Categorization of biologically relevant chemical signals in the medial amygdala

Samuelsen, Chad L.; Meredith, Michael

doi:10.1016/j.brainres.2009.01.048

Cited by 62 publications

(112 citation statements)

References 41 publications

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“…13,14 Many studies using Fos as a marker of neuronal activity have shown strong activation of the MeAm associated with stressful stimuli. 13,15,16 Moreover, inhibition of the MeAm has demonstrated that it does indeed mediate the cardiovascular response to stress in rats, indicating that Fos activity is not merely a response to the stressor.…”

Section: Hypertensionmentioning

confidence: 99%

“…Midfrequency BP power was attenuated in both strains (P lesion <0.05) and the depressor responses to pentolinium after enalaprilat pretreatment was attenuated after lesions in BPH/2J mice (P lesion <0.001; n=3 in the integration of olfactory and chemosensory signaling involved in predator and territorial responses and reproduction. 13,14 Many studies using Fos as a marker of neuronal activity have shown strong activation of the MeAm associated with stressful stimuli. 13,15,16 Moreover, inhibition of the MeAm has demonstrated that it does indeed mediate the cardiovascular response to stress in rats, indicating that Fos activity is not merely a response to the stressor.…”

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confidence: 99%

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Major Contribution of the Medial Amygdala to Hypertension in BPH/2J Genetically Hypertensive Mice

et al. 2014

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BPH/2J mice are a genetic model of hypertension developed in the 1970s by Schlager et al.1 These mice were selectively bred for elevated blood pressure (BP) alongside a normotensive (BPN/3J) and hypotensive control strain (BPL/1J), from a base population of 8 inbred strains of mice. Since then a range of pathophysiological factors have been studied to determine the cause of hypertension in BPH/2J mice, and the relatively modest characterization has been increasing in recent years, possibly because of advances in technology used to study mice. 2,3 Our own findings suggest that hypertension in BPH/2J mice is sympathetically mediated, based on the greater depressor response to ganglion blockade, which ultimately abolishes the hypertension in BPH/2J mice and also greater midfrequency mean arterial pressure variability (MAP power). 4 Even the percentage depressor response to ganglion blockade is greater in BPH/2J mice compared with normotensive controls. 4 This contrasts findings in spontaneously hypertensive rats (SHRs) that are likely confounded by a vascular amplifier effect 5 caused by vascular structural changes, which contribute to hypertension in adult SHRs. 6 Recently, we have also reported that BPH/2J mice have renal sympathetic hyperinnervation and enhanced renin synthesis, which results in a greater contribution of the renin-angiotensin system (RAS) to BP maintenance during the dark period of the 24-hour light cycle in BPH/2J mice compared with BPN/3J mice. 7 Early studies indicated that BPH/2J mice have aberrant brain catecholamine levels, 8 suggesting that the hypertension may be centrally mediated. Furthermore, using Fos as a marker of neuronal activity, BPH/2J mice were also shown to have greater neuronal activity in key cardiovascular regulatory brain regions compared with normotensive control BPN/3J mice. 4 Importantly, of the limbic, hypothalamic, and medullary brain regions analyzed using Fos immunohistochemistry, the medial amygdala (MeAm) was the only region to show greater neuronal activity during the light (inactive) and the dark (active) period in BPH/2J compared with BPN/3J mice, 4 suggesting that this region may be inherently overactive in BPH/2J mice. Furthermore, neuronal activity within the MeAm correlated strongly with BP level (R=0.98), suggesting that neuronal activity in the MeAm may be related to BP level. 4 The MeAm is an important limbic region that integrates sensory information, including stress and fear as well as reproductive-related inputs, and regulates the subsequent cardiovascular, behavioral, and hormonal responses.9-11 The MeAm is activated by stressful stimuli particularly of psychological rather than a physiological nature 12 and is involved Abstract-BPH/2J mice are recognized as a neurogenic model of hypertension primarily based on overactivity of the sympathetic nervous system and greater neuronal activity in key autonomic cardiovascular regulatory brain regions. The medial amygdala (MeAm) is a forebrain region that integrates the autonomic response...

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Section: Hypertensionmentioning

confidence: 99%

mentioning

confidence: 99%

Major Contribution of the Medial Amygdala to Hypertension in BPH/2J Genetically Hypertensive Mice

et al. 2014

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“…The posterior MeA (MeAp) is particularly important in conspecific or socially relevant responses (Meredith and Westberry, 2004;Samuelsen and Meredith, 2009b), and was the focus of these studies. The MeAp has two functionally distinct subdivisions, the dorsal (MeApd) and ventral (MeApv) subdivisions.…”

Section: Introductionmentioning

confidence: 99%

“…The medial nucleus of the amygdala (MeA) has been particularly implicated in prosocial maternal and sexual behavior, as well as agonistic aggressive behaviors. In rodent models, the MeA is activated by socially relevant cues, such as maternal interaction, mating, pheromones of opposite-sex conspecifics, and predators (Fleming and Walsh, 1994;Kollack-Walker and Newman, 1997;Meredith and Westberry, 2004;Choi et al, 2005;Samuelsen and Meredith, 2009b;Bergan et al, 2014), ablation of the MeA impairs recognition of opposite-sex odors (Petrulis, 2009;Maras and Petrulis, 2010), and activation of MeA afferents induces a gradient of social behavior from mating behavior to aggression (Hong et al, 2014;Unger et al, 2015).…”

Section: Introductionmentioning

confidence: 99%

Social Isolation During Postweaning Development Causes Hypoactivity of Neurons in the Medial Nucleus of the Male Rat Amygdala

Adams

Rosenkranz

2015

Neuropsychopharmacol

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Children exposed to neglect or social deprivation are at heightened risk for psychiatric disorders and abnormal social patterns as adults. There is also evidence that prepubertal neglect in children causes abnormal metabolic activity in several brain regions, including the amygdala area. The medial nucleus of the amygdala (MeA) is a key region for performance of social behaviors and still undergoes maturation during the periadolescent period. As such, the normal development of this region may be disrupted by social deprivation. In rodents, postweaning social isolation causes a range of deficits in sexual and agonistic behaviors that normally rely on the posterior MeA (MeAp). However, little is known about the effects of social isolation on the function of MeA neurons. In this study, we tested whether postweaning social isolation caused abnormal activity of MeA neurons. We found that postweaning social isolation caused a decrease of in vivo firing activity of MeAp neurons, and reduced drive from excitatory afferents. In vitro electrophysiological studies found that postweaning social isolation caused a presynaptic impairment of excitatory input to the dorsal MeAp, but a progressive postsynaptic reduction of membrane excitability in the ventral MeAp. These results demonstrate discrete, subnucleus-specific effects of social deprivation on the physiology of MeAp neurons. This pathophysiology may contribute to the disruption of social behavior after developmental social deprivation, and may be a novel target to facilitate the treatment of social disorders.

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“…The importance of the MeA in the regulation of male-type social behaviors has been demonstrated in numerous studies (13)(14)(15)(16)(17)(18). Particularly, the MeA plays a significant role in chemosensory information processing (15,16,33,34) as part of the social behavior network in the CNS (35). It relays socially meaningful signals to activate or inhibit various downstream brain sites, such as the MPOA, anterior hypothalamic area (AHA), and VMN, that are more directly involved in the execution of male sexual and aggressive behaviors (14,(36)(37)(38)(39)(40).…”

Section: Discussionmentioning

confidence: 98%

Pubertal activation of estrogen receptor α in the medial amygdala is essential for the full expression of male social behavior in mice

Sato

Nakata

Musatov

et al. 2016

Proc. Natl. Acad. Sci. U.S.A.

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Testosterone plays a central role in the facilitation of male-type social behaviors, such as sexual and aggressive behaviors, and the development of their neural bases in male mice. The action of testosterone via estrogen receptor (ER) α, after being aromatized to estradiol, has been suggested to be crucial for the full expression of these behaviors. We previously reported that silencing of ERα in adult male mice with the use of a virally mediated RNAi method in the medial preoptic area (MPOA) greatly reduced sexual behaviors without affecting aggressive behaviors whereas that in the medial amygdala (MeA) had no effect on either behavior. It is well accepted that testosterone stimulation during the pubertal period is necessary for the full expression of male-type social behaviors. However, it is still not known whether, and in which brain region, ERα is involved in this developmental effect of testosterone. In this study, we knocked down ERα in the MeA or MPOA in gonadally intact male mice at the age of 21 d and examined its effects on the sexual and aggressive behaviors later in adulthood. We found that the prepubertal knockdown of ERα in the MeA reduced both sexual and aggressive behaviors whereas that in the MPOA reduced only sexual, but not aggressive, behavior. Furthermore, the number of MeA neurons was reduced by prepubertal knockdown of ERα. These results indicate that ERα activation in the MeA during the pubertal period is crucial for male mice to fully express their male-type social behaviors in adulthood.T estosterone plays a central role in the regulation of male-type social behaviors in many mammalian species. It is known that testosterone facilitates the expression of sexual and aggressive behaviors through two kinds of actions. During the developmental period, testosterone exerts its "organizational action" to irreversibly masculinize the sexually undifferentiated brain and build the male-type neural network. In adulthood, testosterone exerts "activational action" to regulate the function of the fully masculinized neural network. As well as acting through androgen receptors (ARs), testosterone also acts through estrogen receptor (ER) α or ERβ, after being aromatized to estradiol (E2). Because the expression of sexual and aggressive behaviors is greatly reduced in aromatase knockout (ArKO) and ERα knockout (αERKO) male mice, aromatization of testosterone and its action via ERα have been suggested to be crucial for the facilitation of male-type social behaviors in mice (1-8). However, the exact timing and brain site(s) of ERα activation crucial for the expression of sexual and aggressive behaviors remain undetermined.In our previous study, we demonstrated site-specific involvement of ERα in the activational action of testosterone by using a virally mediated RNAi method. In this study, knocking down of ERα in the medial preoptic area (MPOA) of gonadally intact adult male mice suppressed sexual behavior while in the ventromedial nucleus (VMN) of hypothalamus reduced both sexual and aggressive behaviors...

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Categorization of biologically relevant chemical signals in the medial amygdala

Cited by 62 publications

References 41 publications

Major Contribution of the Medial Amygdala to Hypertension in BPH/2J Genetically Hypertensive Mice

Major Contribution of the Medial Amygdala to Hypertension in BPH/2J Genetically Hypertensive Mice

Social Isolation During Postweaning Development Causes Hypoactivity of Neurons in the Medial Nucleus of the Male Rat Amygdala

Pubertal activation of estrogen receptor α in the medial amygdala is essential for the full expression of male social behavior in mice

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