Acute stress induces long-lasting alterations in the dopaminergic system of female mice

Abstract

54Stress is a risk factor for many neuropsychiatric disorders, and the mesolimbic dopamine (DA) 55 pathway is a crucial node of vulnerability. Despite the high prevalence of stress-related 56 neuropsychiatric disorders in women, preclinical knowledge on the impact of stress on neural 57 circuitry has predominantly been acquired in males. Here, we examine how a non-social stressor

Medial preoptic area antagonistically mediates stress-induced anxiety and parental behavior

“…1e). These behavioral results suggest an elevated anxiety state after exposure to stressors, consistent with previous studies 7,14,21,22 .…”

“…In the present study, we took a strategy of searching for brain structures that exhibit both acute and prolonged responses to anxiogenic stressors. Considering a close link between anxiety state and prior exposure to noxious stimuli 10,14 , brain structures encoding negative valence may be intimately involved in converting the emotional valence to the expression of anxiety-like phenotypes. Here, by exploiting acute stress-induced anxiety paradigms, we identified a structure previously unrecognized in anxiety-related circuits, the medial preoptic area (mPOA).…”

Neural Circuit Motifs in Valence Processing

“…Many have conceptualized catecholamine release as a proxy for stress (Abercrombie et al, 1989; Arnsten, 2009; Cabib and Puglisi-Allegra, 1996; Morilak et al, 2005). In so doing, this model can be extended to other functions, including social behavior (Shansky and Lipps, 2013; Wichmann et al, 2017) and even valence processing (Lemos et al, 2012). The relationship between stressors of different types, severities, and durations and VTA dopamine activity has led to a confusing literature regarding valence and hedonic signaling, best explained by a model wherein either too much or too little dopamine can lead to depression-like symptoms (Chang and Grace, 2013; Chaudhury et al, 2013; Lammel et al, 2014; Moore et al, 2001; Tye et al, 2013; Valenti et al, 2011).…”

The neural circuitry of social homeostasis: Consequences of acute versus chronic social isolation

“…For instance, adult male mice who undergo a social defeat paradigm and are susceptible to social subordination exhibit changes in mesolimbic dopamine system, including increased firing rate of VTA dopamine neurons and increased brain-derived neurotrophic factor (BDNF) signaling in the NAc, inducing plasticity in the VTA-NAc circuit that is involved in emotion and reward processing (Krishnan et al, 2007). Additionally, while stimulation of VTA-NAc in adult female mice promotes social behavior (Gunaydin et al, 2014), stimulation of the VTA-NAc circuit following recent or remote stress produces an antisocial effect and increases optically induced dopamine release in the NAc (Wichmann et al, 2017), suggesting that stressors can induce circuit plasticity that ultimately changes behavioral output. Given that acute social isolation increases the activity of DRN dopamine neurons in response to social stimuli (Matthews et al, 2016), it is tempting to speculate that the chronic homeostatic correction effort expended by the DRN dopamine neurons may indeed induce downstream plasticity that is ultimately responsible for the shift from prosocial to antisocial behaviors.…”