Granulocyte colony-stimulating factor (G-CSF) enhances cocaine effects in the nucleus accumbens via a dopamine release–based mechanism

Brady, Lillian J.; Erickson, Kirsty R; Lucerne, Kelsey E.; Osman, Aya; Kiraly, Drew D.; Calipari, Erin S.

doi:10.1007/s00213-021-05967-9

Cited by 5 publications

(2 citation statements)

References 52 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In addition to contributing to learning and memory, the NAc participates in the neural circuit responsible for regulation of motivation and reward systems [14]. Addictive substances such as cocaine and morphine induce addictive behaviors by releasing dopamine in the NAc [15]. NAc neurons are predominantly medium-spiny neurons (MSN), consisting of D1R-MSNs and D2R-MSNs, with D1R neurons accounting for most of the MSNs [16], which are important in the generation of attraction and aversion to stimuli [17].…”

Section: Discussionmentioning

confidence: 99%

Inhibition of SIRT1 in the nucleus accumbens attenuates heroin addiction-related behavior by decreasing D1 neuronal autophagy

Huang,

Liu,

Zheng

et al. 2024

NeuroReport

View full text Add to dashboard Cite

This study aimed to investigate the effects of SIRT1 modulation on heroin addiction-like behavior and its possible biological mechanisms. Wild-type C57BL/6J and Sirt1 loxp/loxpD1-Cre mice were used in this experiment, and Sirt1loxp/loxpD1-Cre(−) mice were used as a control for conditional knockout mice. Mice were divided into saline control and heroin-dependent groups. Behavioral methods were used to record the withdrawal response, conditioned place preference (CPP) changes, and open field test results. Transmission electron microscopy (TEM) was used to observe the structure of autophagosomes in nucleus accumbens (NAc) neurons. The expression of SIRT1 and autophagy-related proteins and genes, such as LC3Ⅱ, ATG5, and ATG7, was detected in the NAc of each mouse group via western blot, real-time quantitative PCR (qPCR) analyzes, and immunofluorescence. The results of this experiment showed that compared with the saline group, mice in the wild-type heroin-dependent group showed marked withdrawal symptoms, with more autophagosomes observed in NAc via TEM. Compared with wild-type and Sirt1 loxp/loxpD1-Cre(−) heroin-dependent groups, CPP formation was found to be reduced in the conditional knockout mouse group, with a significant decrease in spontaneous activity. Western blot, qPCR, and immunofluorescence results indicated that the expression of LC3Ⅱ, ATG-5, and ATG-7 was significantly reduced in the NAc of the Sirt1 loxp/loxpD1-Cre(+) group. It was still, however, higher than that in the saline control group. These results suggest that inhibition of Sirt1 expression may prevent heroin-induced addiction-related behaviors via reducing D1 neuronal autophagy.

show abstract

Section: Discussionmentioning

confidence: 99%

Inhibition of SIRT1 in the nucleus accumbens attenuates heroin addiction-related behavior by decreasing D1 neuronal autophagy

Huang,

Liu,

Zheng

et al. 2024

NeuroReport

View full text Add to dashboard Cite

show abstract

“…For mouse targets, this included downregulations of IL-1α and the granulocyte colony stimulating factor (G-CSF) and upregulations in RANTES/CCL5 and IP-10/CXCL10, which have been previously implicated in multiple models of HIV infection and in clinical populations, including in co-occurring cocaine use/expose and infection (Nair et al, 2000;Parikh et al, 2014;Nayak et al, 2020). Elevated G-CSF has also been reported to increase dopamine release in response to cocaine (Brady et al, 2019(Brady et al, , 2021, though as with other considerations this may be mediated by hormonal status in female mice (Brady et al, 2019). Though we did not observe main effects of cocaine itself on mouse G-CSF levels, the cocaine exposure paradigms in the current study were at lower doses (10 mg/kg vs 20 mg/kg) and fewer exposures (3 vs 7 injections), suggesting that a more protracted cocaine exposure regimen may be necessary to observe cocaine effects or cocaine and HIV interactive effects on G-CSF expression.…”

Section: Discussionmentioning

confidence: 99%

Impaired extinction of cocaine seeking in HIV-infected mice is accompanied by peripheral and central immune dysregulation

Barker,

Buck,

Xie

et al. 2023

Preprint

View full text Add to dashboard Cite

Substance use disorders (SUDs) are highly comorbid with HIV infection, necessitating an understanding of the interactive effects of drug exposure and HIV. The relationship between HIV infection and cocaine use disorder is likely bidirectional, with cocaine use directly impacting immune function while HIV infection alters addiction-related behavior. To better characterize the neurobehavioral and immune consequences of HIV infection and cocaine exposure, this study utilized a humanized mouse model to investigate the outcomes of HIV-1 infection on cocaine-related behaviors in a conditioned place preference (CPP) model, and the interactive effects of cocaine and HIV infection on peripheral and central nervous system inflammation. HIV infection selectively impaired cocaine CPP extinction without effecting reinstatement or cocaine seeking under conflict were observed. Behavioral alterations were accompanied by immune changes in HIV infected mice, including increased prefrontal cortex astrocyte immunoreactivity and brain-region specific effects on microglia number and reactivity. Peripheral immune system changes were observed in both mouse and human cytokines, including HIV-induced reductions in mouse IL-1α and G-CSF and human TNFα, and cocaine induced alterations in mouse GM-CSF. Together these data provide new insights into the unique neurobehavioral outcomes of HIV infection and cocaine exposure and how they interact to effect immune responses.

show abstract

Colony-stimulating factor 2 (CSF2) as a gut microbiome dependent immune factor that alters molecular and behavioral responses to cocaine in male mice

Lucerne,

Dean,

Osman

et al. 2024

Brain, Behavior, and Immunity

View full text Add to dashboard Cite

Granulocyte colony-stimulating factor (G-CSF) enhances cocaine effects in the nucleus accumbens via a dopamine release–based mechanism

Cited by 5 publications

References 52 publications

Inhibition of SIRT1 in the nucleus accumbens attenuates heroin addiction-related behavior by decreasing D1 neuronal autophagy

Inhibition of SIRT1 in the nucleus accumbens attenuates heroin addiction-related behavior by decreasing D1 neuronal autophagy

Impaired extinction of cocaine seeking in HIV-infected mice is accompanied by peripheral and central immune dysregulation

Colony-stimulating factor 2 (CSF2) as a gut microbiome dependent immune factor that alters molecular and behavioral responses to cocaine in male mice

Contact Info

Product

Resources

About