671 research outputs found
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 maternal “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. At parturition, or after extensive exposure to young, what emerges appears to be a single stereotyped maternal behavior pattern. However, it is actually a smoothly coordinated constellation of simpler actions with proximate causes that, when sequenced properly, have the appearance of a motivated, purposive, adaptive, pattern of caretaking. Over the past 50 years, much research has focused on finding the principal external and internal factors that convert the nonmaternal behavior patterns of the nonpregnant nullipara, the virgin, to the almost immediate and intense maternal behavior characteristic of the puerpera, the mother. This review is an attempt to summarize the many comprehensive, even encyclopedic, reviews of these factors, with an emphasis on brain mechanisms, and to highlight the gaps that remain in understanding the processes involved in the almost immediate onset of maternal caretaking behaviors observed in mammals at delivery. Where possible, the reader is directed to some of those excellent reviews
Effects of Lateral Hypothalamic Lesions on Placentophagia in Virgin, Primiparous, and Multiparous Rats
Lesions of the lateral hypothalamus (LH) were produced in pregnant and nonpregnant female rats through chronically implanted electrodes to investigate the effect of LH damage on placentophagia. Other variables investigated were prior parturitional experience and stimulus properties of the placenta. Lesions were produced under ether anesthesia 24 hr. prior to parturition in pregnant females and 24 hr. prior to placenta presentation in nonpregnant females.\ud
The LH lesions produced aphagia to a liquid diet. Pregnancy was not a significant variable in the initiation of placentophagia, but prior parturitional experience was a critical variable. Virgin and primiparous females did not exhibit placentophagia following LH damage, but multiparous females would eat placenta whenever the opportunity arose, independently of LH damage and pregnancy
Perinatal maternal and neonatal behaviour in\ud the captive reticulated giraffe
A captive reticulated giraffe was observed constantly for three weeks prior to, and periodically for 90 days subsequent to, the birth of her calf. Extensive observations were made of the birth sequence, feeding, drinking, sleeping and one instance of an infant distress call, as well as observations of the initiation of maternal behaviour (including licking, nursing, placentophagia, and what appeared to be helping the calf to stand, guiding the calf's movements, and attempts to respond to the calf's distress call)
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, 0.01, 0.03, 0.1 or 0.3 µg), on the first three days of a 10-day period of constant exposure to pups. Rats treated with 0.03 µg MS had significantly shorter sensitization latencies than did rats treated with 0.0 µg MS, 0.01 µg MS, or receiving no treatment (higher doses of morphine produced intermediate results). The facilitating effect of intra-VTA MS on the onset of maternal behavior was blocked by pretreatment with naltrexone hydrochloride and was found to have a specific site of action in the VTA (MS injections dorsal to the VTA were ineffective). In Experiment 2, sensitization latencies were determined in periparturitional rats given a bilateral intra-VTA injection of either the opioid antagonist naltrexone methobromide (quaternary naltrexone), its vehicle, a sham injection, or left untreated 40 min after delivery of the last pup. The mothers' own pups were removed at delivery; mothers were nonmaternal at the time of testing. Quaternary naltrexone treatment produced significantly slower sensitization to foster pups than did control conditions. Total activity and pup-directed activity did not differ significantly with treatment. The results demonstrate that increased opioid activity in the VTA facilitates the onset of maternal behavior in inexperienced nonpregnant female rats, and decreased opioid activity in the VTA disrupts the rapid onset of maternal behavior at parturition
Effects of Medial Preoptic Lesions on\ud Placentophagia and on the Onset of Maternal\ud Behavior in the Rat
Lesions of the medial preoptic area (MPO) were produced through permanently indwelling electrodes 24 hr prior to parturition in pregnant rats, or 24 hr prior to donor-placenta presentation in virgin rats determined in a pretest to be placentophages. The lesions had no disruptive effect on placentophagia in the virgin females. However, MPO lesions did delay the onset of placentophagia, pup-retrieval, and nestbuilding in some parturient rats. In others, lesions produced an impairment (in latency and quality) only of nest-building. None showed any impairment of pup-licking, or in the clear tendency to leave excreted waste away from the gathered pups. These results suggest the possibility of at least semi-independent mechanisms for the various components of maternal behavior
The effects of strain, reproductive condition, and strain of placenta donor on placentophagia in nonpregnant mice
The effects on placentophagia of strain, reproductive condition, and strain of placenta donor were observed in nonpregnant mice. Mice of the C57BL/6By and BALB/cBy strains were exposed to placentas of either strain after either no previous parturitional experience, one parturitional experience without nursing experience, or one parturitional experience with nursing experience. There was a significant effect of strain, a significant effect of reproductive condition, but no significant effect of strain of placenta donor. There was a significant interaction between strain and reproductive condition, but no significant interactions with placenta strain. It was inferred that the ability of a mouse to acquire and utilize relevant stimuli during and after parturition, in order to produce an emancipation of placentophagia from the physiological controls associated with parturition, is influenced by genotype
Placentophagia in Nonpregnant Rats:\ud Influence of Estrous Cycle Stage and Birthplace
Prior parturitional experience and genotype have previously been found to affect the proportion of nonpregnant female rats and mice that will eat foster placenta. The present series of experiments was designed to investigate the influence of estrous cycle stage on placentophagia in rats. Foster placenta was presented to nonpregnant Long-Evans females, purchased from a commercial breeder, for 15 min on 5 consecutive days. We found that virgin placentophages were most likely to have eaten placenta on the first presentation, unless the first presentation occurred during proestrus. In fact, virgins would not eat placenta for the first time during proestrus, regardless of test-day. However, once they had eaten placenta, either in a nonproestrus stage, or, in the case of primiparae, during parturition, they would eat placenta during proestrus. Long-Evans rats born in our laboratory differed from the purchased rats, manifesting an incidence of placentophagia that was too low to be analyzed by stage of the estrous cycle; when tested as primiparae, however, there were no differences between the two groups
Enhancement of Opioid-Mediated Analgesia\ud by Ingestion of Amniotic Fluid:\ud Onset Latency and Duration
Ingestion of placenta and amniotic fluid has been shown to enhance opioid-mediated analgesia produced by morphine injection, footshock, vaginal/cervical stimulation, and during late pregnancy in rats. The present study was designed to determine how soon after ingestion the enhancement begins and how long it lasts. Tail-flick latencies in Long-Evans rats were determined before and during vaginal/cervical stimulation; analgesia was measured as the percent increase in tail-flick latency during vaginal stimulation. After determination of baseline, rats were intubated with 0.25 ml of either amniotic fluid or beef bouillon. We found that analgesia enhancement was detectable as early as 5 minutes after ingestion of amniotic fluid, and the effect lasted at least 30 minutes, but no longer than 40 minutes
Amniotic-Fluid Ingestion Enhances\ud Morphine Analgesia During Morphine\ud Tolerance and Withdrawal in Rats
Ingestion of placenta and amniotic fluid has been shown to enhance opioid-mediated analgesia in rats produced by morphine injection. footshock, vaginal/cervical stimulation, and during late pregnancy. The present study was designed to investigate the effects of amniotic fluid ingestion on the characteristics of morphine dependency and withdrawal. Tail-flick latencies in Long-Evans rats were determined before and after repeated daily injections of morphine sulfate. It was found that ingestion of amniotic fluid after establishment of the morphine dependency, coupled with an injection of an otherwise ineffective dose of morphine, enhanced analgesia in morphine-dependent rats, and reversed hyperalgesia seen during withdrawal from morphine dependency
Placenta ingestion by rats enhances d- and k-opioid antinociception, but suppresses m-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 (m, d, k) in the antinociception-modulating effects of Placental Opioid-Enhancing Factor (POEF—presumably the active substance). Antinociception was measured on a 52 C hotplate in adult, female rats after they ingested placenta or control substance (1.0 g) and after they received an intracerebroventricular injection of a d-specific ([D-Pen2,D-Pen5]enkephalin (DPDPE); 0, 30, 50, 62, or 70 nmol), m-specific ([D-Ala2,N-MePhe4,Gly5-ol]enkephalin (DAMGO); 0, 0.21, 0.29, or 0.39 nmol), or k-specific\ud
(U-62066; spiradoline; 0, 100, 150, or 200 nmol) opioid receptor agonist. The results showed that ingestion of placenta potentiated d- and k-opioid antinociception, but attenuated m-opioid antinociception. This finding of POEF action as both opioid receptor-specific and complex\ud
provides an important basis for understanding the intrinsic pain-suppression mechanisms that are activated during parturition and modified by placentophagia, and important information for the possible use of POEF as an adjunct to opioids in pain management
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