Search

To determine whether the neurons of the medial preoptic area (MPOA) are necessary for pup-induced maternal behavior (MB) in juvenile and adult rats, subjects received bilateral injections of the neurotoxin N-Methyl-D-Aspartic acid into the MPOA. Controls were intact or were sham treated by surgical placement of the syringe barrel. The rats were then induced into MB by constant pup exposure. Starting at 27 (juvenile) or 60 (adult) days of age, rats were tested for MB for 12 consecutive days. After histological analysis, rats were categorized as having either large or small lesions of the MPOA. In juveniles, large lesions of the MPOA blocked retrieval and impaired nest-building, but crouching behavior was unaffected; small lesions had no effect on MB. In contrast, in adults, large or small lesions severely impaired all components of MB. The results suggest that in juvenile rats, the role of the MPOA neurons in MB is only partially established, whereas by 60 days of age, the unsubstitutable role of the MPOA in the neural circuit that mediates MB is fully established.

Cocaine was microinfused bilaterally (50 microg/0.5 microl/side) into the medial preoptic area (MPOA) or nucleus accumbens (NA), 2 regions within the rat brain neural circuit known to mediate maternal behavior (MB). Additionally, 2 sites not involved in this neural circuit, the dorsal striatum and dorsal medial hippocampus, were used as control sites. Microinfusion of cocaine into the MPOA or NA impaired MB, whereas infusion into the control sites did not. MB impairment was not temporally coincident with the increased locomotor activity, also documented after cocaine infusion into the MPOA or NA, arguing strongly that impaired MB is a direct, specific effect of cocaine in these areas, not a derivative of increased motor activity. This is the first demonstration that cocaine action on single central nervous system (CNS) sites can impair MB to the same extent as systemic injections. Thus, cocaine's simultaneous effect on multiple CNS sites is not required for MB impairment.

Our research has demonstrated that the lateral habenular nucleus (Lhb) is necessary for the hormonal onset but not the postpartum maintenance of maternal behavior in the rat (K. P. Corodimas, J. S. Rosenblatt, & J. I. Morrell, 1992; K. P. Corodimas, J. S. Rosenblatt, M. E. Canfield, & J. I. Morell, 1993; T. Matthews-Felton, K. P. Corodimas, J. S. Rosenblatt, & J. I. Morell, 1995). To test the role of the Lhb in the nonhormonal onset of maternal behavior, we used the sensitization model in which the continual exposure of females to pups induces maternal behavior. Ovariectomized females received bilateral cytotoxic lesions of neurons of either the Lhb or the dorsal medial cingulate cortex-hippocampus, or they were unoperated. Maternal behavior, activity, and oromotor carrying capability were tested. Complete lesions of the neurons of the Lhb induced significant deficits in pup retrieval and nest building. Sniffing, licking, and crouching behaviors were unaltered. Activity and carrying ability were normal. These results indicate a role for the Lhb that extends to the nonhormonally dependent onset of maternal behavior, but they also indicate a more limited role than in the mediation of the hormonal onset of the behavior.

In 16-day pregnant, hysterectomized-ovariectomized and estradiol benzoate-treated rats, cytotoxic lesions of the lateral habenula (Lhb) produced severe deficits in maternal behavior (K.P. Corodimas, J.S. Rosenblatt, M.E. Canfield, & J.I. Morrell, 1993). To determine if deficits could be found in parturient rats, females were bilaterally injected with kainic acid (KA) to produce cytotoxic lesions of the Lhb. Controls either received bilateral KA-induced lesions to the hippocampus or were unoperated. All females maintained their pregnancies, underwent parturition, and were tested for maternal behavior (pup retrieval, nursing, and nestbuilding), general activity, and oromotor carrying. Females with lesions of the Lhb had severe disruptions of all components of maternal behavior and postpartum estrus. These results extend previous findings that the Lhb is involved in the hormonal onset of maternal behavior and also demonstrate that the Lhb supports the display of postpartum estrus.

Expanding on research showing that radio-frequency-induced lesions of the habenular complex disrupt the hormonal onset of maternal behavior in rats, we explored the importance of neurons in the lateral (Lhb) subdivision of the habenular complex for the onset of maternal behavior. On Day 12 of pregnancy, bilateral cytotoxic lesions were produced in the Lhb with kainic acid or, as a control, just dorsal in the medial hippocampus. A 3rd group had radio-frequency-induced Lhb and medial (Mhb) lesions. On Day 16 of pregnancy, Ss were hysterectomized-ovariectomized, given estradiol, and tested 48 hr later for 10 days. Neuroanatomical tracing with fluoro-gold was then used to directly quantify the extent and location of Lhb neuron loss and to verify that Mhb neurons were intact. Cytotoxic lesions of the entire Lhb prevented the onset of all components of maternal behavior compared with controls. Results show that neurons in the Lhb, not the Mhb, are important for onset of maternal behavior in rats.

Bilateral peripeduncular (PPN) lesions made on the seventh postpartum day (L7) with either radiofrequency (RF) current or N-methyl-d,l-aspartic acid (NMDA)/phosphate buffered saline (PBS) reduced maternal aggression (MA) and partially inhibited lactation without producing significant deficits in other items of maternal behavior (MB). RF-PPN lesions did not interfere with prolactin secretion, which suggests that there was deficient oxytocinergic activity. The deficit in MA was not due to interruption of afferent suckling input to the PPN: either thelectomizing females (day L6) or producing bilateral knifecuts in the mesencephalon (placed caudal to the level of the PPN; Day L7) had no effect on MA, but both procedures impaired lactation. Deficits in MA produced by RF-PPN lesions developed gradually between Days L4 and L7; lesions made either prepartum or on Day L1 did not impair MA or MB. Deficits in lactation first appeared after RF-PPN lesions on Day L1.

The role of the habenular complex (Hbc) in the hormonal onset and nonhormonal maintenance of maternal behavior in rats was examined. In Experiment 1, bilateral lesions were produced in the Hbc on Gestational Day (GD) 12. On GD 16, animals were hysterectomized-ovariectomized and given estradiol benzoate (EB); they were then tested for maternal behavior 48 hr later. Hbc lesions delayed the appearance of all components of maternal behavior for several days. In Experiment 2, large Hbc lesions that were produced on Postpartum Day 4 caused only 1- or 2-day deficits in maternal behavior. These data suggest that the Hbc mediates the hormonal onset of maternal behavior. During the postpartum period, however, the importance of the Hbc for maternal behavior diminishes as the hormones of pregnancy become less important.