Placentophagia and the Tao of POEF.

Placentophagia, ingestion of placenta and amniotic fluid, usually during parturition, is a behavioral feature of nearly all nonaquatic, placental mammals, and is a nexus for several interlocking behavioral phenomena. Placentophagia has not been typical of human cultures, but in recent years, some women in affluent societies have engaged in it, thereby bringing publicity to the behavior. First, we summarized benefits of placentophagia for nonhuman mammals, which include increased attractiveness of neonates, enhanced onset of maternal behavior, suppression of pseudopregnancy, and enhancement of opioid hypoalgesia by Placental Opioid-Enhancing Factor (POEF), a benefit that may extend well outside the context of parturition.

Dual ELISA using SARS-CoV-2 nucleocapsid protein produced in E. coli and CHO cells reveals epitope masking by N-glycosylation.

Spike and nucleocapsid proteins of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2-SP, SARS-CoV-2-NP) are the main immunogenic targets for antibodies. We herein demonstrate that the glycosylation of SARS-CoV-2-NP masks some of its antibody epitopes. In many cases, this can lead to false-negative serological tests.

Amniotic-fluid ingestion enhances central δ-opioid-induced hypoalgesia in rats in the cold-water tail-flick assay in a repeated-measures design.

Placental Opioid Enhancing Factor (POEF) is found in amniotic fluid (AF) and placenta. When ingested, it enhances opioid-mediated pain relief. Our laboratory has shown that ingestion of AF specifically enhances the hypoalgesia associated with δ-opioid receptor activation in the brain.

Placentophagia in humans and nonhuman mammals: causes and consequences.

Afterbirth ingestion by nonhuman mammalian mothers has a number of benefits: (1) increasing the interaction between the mother and infant; (2) potentiating pregnancy-mediated analgesia in the delivering mother; (3) potentiating maternal brain opioid circuits that facilitate the onset of caretaking behavior; and (4) suppressing postpartum pseudopregnancy. Childbirth is fraught with additional problems for which there are no practical nonhuman animal models: postpartum depression, failure to bond, hostility toward infants. Ingested afterbirth may contain components that ameliorate these problems, but the issue has not been tested empirically.

Effect of amniotic-fluid ingestion on vaginal-cervical-stimulation-induced Fos expression in female rats during estrus.

Placental Opioid-Enhancing Factor (POEF) is a substance found in amniotic fluid (AF) that, when ingested, potentiates opioid-mediated, but not non-opioid-mediated, hypoalgesia. Vaginal-cervical stimulation (VCS) produces a stimulus-bound, partially opioid-mediated hypoalgesia that previous research has shown to be potentiated by AF ingestion. To understand the mechanism of opioid enhancement by POEF we investigated the pattern of neural activation after a bout of VCS that produced hypoalgesia, with and without co-administration of AF.

Ingestion of amniotic fluid enhances the facilitative effect of VTA morphine on the onset of maternal behavior in virgin rats.

Previous research has shown that injection of morphine into the ventral tegmental area (VTA) facilitates the onset of maternal behavior in virgin female rats, and injection of the opioid antagonist naltrexone into the VTA disrupts the onset of maternal behavior in parturient rats. Placentophagia -- ingestion of placenta and amniotic fluid, usually at parturition -- modifies central opioid processes. Ingestion of the active substance in placenta and amniotic fluid, Placental Opioid-Enhancing Factor (POEF), enhances the hypoalgesic effect of centrally administered morphine, and more specifically, enhances delta- and kappa-opioid-receptor-mediated hypoalgesia and attenuates mu-opioid-receptor-mediated hypoalgesia.

Evaluation of buprenorphine in a postoperative pain model in rats.

We evaluated the commonly prescribed analgesic buprenorphine in a postoperative pain model in rats, assessing acute postoperative pain relief, rebound hyperalgesia, and the long-term effects of postoperative opioid treatment on subsequent opioid exposure. Rats received surgery (paw incision under isoflurane anesthesia), sham surgery (anesthesia only), or neither and were treated postoperatively with 1 of several doses of subcutaneous buprenorphine. Pain sensitivity to noxious and nonnoxious mechanical stimuli at the site of injury (primary pain) was assessed at 1, 4, 24, and 72 h after surgery.

The biopsychology of maternal behavior in nonhuman mammals.

The term "maternal behavior," when applied to nonhuman mammals, includes the behaviors exhibited in preparation for the arrival of newborn, in the care and protection of the newly arrived young, and in the weaning of those young, and represents a complex predictable pattern that is often regarded as a single, comprehensive, species-specific phenomenon. Although the delivering first-time mammalian mother is immediately and appropriately maternal, a "virgin" with no prior exposure to young does not show immediate and appropriate behavior toward foster young. Nevertheless, the virgin female, and indeed the male, possess the neural circuitry that underlies the pattern referred to as maternal behavior, despite not exhibiting the pattern under normal circumstances.

Lack of analgesic efficacy in female rats of the commonly recommended oral dose of buprenorphine.

Previous work in our laboratory showed that the recommended oral dose of buprenorphine (0.5 mg/kg) was not as effective as the standard therapeutic subcutaneous dose for postoperative analgesia in male Long-Evans (hooded) and Sprague-Dawley (albino) rats. The aim of the current study was to extend this analysis to female rats.

Analgesic efficacy of orally administered buprenorphine in rats: methodologic considerations.

Buprenorphine has been widely recommended for treatment of pain in rodents. We have previously documented that the recommended postoperative oral dose of buprenorphine in male Long-Evans rats, 0.5 mg/kg, is not as effective as the recommended parenteral dose of buprenorphine (0.

Ingested placenta blocks the effect of morphine on gut transit in Long-Evans rats.

Opioids produce antinociception, and ingested placenta or amniotic fluid modifies that antinociception. More specifically, ingested placenta enhances the antinociception produced by selective activation of central kappa-opioid or delta-opioid receptors but attenuates that produced by activation of central mu-opioid receptors. Opioids also slow gut transit by acting on central or peripheral mu-opioid receptors.

Placenta ingestion by rats enhances delta- and kappa-opioid antinociception, but suppresses mu-opioid antinociception.

Ingestion of placenta or amniotic fluid produces a dramatic enhancement of centrally mediated opioid antinociception in the rat. The present experiments investigated the role of each opioid receptor type (mu, delta, kappa) in the antinociception-modulating effects of Placental Opioid-Enhancing Factor (POEF-presumably the active substance). Antinociception was measured on a 52 degrees C hotplate in adult, female rats after they ingested placenta or control substance (1.

Male-induced estrus synchronization in the female Siberian hamster (Phodopus sungorus sungorus).

Olfactory cues play an integral role in the organization of events that mediate reproductive success. In a variety of species, priming pheromones, in particular, are important for ensuring reproductive fitness. To date, very little research has focused on how male-emitted priming pheromones, such as those that regulate the onset of puberty and estrus synchronization in females, affect the reproductive physiology of the female Siberian hamster (Phodopus sungorus sungorus).

Analgesic efficacy of orally administered buprenorphine in rats.

The analgesic effect of orally administered buprenorphine was compared with that induced by a standard therapeutic injected dose (0.05 mg/kg of body weight, s.c.

Ingested bovine amniotic fluid enhances morphine antinociception in rats.

Ingestion by rats of rat placenta or amniotic fluid enhances opioid-mediated, or partly opioid-mediated, antinociception produced by morphine injection, vaginal or cervical stimulation, late pregnancy, and foot shock. This phenomenon is believed to be produced by a placental opioid-enhancing factor (POEF). Ingestion by rats of human or dolphin placenta has also been shown to enhance opioid antinociception, suggesting that POEF may be common to many mammalian species.

Effects of cocaethylene on dopamine and serotonin synthesis in Long-Evans and Sprague-Dawley brains.

We examined the behavioral and neurochemical effects of cocaethylene treatment in Long-Evans (LE) and Sprague-Dawley (SD) rats. Cocaethylene-induced behaviors were significantly less in LE rats. Cocaethylene caused an inhibition of dopamine synthesis in the caudate nucleus and nucleus accumbens that was equivalent in both rat lines.

The analgesia-enhancing component of ingested amniotic fluid does not affect nicotine-induced antinociception in naltrexone-treated rats.

Ingestion of amniotic fluid and placenta by rats has been shown to enhance opioid-mediated antinociception but not affect the nonopioid-mediated antinociception produced by aspirin, suggesting specificity for opioid-mediated processes. However, enhancement by the active substance(s) in amniotic fluid and placenta (POEF, for placental opioid-enhancing factor) of antinociception produced by other nonopioid mechanisms has yet to be examined. The present experiments tested whether ingestion of amniotic fluid enhances the antinociception produced by nicotine injection.

Differential behavioral responses to cocaethylene of Long-Evans and Sprague-Dawley rats: role of serotonin.

Cocaethylene is a neuroactive metabolite derived from the concurrent consumption of cocaine and ethanol. The effects of cocaethylene on locomotor activity, stereotypy, and rearing in Long-Evans and Sprague-Dawley rats were compared. A single cocaine injection (molar equivalent of 60 mumol/kg cocaethylene, intraperitoneal) elicited a robust series of motor output behaviors, including locomotion, stereotypy, and rearing over a 30-minute testing period in Long-Evans rats.

Dopaminergic and glutamatergic mechanisms mediate the induction of FOS-like protein by cocaethylene.

Cocaethylene is a psychoactive metabolite formed during the combined consumption of cocaine and ethanol. As this metabolite has many properties in common with cocaine, it is conceivable that cocaethylene administration may induce the activity of nuclear transcription factors that regulate the expression of late-response genes. Therefore, the temporal induction of FOS-like protein in rat brain was examined following IP administration of 60 micromol/kg cocaethylene.

Opioid stimulation in the ventral tegmental area facilitates the onset of maternal behavior in rats.

This research investigated the effect of an increase or decrease in opioid activity in the ventral tegmental area (VTA) on the onset of maternal behavior in rats. In Experiment 1, the latency to show maternal behavior toward foster rat pups (sensitization latency) was determined in maternally naive female rats given either nothing or a unilateral intra-VTA injection of morphine sulfate (MS) (0.0, 0.

Blockade of digestion by famotidine pretreatment does not interfere with the opioid-enhancing effect of ingested amniotic fluid.

Ingestion of placenta or amniotic fluid by rats has been shown to enhance ongoing opioid-mediated antinociception, but does not, by itself, produce antinociception. This enhancement is produced by an active substance(s) in placenta and amniotic fluid that we have termed POEF for placental opioid-enhancing factor. Previous research has shown that enhancement requires mediation by the gastrointestinal system: gastric vagotomy blocks enhancement produced by ingested placenta; amniotic fluid injected SC or IP does not produce enhancement.

Ingestion of amniotic fluid by postpartum rats enhances morphine antinociception without liability to maternal behavior.

Ingestion of amniotic fluid or placenta by rats has been shown to enhance opioid-mediated analgesia induced by morphine injection, foot shock, vaginal/cervical stimulation, or late pregnancy. The present study was designed to determine whether this mechanism might be a means of providing greater analgesia during the periparturitional period without contributing to the disruption of maternal behavior (measured primarily as retrieval) that can result from excessive opioid levels. Postpartum primiparous rats, injected with either 2 or 3 mg/kg morphine sulfate or vehicle and given orogastric infusions of either amniotic fluid or saline, were tested for maternal behavior.

An adaptable microcomputer program for monitoring behavior.

We describe an improvement of a flexible and easy to use program for monitoring and recording behavior durations with IBM-compatible microcomputers and a companion program that provides additional versatility for handling data. Up to 35 behaviors or events can be monitored, and processing speed is fast enough to measure even very rapidly performed behaviors. No specialized hardware is required, and the data files that are created are compatible with commercially available software packages for statistical analysis.

Gastric vagotomy blocks opioid analgesia enhancement produced by placenta ingestion.

Ingestion of amniotic fluid or placenta by rats has been shown to enhance opioid-mediated analgesia induced by morphine injection, footshock, vaginal/cervical stimulation, or late pregnancy. This enhancement by ingestion appears to be specific to the central actions of opioids. The present study was designed to examine the possibility that information traveling via the vagus nerve might be involved in mediating this effect.