mRNA levels in the hypothalamus. In a second experiment, rats were exposed to 60% N2O or air for 12, 24 and 48 h duration, and hypothalamic levels of preproenkephalin mRNA as well as methionine enkephalin were analyzed. Compared with controls, N2O exposed rats exhibited significant elevations in preproenkephalin mRNA levels. The levels on preproenkephalin mRNA were significantly higher after 48 h of N2O exposure than after 12 h of N2O exposure. Similarly, the concentration of methionine enkephalin was significantly higher after 24 and 48 h of exposure to N2O than after exposure to 12 h of N2O or air. These results indicate that (a) exposure to N2O results in significant elevations in preproenkephalin mRNA levels, (b) the increased preproenkephalin mRNA levels appear to be proportional to the concentration of N2O exposure as well as the duration of N2O exposure, and (c) N2O-induced elevation in preproenkephalin mRNA levels is associated with corresponding increase in tissue concentrations of methionine enkephalin. In total, these results suggest that N2O selectively stimulates synthesis of methionine enkephalin in the diencephalic region of the brain.

The objective of this study was to document, through comprehensive means, normal distribution and concentration of catecholamines in various regions of the CNS of pigs, an increasingly popular animal model used for transgenic manipulation of neural genes. The effects of gonadal steroidal status on this distribution were also assessed by comparing CNS catecholamine concentrations among mature male pigs (boars), immature (gilts) and mature female pigs (sows), and adult male pigs castrated prepuberally (barrows). Dissected tissue samples from the CNS were extracted in 2 N acetic acid, filtered through a 0.2 micron filter, then quantitated by reverse-phase high performance liquid chromatography using a C-18 reverse phase column with electrochemical detection. In both boars and sows the highest concentrations of norepinephrine (NE) were found in the diencephalic areas and brain stem. Gilts exhibited elevated concentrations of NE in the olfactory bulbs (OB), hypothalamus, pons, and corpus trapezoideum-locus ceruleus (LC) compared to lower concentrations in corresponding areas of sows. Prepuberal castration of the male was associated with significantly lower NE concentrations in the striatum, periaqueductal area (PAG), pons, LC, and spinal cord. The sow exhibited significantly lower NE concentrations in the mammillary area (Mam), PAG, pons, and spinal cord than those in corresponding areas of the boar. Dopamine concentrations appeared to be similar in all areas of the brain and spinal cord studied in the sow and boar. Results demonstrated that prepuberal castration of the male appears to significantly alter the DA content of the Mam and dorsal spinal cord, in contrast to gilts who possess significantly higher concentrations of DA. It is concluded from our studies that in general, catecholamine concentrations in various regions of the brain and spinal cord of sexually mature pigs parallel distributions of neuropeptides, substance P, and methionine enkephalin, as previously reported. In addition, significant association was found between gonadal activity and catecholamine concentrations in discrete areas of the pig brain.

Interleukin-1 (IL-1) has been shown to stimulate corticosterone release from the adrenal gland directly, and indirectly through activation of the hypothalamic-pituitary-adrenal axis. The aim of this paper was to determine whether IL-1-stimulated corticosterone release occurs indirectly through the local release of catecholamines from the rat adrenal gland. To accomplish this, experiments were conducted on both quartered rat adrenal glands and primary cultures of dispersed adrenal cells. Incubation of quartered adrenals with adrenocorticotropic hormone (ACTH, 10(-12) to 10(-8) M) or IL-1 beta (10(-12) to 10(-8) M) resulted in dose-dependent increases (P less than 0.05) in corticosterone release. Corticosterone release stimulated by 10(-8) M doses of ACTH and IL-1 beta began to rise 30 min after incubation and peaked at 2 h. In primary cultures of adrenal cells, IL-1 alpha and IL-1 beta elevated corticosterone release after a 24-h incubation period. ACTH elevated corticosterone levels at 4 and 24 h. The stimulatory effect of IL-1 on corticosterone release was mimicked by epinephrine (10(-6) M), and was selectively blocked by the alpha-adrenergic antagonist phentolamine (10(-5) M). The beta-adrenergic antagonist propranolol (10(-5) M) did not change IL-1-induced corticosterone release. Neither phentolamine nor propranolol had an effect on ACTH-stimulated corticosterone release. Both IL-1 alpha and IL-1 beta significantly increased (P less than 0.05) epinephrine levels after a 24-h incubation period compared with media-treated controls.(ABSTRACT TRUNCATED AT 250 WORDS)

The effect of varying doses of purified human interleukin 1 (IL-1) on rectal temperature (Tr), hypothalamic corticotropin-releasing hormone (CRH), pituitary and plasma adrenocorticotropic hormone (ACTH), and plamsa corticosterone was examined in intact male rats at 24 degrees C; plasma ACTH and corticosterone responses were also studied in hypophysectomized rats. In addition, IL-1-induced changes in corticosterone concentration were investigated by means of adrenal organ cultures. Tr was measured with thermocouples. CRH and ACTH levels were determined by radioimmunoassay, and corticosterone by protein-binding assay. Intravenous administration of IL-1 (0.063-1.0 ng) resulted in hyperthermia, which began 20 min postinjection and continued for an additional 30 min. IL-1 at a dose of 0.5 ng resulted in no change in hypothalamic CRH, pituitary ACTH, or plasma ACTH levels compared with saline-treated rats. Plasma corticosterone was significantly (P less than 0.05) elevated 30 min after IL-1 administration and returned to control levels after 1 h. The higher dose of IL-1 (1.0 ng) did not affect hypothalamic CRH content, but pituitary ACTH began to rise at 15 min and was significantly (P less than 0.05) elevated 30 min after injection. Rats receiving this dose displayed elevated (P less than 0.05) plasma ACTH and corticosterone levels 30 and 60 min postinjection. No change in plasma corticosterone was observed in hypophysectomized rats administered either 1 ng of IL-1 or 1 microgram of recombinant IL-1 beta (rIL-1 beta); adrenal organ cultures treated with IL-1 (10(-11) M) responded similarly.(ABSTRACT TRUNCATED AT 250 WORDS)

The effect of acute (1 day) or subchronic (25 days) treatment with delta 9-tetrahydrocannabinol (THC), the major psychoactive constituent of marihuana, on plasma norepinephrine (NE), epinephrine (E), corticosterone, beta-endorphin (beta-end), and splenic natural killer (NK) cell activity of the rat was studied. Groups of animals received subcutaneously, either THC in corn oil + saline (3 mg THC/kg); oil + saline; or THC + naloxone (2 mg naloxone/kg and 3 mg THC/kg). Acute injection of THC with or without naloxone did not significantly change plasma levels of NE, E corticosterone, beta-end, or the NK cell activity. However, subchronic treatment with THC significantly reduced plasma levels of NE, E, corticosterone, and NK cell activity, compared to controls. The plasma beta-end levels were significantly elevated in the THC-treated animals. In the THC + naloxone group of animals, the plasma hormone levels (corticosterone and beta-end) were similar to control levels and the NK cell activity was significantly higher than in THC-treated animals. These results indicate that subchronic exposure to THC results in suppression of splenic NK cell activity. The interaction of THC with the endogenous opiate system appears to be a contributing factor leading to the NK cell suppression in rats. A direct suppressive action of THC or its metabolites on the NK cell is not ruled out by this study.

Adult female golden hamsters were used to study the effect of short photoperiod on the endogenous opioid system and the effect of pinealectomy on the serum β‐endorphin‐iike immunoreactivity (β‐end LI) levels. Hamsters were housed under either long photoperiod (14L:10D) or short photoperiod (2L:22D) and the regularity of the estrous cycles was determined by daily vaginal exfoliative cytology. Hamsters under short photoperiod became acyclic after about 7 wk. At the end of 8 wk, all the hamsters were decapitated and medial basal hypothalamic (MBH) content of LHRH and methionine‐enkephalin (met‐enkephalin) were measured by specific radioimmunoassays (RIA). Both LHRH and met‐enkephalin levels of the MBH were significantly elevated in the short‐photoperiod hamsters as compared to the normally cycling control animals under long photoperiod. In a second experiment, the effect of pinealectomy (PNX) on the serum levels of β‐end LI in the short‐photoperiod hamsters was determined. The serum β‐end LI levels were increased approximately threefold in the noncyclic hamsters housed under 8 wk of short‐photoperiod conditions. Pinealectomized hamsters kept under 8 wk of short‐photoperiod exhibited lower serum β‐end LI levels similar to those of normally cycling hamsters kept under long photoperiod. These results indicate a possible functional relationship between increased pineal activity (as a result of short photoperiod) and increased MBH met‐enkephalin, LHRH, and serum β‐end LI levels.

The present study was undertaken to determine if the effects of delta 9-tetrahydrocannabinol on gonadotropin secretion are mediated through endogenous opioid neurons in the rat. Ovariectomized rats were treated with estradiol-benzoate (EB, day O) and with progesterone (P) at 11:00 h on day 2. At 13:00 h (day 2), these estradiol primed and progesterone-treated (EBP) animals received either delta 9-THC (3mg/kg in oil, i.m.); naloxone (Nal) 3 mg/kg in saline, s.c.) or delta 9-THC + Nal. All animals were decapitated at 16:00 h and trunk sera were assayed for luteinizing hormone (LH) and prolactin (Prl), while medial basal hypothalami (MBH) were assayed for luteinizing hormone-releasing hormone (LHRH). Naloxone enhanced the EBP-induced hypersecretion of LH by 2-fold while delta 9-THC completely blocked the EBP-induced secretion of LH. delta 9-THC slightly diminished the stimulatory effect of Nal on LH secretion and caused a 2-fold increase in serum Prl concentrations, while Nal did not influence the serum PRL levels in these EBP rats. However, Nal did block the stimulatory effects of delta 9-THC on Prl secretion. delta 9-THC caused a significant increase in MBH content of LHRH, an effect which was prevented by Nal. These results suggest that the inhibitory effects of delta 9-THC on serum LH and the stimulatory effect of the cannabinoid on Prl are mediated by an opioid mechanism.

Effect of light deprivation on hypothalamic dopamine (DA) depletion rate and luteinizing hormone releasing hormone (LHRH) content was evaluated in golden hamsters. Hamsters maintained in continuous darkness (CD) became acyclic after about 6 weeks while another group of hamsters maintained vaginal cyclicity under 20 lux light intensity for 14 hours a day. All hamsters were ovariectomized subsequently. Luteinizing hormone releasing hormone levels were significantly higher in the medial basal hypothalamus (MBH) and the serum gonadotropin levels were significantly lower in CD hamsters when compared with 20 lux group. However, gonadotropin release in response to exogenous LHRH was not significantly different in CD or 20 lux group of hamsters. Examination of hypothalamic catecholamine levels one hour after alpha-methyl-p-tyrosine injection indicated that the DA depletion was higher in CD animals. Results indicate that light deprivation probably enhances DA depletion rate in the MBH, suggesting that increased activity in dopaminergic neurons may inhibit the release of MBH LHRH in hamsters kept in continuous darkness.