The Experts below are selected from a list of 294 Experts worldwide ranked by ideXlab platform
Stephen C Gammie - One of the best experts on this subject based on the ideXlab platform.
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gabaa receptor signaling in caudal periaqueductal gray regulates Maternal Aggression and Maternal care in mice
Behavioural Brain Research, 2010Co-Authors: Grace Lee, Stephen C GammieAbstract:Maternal Aggression (Maternal defense) is exhibited by lactating females towards intruders and contributes to the protection of offspring. Enhancement of Gamma-Aminobutyric acid (GABA)(A) receptor signaling by benzodiazepines elevates Maternal Aggression, and we previously found indirect evidence (via c-Fos immunohistochemistry) that caudal periaqueductal gray (cPAG) and lateral septum (LS) could be sites where benzodiazepines increase Aggression. We recently found that GABA(A) receptor signaling in LS modulates Maternal Aggression, and in this study, we tested the hypothesis that GABA(A) receptor signaling in cPAG also regulates this behavior. Site-directed injections to cPAG were made in lactating mice using the GABA(A) receptor antagonist, bicuculline (3-9 ng) or the GABA(A) receptor positive modulator, chlordiazepoxide (CDP), a benzodiazepine (2.5-20 microg). Maternal Aggression, other Maternal behaviors, and anxiety-like measures (using the light-dark box) were then examined. GABA(A) receptor positive modulator did not increase Aggression, which could have resulted from a ceiling effect. However, 8 ng and 9 ng of bicuculline in cPAG significantly decreased Maternal Aggression without altering other Maternal behaviors or light-dark box performance, suggesting some GABA(A) receptor signaling in cPAG is required for full Maternal Aggression expression. Additionally, 7 ng of bicuculline significantly increased licking/grooming of pups, and decreased the number of transitions between the light and dark compartments of the light-dark box without affecting Aggression. Given these results indicating that antagonizing GABA(A) receptor in cPAG dose-dependently promotes offspring grooming behavior while impairing Aggression, it is possible that the cPAG represents a key site for decision making (Aggression versus other behaviors) in the lactating female.
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gabaa receptor signaling in the lateral septum regulates Maternal Aggression in mice
Behavioral Neuroscience, 2009Co-Authors: Grace Lee, Stephen C GammieAbstract:Maternal Aggression (Maternal defense) is a fierce Aggression produced by lactating females toward intruders that plays an important role in protection of vulnerable offspring. Enhancement of GABA(A) receptor signaling by benzodiazepines increases Maternal Aggression, and we recently found indirect evidence that lateral septum (LS) could be a key site where benzodiazepines elevate Aggression. In this study, we directly tested the hypothesis that activation of GABA(A) receptors in LS would promote Maternal Aggression while inhibition of this receptor would decrease Aggression. Site-directed injections to LS were made using the GABA(A) receptor antagonist, bicuculline (3-30 ng), or the GABA(A) receptor agonists, chlordiazepoxide, a benzodiazepine (2.5-5 microg), and muscimol (0.05-5 ng). Maternal Aggression and other behavioral measures were then evaluated in lactating mice. Neither GABA(A) receptor agonist elevated Aggression, which could reflect a ceiling effect. However, 7 ng of the GABA(A) receptor antagonist, bicuculline, in LS significantly decreased Maternal Aggression without altering other Maternal behaviors or light-dark box performance, suggesting some GABA(A) receptor signaling in LS is required for full Maternal Aggression expression. Together, these results confirm a role for GABA(A) receptor signaling in LS in the regulation of Maternal Aggression.
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neurotensin inversely modulates Maternal Aggression
Neuroscience, 2009Co-Authors: Stephen C Gammie, Kimberly L Danna, Hilary Gerstein, Sharon A StevensonAbstract:Abstract Neurotensin (NT) is a versatile neuropeptide involved in analgesia, hypothermia, and schizophrenia. Although NT is released from and acts upon brain regions involved in social behaviors, it has not been linked to a social behavior. We previously selected mice for high Maternal Aggression (Maternal defense), an important social behavior that protects offspring, and found significantly lower NT expression in the CNS of highly protective females. Our current study directly tested NT's role in Maternal defense. Intracerebroventricular (i.c.v.) injections of NT significantly impaired defense in terms of time aggressive and number of attacks at all doses tested (0.05, 0.1, 1.0, and 3.0 μg). Other Maternal behaviors, including pup retrieval, were unaltered following NT injections (0.05 μg) relative to vehicle, suggesting specificity of NT action on defense. Further, i.c.v. injections of the NT receptor 1 (NT1) antagonist, SR 48692 (30 μg), significantly elevated Maternal Aggression in terms of time aggressive and attack number. To understand where NT may regulate Aggression, we examined Fos following injection of either 0.1 μg NT or vehicle. Thirteen of 26 brain regions examined exhibited significant Fos increases with NT, including regions expressing NT1 and previously implicated in Maternal Aggression, such as lateral septum, bed nucleus of stria terminalis, paraventricular nucleus, and central amygdala. Together, our results indicate that NT inversely regulates Maternal Aggression and provide the first direct evidence that lowering of NT signaling can be a mechanism for Maternal Aggression. To our knowledge, this is the first study to directly link NT to a social behavior.
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Trpc2 gene impacts on Maternal Aggression, accessory olfactory bulb anatomy and brain activity
Genes brain and behavior, 2009Co-Authors: Nina S. Hasen, Stephen C GammieAbstract:The Trpc2 gene codes for an ion channel found in the vomeronasal organ (VNO). Studies using the Trpc2−/− (KO) mouse have exploited the gene's role in signal transduction to explore the VNO's role in pheromonally mediated behaviors. To date, no study has evaluated the impact of the Trpc2 gene on activity within the brain. In this study, we examine the gene's effect on brain regions governing Maternal Aggression. We intruder-tested lactating dams and then quantified Fos immunoreactivity (Fos-IR) in the vomeronasal amygdala, hypothalamus, olfactory regions and accessory olfactory bulb (AOB). Our data confirm previous reports that loss of the Trpc2 gene severely diminishes Maternal Aggression. We also show that deletion of the gene results in differential hypotrophy of the glomerular layer (GlA) of the AOB, with the anterior portion the GlA resembling that of wild-type mice, and the posterior portion reduced or absent. This anatomy is suggestive of residual functioning in the apical VNO of these animals. Our Fos study describes an impact of the deletion on a network of 21 brain regions involved in emotion, Aggression and olfaction, suggesting that signals from the VNO mediate activity throughout the brain. Home-cage observations of KO dams show specific deficits in nest-building, suggesting a role for pup pheromones in inducing and maintaining pup-directed Maternal behaviors as well as Maternal Aggression.
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Deletion of corticotropin-releasing factor binding protein selectively impairs Maternal, but not intermale Aggression
Neuroscience, 2008Co-Authors: Stephen C Gammie, Audrey F Seasholtz, Sharon A StevensonAbstract:Corticotropin-releasing factor (CRF) binding protein (CRF-BP) is a secreted protein that acts to bind and limit the activity of the neuropeptides, CRF and urocortin (Ucn) 1. We previously selected for high Maternal defense (protection of offspring) in mice and found CRF-BP to be elevated in the CNS of selected mice. We also previously determined that both CRF and Ucn 1 are potent inhibitors of offspring protection when administered centrally. Thus, elevated CRF-BP could promote defense by limiting endogenous actions of CRF or Ucn 1. To test this hypothesis, we crossed the deletion for CRF-BP into the mice selected for high Maternal defense and evaluated offspring protection and other Maternal behaviors. CRF-BP knockout (KO) mice exhibited significant deficits in Maternal Aggression relative to wild-type (WT) mice in three different measures. Other Maternal features were almost identical between groups, including dam and pup weight, litter size, nursing time, and pup retrieval. Both groups performed similarly in a forced swim stress test and Aggression in both groups was reduced following the swim test. Virgin KO female mice exhibited higher levels of anxiety-like behavior in terms of decreased time in the light portion of the light/dark box test. For males, no differences in light/dark box or swim test were found. However, increased anxiety-like behavior in male KO mice was identified in terms of contact and approach to a novel object both with and without previous exposure to the swim test. No differences in isolation induced resident intruder male Aggression were found between groups. Together, these results indicate that loss of CRF-BP selectively impairs Maternal, but not intermale Aggression and that loss of the gene induces anxiety-like behavior in males and females, but there are sex differences in terms of how that anxiety is revealed.
Inga D Neumann - One of the best experts on this subject based on the ideXlab platform.
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reduced brain corticotropin releasing factor receptor activation is required for adequate Maternal care and Maternal Aggression in lactating rats
European Journal of Neuroscience, 2013Co-Authors: Stefanie M Klampfl, Inga D Neumann, Oliver J BoschAbstract:The brain corticotropin-releasing factor (CRF) system triggers a variety of neuroendocrine and behavioural responses to stress. Whether Maternal behaviour and emotionality in lactation are modulated by CRF has rarely been investigated. In the present study, we measured CRF mRNA expression within the parvocellular part of the paraventricular nucleus in virgin and lactating Wistar rats bred for high (HAB) and low (LAB) anxiety-related behaviour or non-selected for anxiety (NAB). Further, we intracerebroventricularly infused synthetic CRF or the CRF receptor (CRF-R) antagonist D-Phe to manipulate CRF-R1/2 non-specifically in lactating HAB, LAB, and NAB dams, and monitored Maternal care, Maternal motivation, Maternal Aggression, and anxiety. The CRF mRNA expression in the parvocellular part of the paraventricular nucleus was higher in HAB vs. LAB rats independent of reproductive status. The lactation-specific decrease of CRF mRNA was confirmed in LAB and NAB dams but was absent in HAB dams. Intracerebroventricular CRF decreased Maternal care under basal conditions in the home cage in all breeding lines and reduced attack behaviour in HAB and LAB dams during Maternal defence. In contrast, D-Phe rescued Maternal care after exposure to Maternal defence in the home cage without influencing Maternal Aggression. Furthermore, D-Phe decreased and CRF tended to increase anxiety in HAB/NAB and LAB dams, respectively, suggesting an anxiogenic effect of CRF in lactating females. In conclusion, low CRF-R activation during lactation is an essential prerequisite for the adequate occurrence of Maternal behaviour.
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both oxytocin and vasopressin are mediators of Maternal care and Aggression in rodents from central release to sites of action
Hormones and Behavior, 2012Co-Authors: Oliver J Bosch, Inga D NeumannAbstract:Abstract In the mammalian peripartum period, the activity of both the brain oxytocin and vasopressin system is elevated as part of the physiological adaptations occurring in the mother. This is reflected by increased expression and intracerebral release of oxytocin and vasopressin, as well as increased neuropeptide receptor expression and binding. In this review we discuss the functional role of the brain oxytocin and vasopressin system in the context of Maternal behavior, specifically Maternal care and Maternal Aggression in rodents. In order to enable the identification of significant and peptide-specific contributions to the display of Maternal behavior, various complementary animal models of Maternal care and/or Maternal Aggression were studied, including rats selectively bred for differences in anxiety-related behavior (HAB and LAB dams), monitoring of local neuropeptide release during ongoing Maternal behavior, and local pharmacological or genetic manipulations of the neuropeptide systems. The medial preoptic area was identified as a major site for oxytocin- and vasopressin-mediated Maternal care. Furthermore, both oxytocin and vasopressin release and receptor activation in the central amygdala and the bed nucleus of the stria terminalis play an important role for Maternal Aggression. This article is part of a Special Issue entitled Oxytocin, Vasopressin, and Social Behavior.
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changes in the intensity of Maternal Aggression and central oxytocin and vasopressin v1a receptors across the peripartum period in the rat
Journal of Neuroendocrinology, 2011Co-Authors: Sarah Caughey, Stefanie M Klampfl, Oliver J Bosch, Inga D Neumann, Valerie Bishop, J Pfoertsch, Simone MeddleAbstract:Maternal aggressive behaviour, which protects the offspring from harm, is one component of Maternal behaviour. Not only Maternal Aggression, but also Maternal care and social behaviour in general, is regulated by the brain oxytocin (OXT) and vasopressin (AVP) systems. In the present study, we quantified the intensity of Maternal Aggression using the Maternal defence test at key time points throughout pregnancy, parturition and lactation. Furthermore, we quantified changes in central OXT and arginine AVP V1a receptor (V1a-R) binding in brain regions known to be important in regulating Maternal Aggression, aiming to investigate whether central changes coincide with the intensity of this behaviour. The intensity of Aggression was found to dramatically change over the peripartum period, with its first appearance on the day before parturition. Aggression intensity fell immediately after parturition, although it increased during days 4-7 of lactation, before almost disappearing at weaning. OXT receptor (OTR) and V1a-R binding also showed changes through the peripartum period. OTR binding was highest at parturition within the bed nucleus of the stria terminalis and medial preoptic area and on days 4-7 of lactation in the lateral septum (LS) compared to any other time point during the peripartum period. OTR binding positively correlated with the peak of Maternal Aggression, suggesting that OXT may act in the LS to facilitate the expression of aggressive behaviour. At parturition, V1a-R binding was at its highest levels in the paraventricular nucleus and central amygdala (CeA) and, in the LS, V1a-R binding positively correlated with aggressive behaviour. V1a-R mRNA expression was also increased within the CeA at parturition. Taken together, the observed fluctuations in OTR and V1a-R binding in the neural circuitry important for regulating Maternal behaviour may ensure that Maternal Aggression is expressed at the correct time during the peripartum period.
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Vasopressin released within the central amygdala promotes Maternal Aggression.
The European journal of neuroscience, 2010Co-Authors: Oliver J Bosch, Inga D NeumannAbstract:Vasopressin regulates important aspects of social behaviour. Although vasopressin is more prominent in the expression of male social behaviours, we recently demonstrated its role in the fine-tuned maintenance of Maternal care in lactating rats. Here, we investigate the involvement of brain vasopressin in the regulation of Maternal Aggression in lactating Wistar rats selectively bred for either high (HAB) or low (LAB) anxiety-related behaviour. The genetically determined elevation in vasopressin mRNA expression was confirmed within the hypothalamic paraventricular nucleus of virgin and lactating HAB rats and was additionally found in limbic brain areas. Lactating HAB dams are more Maternally aggressive as part of their generally higher level of Maternal care compared with LAB rats. Using intracerebral microdialysis, we describe increased vasopressin release within the central amygdala, but not the paraventricular nucleus, during Maternal Aggression only in HAB dams. Moreover, the release of vasopressin within the central amygdala was positively correlated with the display of offensive behaviour. Blockade of local vasopressin actions by bilateral administration of a selective vasopressin V1a receptor antagonist into the central amygdala reduced Maternal Aggression in HAB dams, whereas synthetic vasopressin increased the low level of Aggression in LAB rats. Vasopressin receptor binding within the central amygdala or the paraventricular nucleus was similar in HAB and LAB females. In conclusion, vasopressin is an important neuropeptide regulating Maternal aggressive behaviour, thus further extending its involvement in female social behaviour. Differences in intracerebral vasopressin release within the central amygdala rather than local vasopressin receptor binding contribute to the level of Maternal Aggression.
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Maternal behaviour is associated with vasopressin release in the medial preoptic area and bed nucleus of the stria terminalis in the rat
Journal of Neuroendocrinology, 2010Co-Authors: Oliver J Bosch, Rainer Landgraf, J Pfortsch, Daniela I Beiderbeck, Inga D NeumannAbstract:The neuropeptide arginine vasopressin was recently shown to be an important regulator of female social behaviour, including Maternal care and Aggression. A key brain site for vasopressin- as well as oxytocin-mediated Maternal care is the medial preoptic area (MPOA). Together with the adjacent bed nucleus of the stria terminalis (BNST), these brain regions are considered to form a 'super-region' for Maternal behaviour. In the present study, we investigated the vasopressin and oxytocin systems within the MPOA and the BNST during Maternal care in lactating rats in more detail. Binding to V1a and oxytocin receptors in the BNST and to oxytocin receptors in the MPOA was increased in lactation. Furthermore, microdialysis revealed that vasopressin release significantly increased (MPOA) or tended to increase (BNST) during different phases of Maternal care (i.e. with or without suckling stimulus). In support, manipulations of V1a receptors in the MPOA are known to alter Maternal care. We now show that local injection of a selective V1a receptor antagonist bilaterally into the BNST did not affect Maternal care, but reduced Maternal Aggression and tended to lower anxiety-related behaviour. The release of oxytocin did not change in any of the brain regions during Maternal care. The results obtained indicate that locally-released vasopressin within the MPOA and the BNST is important for the maintenance of complex Maternal behaviours, including Maternal care and Aggression, respectively.
Oliver J Bosch - One of the best experts on this subject based on the ideXlab platform.
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more than reproduction central gonadotropin releasing hormone antagonism decreases Maternal Aggression in lactating rats
Journal of Neuroendocrinology, 2019Co-Authors: Doris S Bayerl, Stefanie M Klampfl, Oliver J BoschAbstract:Gonadotropin-releasing hormone (GnRH) is a major regulator and activator of the hypothalamic-pituitary-gonadal axis. Many studies have demonstrated the importance of GnRH in reproduction and sexual behaviour. However, to date, only a single study shows an involvement of GnRH in Maternal behaviour where a 30% reduction of GnRH neurones abolishes a mother's motivation to retrieve pups. On this basis, we aimed to investigate the effects of acute central GnRH receptor blockade in lactating rats on Maternal care under non-stress and stress conditions, Maternal motivation in the pup retrieval test, Maternal anxiety on the elevated plus maze, and Maternal Aggression in the Maternal defence test. We found that acute central infusion of a GnRH antagonist ([d-Phe2,6 ,Pro3 ]-luteinising hormone-releasing hormone; 0.5 ng 5 μL-1 ) impaired a mother's attack behaviour against a female intruder rat during the Maternal defence test compared to vehicle controls. However, in contrast to the previous study on reduced GnRH neurones, acute central GnRH antagonism did not affect pup retrieval, nor any other parameter of Maternal behaviour or Maternal anxiety. Taken together, GnRH receptor activation is mandatory for protection of the offspring. These findings shed new light on GnRH as a neuropeptide acting not exclusively on the reproductive axis but, additionally, on Maternal behaviour including pup retrieval and Maternal Aggression.
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Maternal stress and the mpoa activation of crf receptor 1 impairs Maternal behavior and triggers local oxytocin release in lactating rats
Neuropharmacology, 2018Co-Authors: Paula Brunton, Stefanie M Klampfl, Milena M Schramm, Barbara M Gasner, Katharina Hubner, Audrey F Seasholtz, Doris S Bayerl, Oliver J BoschAbstract:Abstract Maternal behavior and anxiety are potently modulated by the brain corticotropin-releasing factor (CRF) system postpartum. Downregulation of CRF in limbic brain regions is essential for appropriate Maternal behavior and an adaptive anxiety response. Here, we focus our attention on arguably the most important brain region for Maternal behavior, the hypothalamic medial preoptic area (MPOA). Within the MPOA, mRNA for CRF receptor subtype 1 (protein: CRFR1, gene: Crhr1) was more abundantly expressed than for subtype 2 (protein: CRFR2, gene: Crhr2), however expression of Crhr1, Crhr2 and CRF-binding protein (protein: CRFBP, gene: Crhbp) mRNA was similar between virgin and lactating rats. Subtype-specific activation of CRFR, predominantly CRFR1, in the MPOA decreased arched back nursing and total nursing under non-stress conditions. Following acute stressor exposure, only CRFR1 inhibition rescued the stress-induced reduction in arched back nursing while CRFR1 activation prolonged the decline in nursing. Furthermore, inhibition of CRFR1 strongly increased Maternal Aggression in the Maternal defense test. CRFR1 activation had anxiogenic actions and reduced locomotion on the elevated plus-maze, however neither CRFR1 nor R2 manipulation affected Maternal motivation. In addition, activation of CRFR1, either centrally or locally in the MPOA, increased local oxytocin release. Finally, inhibition of CRFBP (a potent regulator of CRFR activity) in the MPOA did not affect any of the Maternal parameters investigated. In conclusion, activity of CRFR in the MPOA, particularly of subtype 1, needs to be dampened during lactation to ensure appropriate Maternal behavior. Furthermore, oxytocin release in the MPOA may provide a regulatory mechanism to counteract the negative impact of CRFR activation on Maternal behavior.
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central v1b receptor antagonism in lactating rats impairment of Maternal care but not of Maternal Aggression
Journal of Neuroendocrinology, 2014Co-Authors: Doris S Bayerl, Stefanie M Klampfl, Oliver J BoschAbstract:Maternal behaviour in rodents is mediated by the central oxytocin and vasopressin systems, among others. The role of vasopressin, acting via the V1a receptor (V1aR), on Maternal care and Maternal Aggression has recently been described. However, a potential involvement of the V1b receptor (V1bR) in Maternal behaviour has only been demonstrated in knock-out mice. Therefore, we aimed to examine the effects of central pharmacological manipulation of the V1bR on Maternal behaviour in lactating Wistar rats. On pregnancy day 18, female rats were implanted with a guide cannula targeting the lateral ventricle. After parturition, dams received once daily an acute central infusion of a specific V1bR agonist (d[Leu4,Lys8]VP) or V1bR antagonist (SSR149415) followed by observations of Maternal care (lactation day (LD) 1), Maternal motivation in the pup retrieval test (LD 2), anxiety-related behaviour on the elevated plus-maze (LD 3), and Maternal Aggression in the Maternal defence test followed by Maternal care monitoring (LD 4). Our data demonstrate that under non-stress conditions the V1bR antagonist decreased the occurrence of both nursing and mother-pup interaction, while the V1bR agonist did not affect either parameter. Under stress conditions, i.e. after the Maternal defence test, mother-pup interaction was decreased by infusion of the V1bR antagonist. During the Maternal defence test, neither treatment affected aggressive or non-aggressive behaviour. Finally, neither treatment altered Maternal motivation or anxiety. In conclusion, central V1bR antagonism modulates aspects of Maternal care, but not of Maternal Aggression or Maternal motivation, in lactating rats. These findings further extend our knowledge on the vasopressin system as a vital mediator of Maternal behaviour. This article is protected by copyright. All rights reserved. Language: en
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Maternal Aggression in rodents brain oxytocin and vasopressin mediate pup defence
Philosophical Transactions of the Royal Society B, 2013Co-Authors: Oliver J BoschAbstract:The most significant social behaviour of the lactating mother is Maternal behaviour, which comprises Maternal care and Maternal Aggression (MA). The latter is a protective behaviour of the mother serving to defend the offspring against a potentially dangerous intruder. The extent to which the mother shows aggressive behaviour depends on extrinsic and intrinsic factors, as we have learned from studies in laboratory rodents. Among the extrinsic factors are the pups’ presence and age, as well as the intruders’ sex and age. With respect to intrinsic factors, the mothers’ innate anxiety and the prosocial brain neuropeptides oxytocin (OXT) and arginine vasopressin (AVP) play important roles. While OXT is well known as a Maternal neuropeptide, AVP has only recently been described in this context. The increased activities of these neuropeptides in lactation are the result of remarkable brain adaptations peripartum and are a prerequisite for the mother to become Maternal. Consequently, OXT and AVP are significantly involved in mediating the fine-tuned regulation of MA depending on the brain regions. Importantly, both neuropeptides are also modulators of anxiety, which determines the extent of MA. This review provides a detailed overview of the role of OXT and AVP in MA and the link to anxiety.
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reduced brain corticotropin releasing factor receptor activation is required for adequate Maternal care and Maternal Aggression in lactating rats
European Journal of Neuroscience, 2013Co-Authors: Stefanie M Klampfl, Inga D Neumann, Oliver J BoschAbstract:The brain corticotropin-releasing factor (CRF) system triggers a variety of neuroendocrine and behavioural responses to stress. Whether Maternal behaviour and emotionality in lactation are modulated by CRF has rarely been investigated. In the present study, we measured CRF mRNA expression within the parvocellular part of the paraventricular nucleus in virgin and lactating Wistar rats bred for high (HAB) and low (LAB) anxiety-related behaviour or non-selected for anxiety (NAB). Further, we intracerebroventricularly infused synthetic CRF or the CRF receptor (CRF-R) antagonist D-Phe to manipulate CRF-R1/2 non-specifically in lactating HAB, LAB, and NAB dams, and monitored Maternal care, Maternal motivation, Maternal Aggression, and anxiety. The CRF mRNA expression in the parvocellular part of the paraventricular nucleus was higher in HAB vs. LAB rats independent of reproductive status. The lactation-specific decrease of CRF mRNA was confirmed in LAB and NAB dams but was absent in HAB dams. Intracerebroventricular CRF decreased Maternal care under basal conditions in the home cage in all breeding lines and reduced attack behaviour in HAB and LAB dams during Maternal defence. In contrast, D-Phe rescued Maternal care after exposure to Maternal defence in the home cage without influencing Maternal Aggression. Furthermore, D-Phe decreased and CRF tended to increase anxiety in HAB/NAB and LAB dams, respectively, suggesting an anxiogenic effect of CRF in lactating females. In conclusion, low CRF-R activation during lactation is an essential prerequisite for the adequate occurrence of Maternal behaviour.
Judith M Stern - One of the best experts on this subject based on the ideXlab platform.
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functions of the caudal periaqueductal gray in lactating rats kyphosis lordosis Maternal Aggression and fearfulness
Behavioral Neuroscience, 1998Co-Authors: Joseph S Lonstein, Danielle A Simmons, Judith M SternAbstract:Severe impairment of the kyphotic nursing posture in lactating rats found previously after prepartum lesions of the caudal intercollicular periaqueductal gray (cPAG-x) was confirmed and was extended to a continuous 24-hr period. Litters of cPAG-x dams gained ~ 10% less weight postnatally than controls, which was in part related to their dams' compensatory prone nursing posture that was ineffective for milk letdown. Sexual proceptivity and receptivity (lordosis) during the postpartum estrus were virtually eliminated in subjects with relatively large bilateral cPAG lesions. The doubling of Maternal attacks toward a male intruder after lesioning was also confirmed and was related to reduced tearfulness in an elevated plus-maze. Thus, the cPAG plays a multifaceted role in parturient rats; it is involved in the mediation of nursing, sexual, aggressive, and fear behaviors. During the early postpartum (PP) period, lactating rats are in physical contact with their litters for approximately
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role of the midbrain periaqueductal gray in Maternal nurturance and Aggression c fos and electrolytic lesion studies in lactating rats
The Journal of Neuroscience, 1997Co-Authors: Joseph S Lonstein, Judith M SternAbstract:the upright, crouched, or kyphotic, nursing posture of lactating rats is dependent on suckling stimulation from pups. Because of the neuroanatomical connections of the periaqueductal gray (PAG) and its sensorimotor integration of the analogous lordosis posture displayed by sexually receptive female rats, the possible role of the PAG in kyphosis was investigated using c-fos immunocytochemistry and electrolytic lesions. Lactating rats interacting with and nursing a litter of suckling pups showed greater Fos-immunoreactive nuclei in the lateral and ventrolateral caudal PAG (cPAGl,vl) compared with dams receiving nonsuckling somatosensory, distal, or no stimulation from pups. In contrast, this pattern was not evident in the rostral PAG, where the highest Fos levels occurred in nonsuckled dams, or in five other brainstem sites with either no group differences (peripenduncular, dorsal raphe, and pontine nuclei) or negligible Fos (ventral tegmental area, spinal trigeminal nuclei). After bilateral electrolytic lesions of the cPAGl,vl during gestation or on day 7 postpartum, active Maternal behaviors, such as retrieval and licking of pups, and total nursing time were essentially normal. Kyphotic nursing, however, was reduced by 85%, nursing in prone and supine postures increased substantially, and 24 hr litter weight gains were reduced, particularly early in lactation (by 26%). Furthermore, lesioned rats attacked a strange male twice as often as controls did, which is suggestive of reduced fearfulness. These results extend the known roles of the PAG in reproductive and defensive behaviors to the postural control of suckling-induced kyphotic nursing and the modulation of Maternal Aggression.
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Maternal Aggression in rats effects of olfactory bulbectomy znso4 induced anosmia and vomeronasal organ removal
Hormones and Behavior, 1995Co-Authors: Jane M Kolunie, Judith M SternAbstract:Abstract Previous studies from our laboratory indicate that somatosensory inputs to the snout and ventral trunk, but not visual or auditory stimuli, play critical roles in the elicitation and maintenance of Maternal Aggression by lactating Norway rats toward a strange male intruder. There are conflicting reports on the influence of olfaction on Maternal Aggression. We explored the possible roles of central or peripheral anosmia on Maternal Aggression in Long–Evans rats during early lactation. In Experiment 1, responsiveness to both volatile and non-volatile odors was eliminated by bilateral olfactory bulbectomy (BOB), carried out during mid-gestation. BOB resulted in a reduced likelihood and intensity of Maternal Aggression on days 1 and 5 of lactation (L1 and L5), but also severe deficiencies in Maternal behavior and litter growth and survival. In Experiment 2, anosmia to volatile odors was induced by spraying zinc sulfate intranasally on gestation day 21 and L1. This treatment had little or no effect on Maternal Aggression on L1 or L2 or on Maternal behavior, especially if there was a 1-day recovery between the second treatment and testing. In Experiment 3, responsiveness to non-volatile odors was eliminated by vomeronasal-organ removal (VNX) carried out prior to mating. VNX did not disturb Maternal behavior on L2–L8 or Maternal Aggression on L1 or L5. These results and others suggest that the expression of Maternal Aggression is affected by volatile odors, mediated possibly by accessory chemosensory systems such as the septal organ, or by neural changes that follow olfactory deafferentation, or both.
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Maternal Aggression in rats effects of olfactory bulbectomy znso4 induced anosmia and vomeronasal organ removal
Hormones and Behavior, 1995Co-Authors: Jane M Kolunie, Judith M SternAbstract:Abstract Previous studies from our laboratory indicate that somatosensory inputs to the snout and ventral trunk, but not visual or auditory stimuli, play critical roles in the elicitation and maintenance of Maternal Aggression by lactating Norway rats toward a strange male intruder. There are conflicting reports on the influence of olfaction on Maternal Aggression. We explored the possible roles of central or peripheral anosmia on Maternal Aggression in Long–Evans rats during early lactation. In Experiment 1, responsiveness to both volatile and non-volatile odors was eliminated by bilateral olfactory bulbectomy (BOB), carried out during mid-gestation. BOB resulted in a reduced likelihood and intensity of Maternal Aggression on days 1 and 5 of lactation (L1 and L5), but also severe deficiencies in Maternal behavior and litter growth and survival. In Experiment 2, anosmia to volatile odors was induced by spraying zinc sulfate intranasally on gestation day 21 and L1. This treatment had little or no effect on Maternal Aggression on L1 or L2 or on Maternal behavior, especially if there was a 1-day recovery between the second treatment and testing. In Experiment 3, responsiveness to non-volatile odors was eliminated by vomeronasal-organ removal (VNX) carried out prior to mating. VNX did not disturb Maternal behavior on L2–L8 or Maternal Aggression on L1 or L5. These results and others suggest that the expression of Maternal Aggression is affected by volatile odors, mediated possibly by accessory chemosensory systems such as the septal organ, or by neural changes that follow olfactory deafferentation, or both.
Randy J. Nelson - One of the best experts on this subject based on the ideXlab platform.
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paternal Aggression in a biparental mouse parallels with Maternal Aggression
Hormones and Behavior, 2008Co-Authors: Brian C Trainor, Sima M Finy, Randy J. NelsonAbstract:Environmental and social factors have important effects on aggressive behaviors. We examined the effect of reproductive experience on Aggression in a biparental species of mouse, Peromyscus californicus. Estrogens are important in mediating aggressive behavior so we also examined estrogen receptor expression and c-fos for insights into possible mechanisms of regulation. Parental males were significantly more aggressive than virgin males, but no significant differences in estrogen receptor alpha or beta expression were detected. Patterns of c-fos following Aggression tests suggested possible parallels with Maternal Aggression. Parental males had more c-fos positive cells in the medial amygdala, and medial preoptic area relative to virgin males. The medial preoptic area is generally considered to be relatively less important for male-male Aggression in rodents, but is known to have increased activity in the context of Maternal Aggression. We also demonstrated through habituation-dishabituation tests that parental males show exaggerated investigation responses to chemical cues from a male intruder, suggesting that heightened sensory responses may contribute to increased parental Aggression. These data suggest that, in biparental species, reproductive experience leads to the onset of paternal Aggression that may be analogous to Maternal Aggression.
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Maternal Aggression persists following lipopolysaccharide induced activation of the immune system
Physiology & Behavior, 2006Co-Authors: Zachary M Weil, Eliot Dow, Stephanie L K Bowers, Randy J. NelsonAbstract:Lactating females direct aggressive behaviors towards intruders presumably to reduce the likelihood of infanticide of their pups. Infected animals display a constellation of responses that include lethargy, anorexia, and decreased social interactions. This suite of responses is referred to as sickness behavior, and is putatively part of an adaptive strategy to aid the organism in recovery from infection. Previous work has suggested that animals can suppress the behavioral symptoms of sickness in order to engage in adaptive behaviors. To test whether adaptive nest defense is affected by illness, dams received a peripheral injection of either saline or lipopolysaccharide (LPS [50, 400, or 1000 μg/kg]), a non-replicating component of bacterial cell walls that activates the immune system. Simulated infection with LPS reduced body mass and food intake in dams and interfered with litter growth in a dose-dependent manner. Generally, nest defense was unaffected by LPS; the proportion of dams displaying Maternal Aggression against a male intruder, as well as the latency and duration of aggressive encounters were only suppressed at the highest LPS dose tested. Further, LPS treatment also altered non-agonistic behavior during the Aggression test as indicated by reduced social investigation of the intruder and an increased time spent immobile during the session. LPS administration also significantly increased serum corticosterone concentrations in lactating females. These findings suggest that Maternal Aggression is not suppressed by LPS-evoked immune activation at doses that attenuate other aspects of Maternal and social behavior.
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High Maternal Aggression in dwarf hamsters (Phodopus campbelli and P. sungorus)
Aggressive Behavior, 2005Co-Authors: Stephen C Gammie, Randy J. NelsonAbstract::::::::::::::::: :::::::::::::::: : The defense of offspring, termed Maternal Aggression, is a highly conserved behavior in mammals, including rodents. This study examined relative levels of Maternal Aggression in two closely related dwarf hamster species, Phodopus campbelli and P. sungorus, that normally inhabit high latitude, boreal environments. When tested with first litters and with the breeder male remaining with the female (for P. campbelli the male is necessary for successful rearing of offspring), both species exhibited high levels of Maternal Aggression with average duration of aggressive behavior480 sec for a 10 min test. For P. sungorus, males are not required to rear offspring. P. sungorus females with either one or multiple litters (singly housed after impregnation) exhibited significantly higher levels of Aggression (4300 sec) relative to females co-housed with the sires. In terms of species differences in attack style, P. campbelli exhibited a boxing or clawing strategy for B50% of total attack time, but for P. sungorus, this form of attack occurredo5% of the time. For P. sungorus, attacks to the vulnerable belly and flank constituted490% of all attacks, but these regions were attacked B50% of the time for P. campbelli. A survey of levels of Maternal Aggression of rodents in other genera suggests that Maternal Aggression in Phodopus is at the high end of the spectrum. Results of this study suggest that the presence of the breeder male may actually suppress Aggression in P. sungorus. This fact, as well as its high level of Aggression and its distant relationship to mice and rats, suggest P. sungorus as a possible model for future studies on the neurobiological basis of Maternal Aggression. The relationship between the high rates of Maternal Aggression and life history strategy in Phodopus is discussed. Aggr. Behav. 31:294–302, 2005. r 2005 Wiley-Liss, Inc.
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cfos and pcreb activation and Maternal Aggression in mice
Brain Research, 2001Co-Authors: Stephen C Gammie, Randy J. NelsonAbstract:Lactating mice exhibit a dramatic increase in Aggression, termed Maternal Aggression, only in association with the rearing and protection of their offspring. Previous work indicates that the neural mechanisms underlying Maternal and male Aggression are different in rodents. In this study, we sought to examine possible neural regions involved in the control of Maternal Aggression by combining behavioral testing with immunohistochemistry for both cFOS and pCREB, two indirect markers of neuronal activity. All lactating female mice were exposed to a male intruder for 20 min and those exhibiting Maternal Aggression were placed in one group and those that were non-aggressive were placed in a second group. Thus, the sensory stimuli were similar and the main difference between the two groups was the behavior. cFOS expression increased significantly in the claustrum, bed nucleus of the stria terminalis, medial preoptic nucleus, paraventricular nucleus, medial amygdala, and cortical amygdala in association with Maternal Aggression. In contrast, the number of pCREB-positive cells significantly increased only in the ventrolateral portion of the caudal periaqueductal gray and in the lateral septum in aggressive lactating mice. Due to large variance in the counts of pCREB-positive cells, the data were log transformed prior to statistical analysis. Thus, the sites of cFOS and pCREB increases do not overlap, but provide complementary indirect information on neural regions active during Maternal Aggression. These results complement previous studies of nitric oxide release during Maternal Aggression to create a possible map of the functional neural circuitry underlying Maternal Aggression.
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Maternal Aggression in endothelial nitric oxide synthase deficient mice
Hormones and Behavior, 2000Co-Authors: Stephen C Gammie, Paul L Huang, Randy J. NelsonAbstract:Lactating female rodents protect their pups by expressing fierce Aggression, termed Maternal Aggression, toward intruders. Mice lacking the neuronal nitric oxide synthase gene (nNOS-/-) exhibit significantly impaired Maternal Aggression, but increased male Aggression, suggesting that nitric oxide (NO) produced by nNOS has opposite actions in Maternal and male Aggression. In contrast, mice lacking the endothelial nitric oxide synthase gene (eNOS-/-) exhibit almost no male Aggression, suggesting that NO produced by eNOS facilitates male Aggression. In the present study, Maternal Aggression in eNOS-/- mice was examined and found to be normal relative to wild-type (WT) mice in terms of the percentage displaying Aggression, the average number of attacks against a male intruder, and the total amount of time spent attacking the male intruder. The eNOS-/- females also displayed normal pup retrieval behavior. Because a significant elevation of citrulline, an indirect marker of NO synthesis, occurs in neurons of the hypothalamus of lactating WT mice in association with Maternal Aggression, we examined the brains of eNOS-/- females for citrulline immunoreactivity following an aggressive encounter. The aggressive eNOS-/- females exhibited a significant elevation of citrulline in the medial preoptic nucleus and the subparaventricular zone of the hypothalamus relative to unstimulated lactating eNOS-/- females. Taken together, these results suggest that NO produced by eNOS neither facilitates nor inhibits Maternal Aggression and that NO produced by eNOS has a different role in Maternal and male Aggression.