Noradrenaline effects on social behaviour, intergroup relations, and moral decisions

Terbeck, Sylvia; Savulescu, Julian; Chesterman, L; Cowen, Philip J.

doi:10.1016/j.neubiorev.2016.03.031

Cited by 61 publications

(35 citation statements)

References 72 publications

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“…Taken together, it suggests that social contact with a familiar conspecific in pain results in social approach (empathy-associated hyperalgesia) driven by activation of the mPFC-LC/NE-SAM axis, however, social contact with an unfamiliar conspecific in pain results in social stress (stress-associated analgesia) initially co-driven by the HPA and SAM hyperactivity and then driven by the SAM axis mediated by a non-LC/NE input. The involvement of the LC/NE-SAM system in empathy for pain can be largely supported by human studies showing enhancing effects of the NE (noradrenaline) on empathy-based prosocial behavior, intergroup relations and moral decisions (Terbeck et al, 2016 ).…”

Section: Discussionmentioning

confidence: 99%

The Locus Coeruleus–Norepinephrine System Mediates Empathy for Pain through Selective Up-Regulation of P2X3 Receptor in Dorsal Root Ganglia in Rats

Yang

et al. 2017

Front. Neural Circuits

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Empathy for pain (vicariously felt pain), an ability to feel, recognize, understand and share the painful emotions of others, has been gradually accepted to be a common identity in both humans and rodents, however, the underlying neural and molecular mechanisms are largely unknown. Recently, we have developed a rat model of empathy for pain in which pain can be transferred from a cagemate demonstrator (CD) in pain to a naïve cagemate observer (CO) after 30 min dyadic priming social interaction. The naïve CO rats display both mechanical pain hypersensitivity (hyperalgesia) and enhanced spinal nociception. Chemical lesions of bilateral medial prefrontal cortex (mPFC) abolish the empathic pain response completely, suggesting existence of a top-down facilitation system in production of empathy for pain. However, the social transfer of pain was not observed in non-cagemate observer (NCO) after dyadic social interaction with a non-cagemate demonstrator (NCD) in pain. Here we showed that dyadic social interaction with a painful CD resulted in elevation of circulating norepinephrine (NE) and increased neuronal activity in the locus coeruleus (LC) in the CO rats. Meanwhile, CO rats also had over-expression of P2X3, but not TRPV1, in the dorsal root ganglia (DRG). Chemical lesion of the LC-NE neurons by systemic DSP-4 and pharmacological inhibition of central synaptic release of NE by clonidine completely abolished increase in circulating NE and P2X3 receptor expression, as well as the sympathetically-maintained development of empathic mechanical hyperalgesia. However, in the NCO rats, neither the LC-NE neuronal activity nor the P2X3 receptor expression was altered after dyadic social interaction with a painful NCD although the circulating corticosterone and NE were elevated. Finally, in the periphery, both P2X3 receptor and α1 adrenergic receptor were found to be involved in the development of empathic mechanical hyperalgesia. Taken together with our previous results, empathy for pain observed in the CO rats is likely to be mediated by activation of the top-down mPFC-LC/NE-sympathoadrenomedullary (SAM) system that further up-regulates P2X3 receptors in the periphery, however, social stress observed in the NCO rats is mediated by activation of both hypothalamic-pituitary-adrenocortical axis and SAM axis.

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Section: Discussionmentioning

confidence: 99%

The Locus Coeruleus–Norepinephrine System Mediates Empathy for Pain through Selective Up-Regulation of P2X3 Receptor in Dorsal Root Ganglia in Rats

Yang

et al. 2017

Front. Neural Circuits

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“…Second, vicariously felt pain (or fear) seen as empathy for distress among familiar rodents has been demonstrated to be mediated by the mPFC (Jeon et al, 2010 ; Li et al, 2014 ; Burkett et al, 2016 ) where has also been demonstrated to be one of the major brain regions activated by empathy for distress (pain and social loss) in humans (Singer et al, 2004 ; Lamm et al, 2011 ; Iannetti et al, 2013 ; Eisenberger, 2015 ). Third, vicariously felt pain (or fear) seen as empathy for distress among familiar rodents has been shown to be facilitated by both hypothalamic-neurohypophysial (oxytocin) system (Neumann et al, 2000 ; Heinrichs et al, 2003 ; Lukas et al, 2011 ; Burkett et al, 2016 ) and the SAM system (LC-NE system) (Lü et al, 2017 ) which have been demonstrated to be essential for induction of empathy and pro-social behaviors in humans (Insel and Young, 2000 , 2001 ; Donaldson and Young, 2008 ; Heinrichs and Domes, 2008 ; Lee et al, 2009 ; Terbeck et al, 2016 ). Fourth, vicariously felt pain (or fear) seen as empathy for distress has been demonstrated to be prevented by activation of the HPA axis in both humans and animals due to social stress (Neumann et al, 2000 ; Heinrichs et al, 2003 ; Lukas et al, 2011 ; Martin et al, 2015 ; Lü et al, 2017 ).…”

Section: Discussionmentioning

confidence: 99%

Validating Rat Model of Empathy for Pain: Effects of Pain Expressions in Social Partners

et al. 2018

Front. Behav. Neurosci.

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Pain can be socially transferred between familiar rats due to empathic responses. To validate rat model of empathy for pain, effects of pain expressions in a cagemate demonstrator (CD) in pain on empathic pain responses in a naïve cagemate observer (CO) after 30 min priming dyadic social interactions (PDSI) were evaluated. The CD rats were prepared with four pain models: bee venom (BV), formalin, complete Freund's adjuvant (CFA), and spared nerve injury (SNI). Both BV and formalin tests are characterized by displayable and eye-identifiable spontaneous pain-related behaviors (SPRB) immediately after treatment, while CFA and SNI models are characterized by delayed occurrence of evoked pain hypersensitivity but with less eye-identifiable SPRB. After 30 min PDSI with a CD immediately after BV and formalin, respectively, the empathic mechanical pain hypersensitivity (EMPH) could be identified at both hind paws in CO rats. The BV—or formalin-induced EMPH in CO rats lasted for 4–5 h until full recovery. However, EMPH failed to develop in CO after socially interacting with a CD immediately after CFA, or 2 h after BV when SPRB completely disappeared. The CO's EMPH was partially relieved when socially interacting with an analgecized CD whose SPRB had been significantly suppressed. Moreover, repeated exposures to a CD in pain could enhance EMPH in CO. Finally, social transfer of pain hypersensitivity was also identified in CO who was being co-housed in pairs with a conspecific treated with CFA or SNI. The results suggest that development of EMPH in CO rats would be determined not only by extent of familiarity but also by visually identifiable pain expressions in the social partners during short period of PDSI. However, the visually unidentifiable pain can also be transferred to naïve cagemate when being co-housed in pairs with a distressed conspecific. In summary, the vicariously social contagion of pain between familiar rats is dependent upon not only expressions of pain in social partners but also the time that dyads spent in social communications. The rat model of empathy for pain is a highly stable, reproducible and valid model for studying the neural mechanisms of empathy in lower animals.

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“…The catecholaminergic system was the first to be found to mediate host-microbe crosstalk. Catecholamines play many roles in the host physiology, from stress-induced fight-or-flight response [89] to influencing gut integrity [90] and affecting host motivational behavior and decision-making [91]. In bacteria, norepinephrine and epinephrine induce a wide range of responses from the promotion of pathogenesis and growth [92] to susceptibility to illness under acute stress caused by norepinephrine-induced bacterial virulence genes, thereby driving infection and mortality [49].…”

Section: Catecholaminesmentioning

confidence: 99%

Obesity Affects the Microbiota–Gut–Brain Axis and the Regulation Thereof by Endocannabinoids and Related Mediators

Forte

Fernández-Rilo

Palomba

et al. 2020

IJMS

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The hypothalamus regulates energy homeostasis by integrating environmental and internal signals to produce behavioral responses to start or stop eating. Many satiation signals are mediated by microbiota-derived metabolites coming from the gastrointestinal tract and acting also in the brain through a complex bidirectional communication system, the microbiota–gut–brain axis. In recent years, the intestinal microbiota has emerged as a critical regulator of hypothalamic appetite-related neuronal networks. Obesogenic high-fat diets (HFDs) enhance endocannabinoid levels, both in the brain and peripheral tissues. HFDs change the gut microbiota composition by altering the Firmicutes:Bacteroidetes ratio and causing endotoxemia mainly by rising the levels of lipopolysaccharide (LPS), the most potent immunogenic component of Gram-negative bacteria. Endotoxemia induces the collapse of the gut and brain barriers, interleukin 1β (IL1β)- and tumor necrosis factor α (TNFα)-mediated neuroinflammatory responses and gliosis, which alter the appetite-regulatory circuits of the brain mediobasal hypothalamic area delimited by the median eminence. This review summarizes the emerging state-of-the-art evidence on the function of the “expanded endocannabinoid (eCB) system” or endocannabinoidome at the crossroads between intestinal microbiota, gut-brain communication and host metabolism; and highlights the critical role of this intersection in the onset of obesity.

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Noradrenaline effects on social behaviour, intergroup relations, and moral decisions

Cited by 61 publications

References 72 publications

The Locus Coeruleus–Norepinephrine System Mediates Empathy for Pain through Selective Up-Regulation of P2X3 Receptor in Dorsal Root Ganglia in Rats

The Locus Coeruleus–Norepinephrine System Mediates Empathy for Pain through Selective Up-Regulation of P2X3 Receptor in Dorsal Root Ganglia in Rats

Validating Rat Model of Empathy for Pain: Effects of Pain Expressions in Social Partners

Obesity Affects the Microbiota–Gut–Brain Axis and the Regulation Thereof by Endocannabinoids and Related Mediators

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