Investigating the role of dopamine receptor- and parvalbumin-expressing cells in extinction of conditioned fear

Madsen, Heather B.; Guerin, Alexandre A.; Kim, Jee Hyun

doi:10.1016/j.nlm.2017.08.009

Cited by 23 publications

(25 citation statements)

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“…Activation of D1 and D2 leads to opposing changes in intracellular signaling cascades and cell physiology (Stoof & Kebabian, ), and their activity must be balanced for normal brain function. Alterations in this physiological balance increase the risk for numerous developmental disorders (Brenhouse & Andersen, ; Flores et al, ; Madsen, Guerin, & Kim, ; Maldonado, Robledo, Chover, Caine, & Koob, ; Slifstein et al, ; Spear, ; Volkow et al, ; Volkow et al, ; Weinberger, ). Thus, of the five dopamine receptors, D1 and D2 have been studied the most in the context of mental disorders (Brenhouse, Sonntag, & Andersen, ; Goldsmith, Shapiro, & Joyce, ; Madsen et al, ; O'Donnell, ; Suhara et al, ; Zbukvic et al, ).…”

Section: Introductionmentioning

confidence: 99%

“…To achieve our aim, we used transgenic mice expressing green fluorescent protein (GFP)‐tagged D1 or D2 (D1‐ or D2‐GFP) mice in combination with immunohistochemistry for GFP. These mice are well validated and widely used to examine cells containing specific mRNA for D1 or D2 (Gong et al, ; Ketzef et al, ; Lee et al, ; Madsen et al, ; Nelson et al, ). Unbiased stereological sampling across many sections was used to estimate the D1+ and D2+ cell population and density within each region.…”

Section: Introductionmentioning

confidence: 99%

“…To achieve our aim, we used transgenic mice expressing green fluorescent protein (GFP)-tagged D1 or D2 (D1-or D2-GFP) mice in combination with immunohistochemistry for GFP. These mice are well validated and widely used to examine cells containing specific mRNA for D1 or D2 (Gong et al, 2003;Ketzef et al, 2017;Lee et al, 2006;Madsen et al, 2017;Nelson et al, 2012).…”

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Postnatal developmental trajectory of dopamine receptor 1 and 2 expression in cortical and striatal brain regions

Cullity

Madsen

Perry

et al. 2018

J of Comparative Neurology

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Healthy brain function requires a balance between the activity of dopamine receptor 1 (D1) and dopamine receptor 2 (D2). Alterations in this balance increase the risk for numerous developmental brain disorders. Indeed, D1 and D2 expression fluctuates throughout maturation, although there is conflicting evidence regarding the precise changes that occur. Here, we used stereology to investigate the developmental changes in the number of D1‐ or D2‐expressing neurons in the prelimbic cortex, infralimbic cortex (IL), insula cortex, dorsal striatum, and ventral striatum of female and male mice with green fluorescent protein‐tagged D1 or D2. Postnatal day 17, 25, 35, 49, and 70 were examined to cover juvenility to adulthood. In all regions, analysis of D1 density compared to D2 density within each sex seldom detected effects or interactions involving age. However, D1:D2 density ratio changed across age depending on sex. In the IL, D1:D2 density ratio increased in females from adolescence, whereas it was stable in males. In the insula cortex, D1:D2 ratio initially increased in males but decreased in females from juvenility to preadolescence. The ratio then increased in males and females from adolescence to adulthood, with males showing a more dramatic increase. In both the dorsal and ventral striatum, the ratio increased from adolescence. In all regions, females had a higher ratio compared to males throughout maturation except in the insula cortex at P25. These comprehensive observations are novel, and highlight how the maturational changes in the expression of these receptors may contribute to developmental disorders.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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confidence: 99%

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Postnatal developmental trajectory of dopamine receptor 1 and 2 expression in cortical and striatal brain regions

Cullity

Madsen

Perry

et al. 2018

J of Comparative Neurology

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“…GraphPad prism 6.0 (GraphPad software, Inc., La Jolla, CA. All behaviors were analyzed as described previously (Madsen, Guerin, & Kim, 2017;Short et al, 2017). For conditioning, percentage freezing during the first 9 seconds of each CS-US trial was analyzed to avoid analyzing shock-related movement.…”

Section: Overallmentioning

confidence: 99%

Sex-dependent effects of chronic exercise on cognitive flexibility in aging mice

Short

Bui

Zbukvic

et al. 2020

Preprint

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Cognitive impairments associated with advanced age are a growing concern in our aging society. Such impairments are associated with alterations in brain structure and function, especially in the hippocampus, which changes to experience throughout life. It is well-known that regular exercise can maintain hippocampus volume. The hippocampus is critical for cognitive flexibility involved with extinction and reinstatement of conditioned fear. Therefore, we asked whether voluntary chronic exercise in middle-aged mice can improve extinction and/or reinstatement of conditioned fear compared to standard housing. Eight-month-old male and female C57Bl/6J mice had access to a running wheel or remained in standard housing until 11 months of age. Alongside control standard-housed young adult (3-monthold) mice, they received tone-footshock pairings, which were subsequently extinguished with tone-alone presentations the next day. Half of the mice then received a reminder treatment in the form of a single footshock. Both male and female 11-month-old mice housed in standard conditions exhibited impaired reinstatement compared to young adult mice.However, for males that had access to a running wheel from 8 months of age, the reminder treatment rescued reinstatement ability. This was not observed in females. Additionally, exercise during middle age in both sexes increased expression of Bdnf mRNA in the hippocampus, specifically exon 4 mRNA. These results show that, at least for males, physical exercise is beneficial for reducing age-related decline in cognitive abilities. Despite not rescuing their impaired reinstatement, exercise also increased Bdnf gene expression in the female hippocampus, which could potentially benefit other forms of hippocampaldependent cognition.

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“…Consistent with the idea that IL serves as a “stop” structure, it has been shown that the IL is critically involved in the suppression of conditioned fear and reward-seeking behavior (Rhodes and Killcross 2004 ; Quirk and Mueller 2008 ; Peters et al 2009 ; Sierra-Mercado et al 2011 ); the essential role of IL in acquisition and consolidation of extinction memories has been an area of intense study (Quirk and Mueller 2008 ; LaLumiere et al 2010 ; Gass and Chandler 2013 ; Van den Oever et al 2013 ; Barker et al 2014 ; Jasinska et al 2015 ). Indeed, successful retrieval of extinguished fear is associated with enhanced activity in the IL [(Milad and Quirk 2002 ; Milad et al 2007 ; Knapska and Maren 2009 ; Madsen et al 2017 ); but, see (Chang et al 2010 ; Fitzgerald et al 2014 )] whereas fear relapse is associated with a decrease in IL activation (Hefner et al 2008 ; Knapska and Maren 2009 ; Hitora-Imamura et al 2015 ; Kutlu et al 2016 ). Interestingly, acute treatment with nicotine enhances the spontaneous recovery of extinguished contextual fear, which coincides with reductions in IL activation (Kutlu et al 2016 ).…”

Section: Introductionmentioning

confidence: 99%

Common neurocircuitry mediating drug and fear relapse in preclinical models

Goode

2018

Psychopharmacology

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Background Comorbidity of anxiety disorders, stressor- and trauma-related disorders, and substance use disorders is extremely common. Moreover, therapies that reduce pathological fear and anxiety on the one hand, and drug-seeking on the other, often prove short-lived and are susceptible to relapse. Considerable advances have been made in the study of the neurobiology of both aversive and appetitive extinction, and this work reveals shared neural circuits that contribute to both the suppression and relapse of conditioned responses associated with trauma or drug use. Objectives The goal of this review is to identify common neural circuits and mechanisms underlying relapse across domains of addiction biology and aversive learning in preclinical animal models. We focus primarily on neural circuits engaged during the expression of relapse. Key findings After extinction, brain circuits involving the medial prefrontal cortex and hippocampus come to regulate the expression of conditioned responses by the amygdala, bed nucleus of the stria terminalis, and nucleus accumbens. During relapse, hippocampal projections to the prefrontal cortex inhibit the retrieval of extinction memories resulting in a loss of inhibitory control over fear- and drug-associated conditional responding. Conclusions The overlapping brain systems for both fear and drug memories may explain the co-occurrence of fear and drug-seeking behaviors.

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Investigating the role of dopamine receptor- and parvalbumin-expressing cells in extinction of conditioned fear

Cited by 23 publications

References 44 publications

Postnatal developmental trajectory of dopamine receptor 1 and 2 expression in cortical and striatal brain regions

Postnatal developmental trajectory of dopamine receptor 1 and 2 expression in cortical and striatal brain regions

Sex-dependent effects of chronic exercise on cognitive flexibility in aging mice

Common neurocircuitry mediating drug and fear relapse in preclinical models

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