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PubMed2007

Evidence for non-genomic transmission of ecological information via maternal behavior in female rats.

Maternal behavior is flexible and programs offspring development. Using a novel manipulation, we demonstrate that rat maternal behavior is sensitive to ecologically relevant stimuli. Long-Evans hooded rat dams (F0) and pups were exposed to a predator condition (cat odor) or a control condition (no odor) for 1 h on the day of parturition. Predator-exposed F0 dams displayed significantly more maternal behavior (licking/grooming, arched-back nursing) relative to control-exposed dams across five subsequent observation days. Female offspring (F1) were raised to adulthood, bred and maternal behavior was observed. F1 dams reared by a predator-exposed F0 dam displayed significantly higher maternal behavior relative to F1 dams reared by a control-exposed F0 dam across 5 days of observation. Increased levels of maternal behavior in predator-reared (PR) F1 dams were evident even in F1 females that had been cross-fostered (CF) from a control-exposed F0 dam, suggesting a non-genomic transmission of increased levels of maternal behavior. Lactating PR F1 dams had significantly elevated estrogen receptor alpha and beta mRNA in the medial preoptic area relative to control-reared (CR) F1 dams. Furthermore, among CR F1 dams, there was no significant difference between those dams that had been CF from predator-exposed F0 dams and those that had been sham CF. These results support the hypothesis that flexible rat maternal behavior can shape offspring development according to current environmental conditions. The results also suggest that estrogen signaling may be part of an epigenetic mechanism by which changes in maternal behavior are passed from F0 to F1 dams.

Animals↗
PubMed2004

Effects of typical and atypical antipsychotic drugs on maternal behavior in postpartum female rats.

Understanding the effects of antipsychotic drugs (APDs) on social behaviors such as maternal behavior is valuable for understanding the complete spectrum of therapeutic and side-effects of antipsychotics. Although previous studies have suggested that typical antipsychotics impair maternal behavior, the effects of the atypical antipsychotics have not been systematically explored. The purpose of the present report was to examine the effects of typical (haloperidol, HAL) and several atypical (clozapine, CLZ; risperidone, RIS; quetiapine, QUE) antipsychotics on maternal behavior in female rats. Maternal behaviors were examined repeatedly over a period of 24 h after a single injection of a range of doses of HAL, CLZ, RIS or QUE on Day 6 postpartum. All antipsychotic drugs, typical or atypical, elicited a qualitatively similar disruptive effect on the active components of maternal behavior such as pup approach, pup retrieval and nest building at clinically relevant doses. However, HAL caused a prolonged disruption, whereas CLZ, RIS and QUE induced an early onset but shorter duration disruption. In addition, only the atypical antipsychotics showed some inhibitory effects on nursing behavior, possibly due to sedative side-effects shared by all atypical antipsychotics. The current generation of atypical antipsychotics shows a disruptive influence on maternal behavior similar to that of the typical antipsychotics. This effect may be intrinsic to antipsychotic activity or may be reflective of a side-effect. Since the latter is more likely, this may be an effect to avoid in the design of future antipsychotics.

Animals↗
PubMed2005

Current models and future directions for understanding the neural circuitries of maternal behaviors in rodents.

Maternal behaviors in rodents include a number of subcomponents, such as nursing, nest building, licking and grooming of pups, pup retrieval, and maternal aggression. Because each behavior involves a unique motor pattern, a unique ensemble neural circuitry must underlie each behavior. To what extent there is overlap in terms of brain regions and specific neurons for each circuit is being actively investigated. This review will first examine overlapping and separate components of pup retrieval and maternal aggression circuitries while examining a central role for medial preoptic area (MPA) in both behaviors. With an emphasis on experimental approaches, the review will then highlight recent findings and propose future directions for understanding maternal behavior regulation. Finally, examples for why studying the neural basis of maternal behaviors can bring insights to other areas of neuroscience, such as feeding, addiction, and anxiety and aggression regulation will be provided.

Aggression↗
PubMed2004

Predicting stability and change in toddler behavior problems: contributions of maternal behavior and child gender.

This study examined the stability and continuity of early-identified behavior problems and the factors associated with this stability. Children and their mothers (N=125) were seen when the children were 2 and 4 years of age. Maternal reports of child externalizing behavior and laboratory observations of child noncompliance were stable from age 2 to age 4. Early externalizing behaviors decreased over time; however, child noncompliance in the laboratory did not. Although few associations were found between maternal positive behavior and child behavior problems, maternal controlling behavior was related to increases in child behavior problems, particularly at high levels of both prior noncompliance and prior maternal control. Child noncompliance was predictive of increases in maternal controlling behavior over time.

Attention Deficit and Disruptive Behavior Disorder↗
PubMed2005

Effects of novel antipsychotics, amisulpiride and aripiprazole, on maternal behavior in rats.

RATIONALE: Rat maternal behavior, which entails complex motivational and social factors, is disrupted by the currently available typical and atypical antipsychotics. It is thought that this disruption reflects a side effect of antipsychotics, modeling the neuroleptic-induced negative or deficit state. Amisulpiride and aripiprazole are new atypical antipsychotics with mechanisms of action distinct from the current typical and atypical antipsychotics. The effects of these drugs on maternal behavior have not been explored. OBJECTIVE: In the present study, we systematically examined the behavioral effects of amisulpiride and aripiprazole on maternal behavior in postpartum female rats. METHODS: Various components of maternal behavior (pup retrieval, pup licking, nest building and pup nursing) were examined repeatedly over a period of 24 h after a single injection of three doses of amisulpiride (10, 30, and 100 mg/kg s.c.) and aripiprazole (3, 10, and 30 mg/kg). RESULTS: Amisulpiride at the lower doses (10 and 30 mg/kg) enhanced pup licking, and only at the highest dose disrupted the active components of maternal behavior such as pup retrieval and nest building. Its effect was delayed in onset and prolonged as compared to other antipsychotics. Aripiprazole, even at the highest dose (30 mg/kg) did not impair pup retrieval or pup licking. However, it did disrupt nest building and led to enhanced pup nursing. CONCLUSIONS: The unique effects of these two drugs may be due to their unique actions at the mesolimbic dopamine synapses. The sparing of the major components of maternal behavior by aripiprazole may be related to its partial agonist effects, whereas the enhancement of pup licking by amisulpiride may be related to its dose-dependent preferential effect on the presynaptic autoreceptors. The potential clinical implications of these findings are discussed.

Amisulpride↗
PubMed2002

Estrogen, progesterone, and pregnancy termination alter neural activity in brain regions that control maternal behavior in rats.

Estrogen stimulates maternal behavior in rats, but does so most potently when its administration is temporally coupled with the termination of pregnancy. In contrast, this effect of estrogen is blocked when subjects are administered a large dose of progesterone concurrent with estrogen. The current study was performed to examine the neural circuitry influenced by these treatments and pup presentation during the hormonally-mediated onset and inhibition of maternal behavior. In experiment I, estrogen induced c-Fos immunoreactivity (Fos-IR) in the medial preoptic area (MPOA) in virgin rats, but was much more effective when administered to pregnancy-terminated rats, suggesting that pregnancy termination increases MPOA's susceptibility to the physiological effects of estrogen. In experiment II, administering progesterone concurrently with estrogen in pregnancy-terminated rats strongly inhibited estrogen-stimulated Fos-IR in the MPOA, indicating that the physiological effects of estrogen on the MPOA are blocked if high progesterone levels are maintained. In experiment III, pregnancy-terminated subjects were administered estrogen, progesterone, or both hormones and presented with pups for 2 h. Approximately half of the subjects administered estrogen alone showed maternal behavior, but subjects receiving the other treatments were not maternal. In the MPOA, ventral bed nucleus of the stria terminalis (BSTv), and dorsal and intermediate lateral septum (LSd,i), maternal subjects showed the highest levels of Fos-IR, whereas subjects treated with progesterone alone or progesterone in combination with estrogen showed low levels of Fos-IR. These experiments suggest that estrogen could promote maternal behavior by enhancing pup-stimulated activity in the MPOA, BSTv, and LSd,i, regions believed to constitute the neural circuit that promotes maternal behavior, whereas progesterone could inhibit maternal behavior by inhibiting neural activity in some of these regions.

Animals↗
PubMed1991

Importance of progesterone and estrogen priming for the induction of maternal behavior by vaginocervical stimulation in sheep: effects of maternal experience.

The effects of treating ovariectomised nulliparous and multiparous ewes with progesterone and estrogen on maternal behavior with or without vagino-cervical stimulation were investigated. Following 48 h of estrogen treatment there was neither evidence for stimulation of maternal behavior, nor a reduction in aggressive behavior, towards lambs by either multiparous or nulliparous ewes compared with control treatment (injections of the oil vehicle). Following 5 min of mechanical vaginocervical stimulation, the multiparous estrogen-treated ewes showed both positive maternal responses (low pitch bleats, licking, sniffing and approaching the lamb) and a reduction in aggression (butts) and negative behavior (withdrawal from the lamb) towards the lambs, whereas the nulliparous ewes showed only a reduction in aggression and negative behavior. Neither group showed positive maternal responses following vaginocervical stimulation without steroid priming. When the ewes received two weeks of progesterone priming prior to estrogen treatment, both multiparous and nulliparous ewes showed reduced aggression towards, and withdrawal from, the lambs compared to the control condition, but no positive maternal responses apart from an increased sniffing of the lamb. After vaginocervical stimulation positive maternal responses showed by multiparous ewes were significantly potentiated compared to those shown following estrogen treatment alone. Nulliparous ewes remained unresponsive on positive maternal behaviors. These studies show that hormonal priming has little effect in inducing the onset of maternal behavior in multiparous or nulliparous sheep but is an essential prerequisite for vaginocervical stimulation to do so in multiparous animals.

Animals↗
PubMed1996

Maternal behavior in male rats: effects of medial preoptic area lesions and presence of maternal aggression.

Male rats exhibit maternal behavior prepuberally and in adulthood, but the neural mechanisms and the ability of males to respond to hormones that stimulate maternal aggression (following arousal of maternal behavior) in females have not been studies. In Experiment 1, males were exposed to pups to stimulate maternal behavior (sensitization) after either radiofrequency lesions of the MPOA or sham lesions with nonactivated electrodes that penetrated the MPOA. Nonsurgical males served as a CONTROL group. The LESION male group showed severe deficits in all components of maternal behavior compared to the latter two groups that showed no behavioral deficits. Females in the LESION group and those given SHAM 1 lesions (produced by electrodes without current introduced into the MPOA) also showed severe deficits in maternal behavior compared to SHAM 2 females (electrode lowered to above the MPOA without current) and nonsurgical CONTROL females. In Experiment 2, prolonged estradiol (E2), progesterone (P) treatment followed by an injection of either 20 micrograms or 100 micrograms/ kg estradiol benzoate (EB) or oil in castrated males was effective in stimulating short-latency maternal behavior, mainly in the 100 micrograms/kg EB group. Males of this group also showed a high level of maternal aggression that was inversely correlated with their latencies for maternal behavior. All groups showed maternal aggression when maternal behavior was established. The results indicate the MPOA mediates maternal behavior in males as it does in females; maternal aggression in males accompanies the stimulation of maternal behavior and may be stimulated by the same hormones.

Aggression↗
PubMed1995

Investigation into the role of cholecystokinin (CCK) in the induction and maintenance of maternal behavior in rats.

The biochemical regulation of maternal behavior has been extensively studied. Cholecystokinin (CCK), a gut peptide that is also present in the brain, recently has been implicated in the onset of maternal behavior in estrogen-primed virgin rats. The objective of the present set of studies was to delineate the role of CCK in the onset (Experiments 1-3) and maintenance (Experiments 4 and 5) of maternal behavior in rats. In the first study intracerebroventricular (i.c.v.) administration of CCK was unable to stimulate the onset of maternal behavior in estrogen-primed virgin rats. Similarly, i.c.v. infusions of CCK into pregnant rats, starting on Day 17 of gestation (Experiment 2), did not advance the onset of maternal behavior. Moreover, when CCK-filled minipumps were implanted intraperitoneally in estrogen-primed virgin rats, the rate of onset of maternal behavior was unaffected (Experiment 3). In contrast, direct infusions of CCK into the MPOA blocked the disruptive effects of beta-endorphin on the maintenance of maternal behavior in postpartum lactating rats (Experiment 4). In addition, proglumide, a CCK receptor antagonist, disrupted maternal behavior in postpartum lactating rats by increasing latencies to retrieve and crouch over the young (Experiment 5). These results support an involvement of CCK in the maintenance, but not the onset, of maternal behavior in rats.

Animals↗
PubMed1992

Effects of transections to the vomeronasal nerves or to the main olfactory bulbs on the initiation and long-term retention of maternal behavior in primiparous rats.

While the onset of maternal behavior at parturition is mediated by hormones, the maintenance of maternal behavior during the first few postpartum weeks depends on experiences acquired while the dam interacts with pups (Rosenblatt, 1990). In fact, if female rats are permitted as little as 2 h or maternal experience within 36 h after Cesarean delivery, they exhibit heightened maternal behavior during maternal induction tests 10 days later; in contrast, dams separated from young at the time of Cesarean delivery and not permitted a maternal experience fail to respond maternally in tests 10 days later (Orpen & Fleming, 1987). In this study we investigated the role of chemosensory input through the vomeronasal and main olfactory systems in this maternal experience effect. Six groups of primiparous females were tested for maternal behavior to foster pups presented 9-10 days after Cesarean delivery: three groups were permitted to interact with pups for a 2-h period 36 h after Cesarean delivery; and three groups were separated from pups until testing and were given no maternal experience. Within each experience condition, one group sustained bilateral section of the vomeronasal nerves, one sustained bilateral coronal cuts through the midsection of the main olfactory bulbs, and one group sustained small medial olfactory bulb cuts. The results showed that animals sustaining vomeronasal or olfactory transections, regardless of experience condition, exhibited significantly reduced latencies to maternal behavior in maternal induction tests. However, these chemosensory disruptions did not prevent an additional facilitation of maternal behavior produced by a prior maternal experience.

Animals↗
PubMed2005

The effects of adrenalectomy and corticosterone replacement on induction of maternal behavior in the virgin female rat.

Maternal behavior of the sensitized virgin rat is affected by approach-avoidance systems as well as by hypothalamic-pituitary-adrenal (HPA) axis, which is also activated during stress. The present experiments investigated the effects of adrenalectomy and of varying corticosterone concentrations on the onset and expression of maternal behavior in sensitized virgin rats. In the first experiment, latency to onset of maternal behavior and time spent licking once maternal were positively related to endogenous levels of corticosterone. However, few rats showed licking. In the second experiment, virgin rats were adrenalectomized or given sham surgeries before being sensitized and being given 0, 25, 100, 300, or 500 microg/mL of corticosterone in their drinking water. In the third experiment, virgin rats were adrenalectomized or given sham surgeries and given either control or corticosterone time-release pellets after being sensitized. Maternal behavior was then tested. Adrenalectomy increased licking in the second experiment and time over pups in the third experiment. Corticosterone replacement reduced licking in the second experiment and both licking and time over pups in the third experiment. In conclusion, exogenous corticosterone had an inhibitory effect on the expression of maternal behavior in the sensitized virgin rat, unlike the facilitatory effect previously found in the postpartum rat.

Administration, Oral↗
PubMed1988

Growth hormone is secreted by ectopic pituitary grafts and stimulates maternal behavior in rats.

The onset of maternal behavior at parturition in rats is hormonally regulated. Recently, we reported that treatment of behaviorally inexperienced, hypophysectomized (hypox), ovariectomized (ovx) rats with a sequential steroid treatment of progesterone (P) and estradiol (E2), and either ectopic anterior pituitary grafts or prolactin (PRL), stimulated maternal responsiveness toward foster young. That growth hormone (GH) has a number of PRL-like activities led us to ask whether the actions of PRL on maternal behavior were specific to PRL or might be shared by other PRL-like protein hormone, i.e., GH. In Experiment 1 we quantified plasma concentrations of GH and PRL by RIA in groups of hypox female rats that were ovariectomized and treated with a combination of ectopic pituitary grafts (Days 1-23) and Silastic capsules filled with P (Days 1-11) and E2 (Days 11-23). Blood samples were collected from Days 1 to 23 of treatment. Both plasma PRL and GH levels increased after grafting, initially rising 10- to 60-fold by Day 4 and gradually declining throughout the remainder of the 23-day sampling period. Throughout the 3-week period after grafting plasma GH levels were as high or higher than those of PRL. In Experiment 2 the behavioral effects of exogenously administered ovine (o)-GH were measured in groups of hypox, ovx rats that were treated with P and E2 as in Experiment 1. Experimental rats were injected twice daily with 0.25 mg oGH beginning on Day 1. Testing for maternal behavior toward foster young was conducted daily from Day 12 to Day 22. In steroid-treated rats, GH treatment stimulated a more rapid onset of maternal behavior (latencies of 3 vs greater than 10 days for vehicle-injected controls). These data indicate that GH, like PRL, is secreted by ectopic pituitary grafts and is capable of stimulating maternal behavior.

Animals↗
PubMed1999

Estrogen implants in the lateral habenular nucleus do not stimulate the onset of maternal behavior in female rats.

The natural onset of maternal behavior in the rat is hormonally mediated. Estrogen, progesterone, and prolactin administered to ovariectomized females in amounts and sequences that produce circulating levels similar to those found during pregnancy stimulate the onset of maternal behavior. In fact, maternal behavior can be stimulated by estrogen alone, administered either peripherally or by implant in the central nervous system. The lateral habenula (Lhb), which is a necessary component in the neural circuit that supports maternal behavior, contains a subset of neurons with estrogen receptors. The present study investigated whether estradiol implants directly in the Lhb are sufficient to stimulate maternal behavior. Female rats, hysterectomized and ovariectomized on day 16 of pregnancy, received estrogen implants in the Lhb or, as a positive control, in the medial preoptic area (MPOA). An additional control group received cholesterol implants in the Lhb. All females were tested for pup retrieval, nest building, crouching behavior, locomotor activity, and carrying behavior. Estradiol implants into the Lhb did not stimulate the onset of maternal behavior. Females with estrogen implants in the Lhb scored significantly lower in pup retrieval and crouching behavior compared to females with implants in the MPOA and were not significantly different from females with cholesterol implants in the Lhb. There were also no significant differences in overall activity or carrying behavior among the groups.

Animals↗
PubMed1982

Oxytocin induces maternal behavior in virgin female rats.

Intracerebroventricular administration of oxytocin to virgin female rats that had been ovariectomized and primed with estrogen 48 hours previously induced a rapid onset of full maternal behavior. The maternal behavior persisted and its incidence was dose-related. Tocinoic acid, the ring structure of oxytocin, also rapidly induced the onset of persistent, full maternal behavior. Arginine vasopressin induced persistent maternal behavior, but this behavior had a later onset. Prostaglandin F2 alpha induced strong partial maternal behavior, which showed early onset but did not persist. Many other peptides, ovarian steroids, and prostaglandin E2 were no more effective than saline. These findings suggest that the release of oxytocin and prostaglandin F2 alpha during labor may promote maternal behavior in rats.

Animals↗
PubMed2005

Effects of chronic typical and atypical antipsychotic drug treatment on maternal behavior in rats.

Understanding the effects of antipsychotics on maternal behavior is important for understanding the poor quality of mother-infant interaction in schizophrenia. Previous preclinical work has demonstrated that acute treatment with typical and atypical antipsychotics disrupts maternal behavior. However, the effects of chronic antipsychotic treatment on maternal behavior are unknown. This issue is of importance since clinical use of antipsychotic medication requires continuous exposure to these drugs. In this study, we treated postpartum rats with haloperidol (0.25 mg/kg/day) or olanzapine (7.5 mg/kg/day), via osmotic minipumps or daily injections for 3 weeks. Maternal behavior was assessed every third day. On each observation day, maternal behavior was observed twice, once just prior to the daily injection ("trough" as this was 24 h after last injection) and again 2 h after the injection ("peak"). Daily injections of haloperidol and olanzapine significantly disrupted pup retrieval, pup licking, nest building at peak, but this effect was gone by trough. Drug administration via minipumps also disrupted these behaviors, but the effects were less severe. Pup nursing was enhanced by either method of drug administration. No evidence of sensitization or tolerance associated with chronic drug treatment was found. It is concluded that chronic antipsychotic treatment disrupts active maternal behaviors and this disruption, most likely to lead to side effects in humans, should be avoided in future drug development.

Animals↗
PubMed1993

Persistent effects on maternal aggression of pregnancy but not of estrogen/progesterone treatment of nonpregnant ovariectomized rats revealed when initiation of maternal behavior is delayed.

Two experiments explored the effects on subsequent maternal aggression of interspersing 5-24 days between pregnancy termination and pup exposure to elicit maternal behavior. Pregnancy-terminated females displaying maternal behavior were compared to nonpregnant females also stimulated by pups to behave maternally and to pregnancy-terminated groups that were not exposed to pups. Pregnancies were terminated by hysterectomy-ovariectomy on Gestation Day 19 (G19), with pup exposure commencing after 6 days (Expt. 1), and by Cesarean section + ovariectomy (OVX), after delays of 5, 10, or 24 days (Expt. 2). In each study pregnancy-terminated, maternal groups were more aggressive than both nonpregnant, maternal groups and pregnancy-terminated, nonmaternal groups regardless of the imposed delays. In Expt. 2, postsurgical interval also was a significant factor, suggesting that surgical stress may elevate maternal aggression for several days. Prolonged treatment of nonpregnant OVX females (Expt. 3) with estrogen and progesterone elevated maternal aggression when pup exposure commenced 2 but not 7 days after termination of hormone treatment (Expt. 3). Therefore the physiological changes initiated during pregnancy that support maternal aggression persist for at least 4 weeks and may involve factors in addition to ovarian hormones that stimulate maternal behavior and maternal aggression. An additional unexpected finding was that nonpregnant (OVX) females had significantly higher Aggression scores after initiating maternal behavior.

Aggression↗
PubMed1991

Opioid receptor subtype involvement in maternal behavior in lactating rats.

Central or systemic administration of morphine disrupts maternal behavior in steroid-primed, pup-induced virgin and lactating rats. Morphine, the prototypical mu agonist, also interacts with different opioid receptor subtypes. The present study examined the effectiveness of five receptor-selective agonists, in addition to morphine, to disrupt maternal behavior in primiparous lactating rats following intracerebroventricular (i.c.v.) infusions in order to characterize opioid receptor subtype involvement in maternal behavior in the female rat. Virgin, Sprague-Dawley rats were mated and implanted with lateral ventricle cannulae on days 13-15 of gestation. On postpartum day 5, mothers were tested for maternal behavior 30 min after i.c.v. vehicle infusion (5 microliters). On day 6, rats received one of the following opioid receptor agonists 30 min before testing: beta-endorphin (mu/epsilon receptor subtype; 0.29, 0.72, 1.45, 2.9 nmol), DAGO (mu; 0.29, 0.72, 1.45, 2.9 nmol), morphine (mu; 0.29, 0.72, 1.45, 2.9, 14.5 nmol), DPDPE (delta; 2.9, 29 nmol), U50488H (kappa l; 2.9, 29, 145 nmol) and SKF10047 (sigma; 2.9, 29, 145 nmol). Only activation of mu opioid receptors dose-dependently disrupted maternal behavior in primiparous lactating rats. DPDPE, U50488 and SKF10047 had no discernible effect on maternal behavior. DAGO, a highly selective mu agonist, was even more potent than beta-endorphin and morphine in disrupting maternal behavior suggesting that maternal behavior is regulated by opioids interacting with the mu opioid receptor.

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗
PubMed1984

A quantitative analysis of the roles of dosage, sequence, and duration of estradiol and progesterone exposure in the regulation of maternal behavior in the rat.

The regulation of the onset of maternal behavior in the rat is under hormonal control. This study reports a new endocrine model for the study of the hormonal regulation of maternal responsiveness. The model employs the administration of physiological amounts of the steroids estradiol (E2) and progesterone (P) via Silastic implants to inexperienced nulliparous rats and measurement of the effects of these implants on maternal behavior. In the first two experiments, the levels of E2 and P in the sera of pregnant and hormone-treated rats were measured by RIA. Using known physiological treatments of E2 given in combination with P, the effects of E2 and P on maternal behavior were measured. Treatment with a combination of E2 at all dosages plus P for 2 weeks before P removal and behavioral testing stimulated a fast onset of maternal behavior in ovariectomized nulliparous rats. Exposure for 2 weeks to small E2 implants (1 or 2 mm; approximately 20-30 pg/ml serum) did not affect maternal responsiveness, whereas large E2 implants (10 mm; approximately 110 pg/ml serum) stimulated maternal behavior. P treatment alone had no behavioral effect. Simultaneous removal of E2 plus P before exposure to foster young also resulted in a stimulation of behavioral responsiveness, indicating that the presence of elevated titers of circulating E2 is not a requirement for stimulation to occur. In addition to facilitating a rapid onset of behavior, the quality of the response in steroid-primed rats was similar to that measured in lactating rats in a T-maze test. In another experiment, when female rats were treated with P before E2 administration, maternal behavior was rapidly induced. Thus, P itself can sensitize the female to the behavioral effects of E2. Finally, the duration of steroid-exposure before testing was found to influence maternal behavior. Increased durations of E2 plus P exposure before testing were accompanied by decreased latencies to respond maternally to foster young. These data indicate that during pregnancy, E2 and P prime the female to respond to her young at birth. The intensity of the steroidal priming increases as pregnancy progresses, and this primed potential is subsequently unmasked by the decline in P and the maintenance of E2 secretion around parturition. These findings demonstrate that behavioral processes can be modified in the adult animal as a result of long term changes in endocrine state, i.e. pregnancy.

Animals↗