Enduring dysregulation of nucleus accumbens catecholamine and glutamate transmission by developmental exposure to phenylpropanolamine

2020 ◽  
Vol 1748 ◽  
pp. 147098
Author(s):  
Karen K. Szumlinski ◽  
Daria L. Thompson ◽  
Rachel M. Renton ◽  
Alexis W. Ary ◽  
Kevin D. Lominac
Keyword(s):  
Nucleus Accumbens ◽  
Developmental Exposure ◽  
Glutamate Transmission

scholarly journals Endogenous enkephalin is necessary for cocaine‐induced alteration in glutamate transmission within the nucleus accumbens

2020 ◽  
Author(s):  
Bethania Mongi‐Bragato ◽  
María Paula Avalos ◽  
Andrea S. Guzmán ◽  
Constanza García‐Keller ◽  
Flavia A. Bollati ◽  
...  
Keyword(s):  
Nucleus Accumbens ◽  
Glutamate Transmission

Author response for "Endogenous enkephalin is necessary for cocaine‐induced alteration in glutamate transmission within the nucleus accumbens"

2020 ◽  
Author(s):  
Bethania Mongi‐Bragato ◽  
María Paula Avalos ◽  
Andrea S. Guzmán ◽  
Constanza García‐Keller ◽  
Flavia A. Bollati ◽  
...  
Keyword(s):  
Nucleus Accumbens ◽  
Author Response ◽  
Glutamate Transmission

scholarly journals Mitochondria-Related Nuclear Gene Expression in the Nucleus Accumbens and Blood Mitochondrial Copy Number After Developmental Fentanyl Exposure in Adolescent Male and Female C57BL/6 Mice

2021 ◽  
Vol 12 ◽  
Author(s):  
Cali A. Calarco ◽  
Megan E. Fox ◽  
Saskia Van Terheyden ◽  
Makeda D. Turner ◽  
Jason B. Alipio ◽  
...  
Keyword(s):  
Gene Expression ◽  
Nucleus Accumbens ◽  
Mitochondrial Function ◽  
Copy Number ◽  
Drug Exposure ◽  
Related Gene ◽  
Developmental Exposure ◽  
Neuronal Signaling ◽  
Mitochondrial Copy Number ◽  
The Brain

The potency of the synthetic opioid fentanyl and its increased clinical availability has led to the rapid escalation of use in the general population, increased recreational exposure, and subsequently opioid-related overdoses. The wide-spread use of fentanyl has, consequently, increased the incidence of in utero exposure to the drug, but the long-term effects of this type of developmental exposure are not yet understood. Opioid use has also been linked to reduced mitochondrial copy number in blood in clinical populations, but the link between this peripheral biomarker and genetic or functional changes in reward-related brain circuitry is still unclear. Additionally, mitochondrial-related gene expression in reward-related brain regions has not been examined in the context of fentanyl exposure, despite the growing literature demonstrating drugs of abuse impact mitochondrial function, which subsequently impacts neuronal signaling. The current study uses exposure to fentanyl via dam access to fentanyl drinking water during gestation and lactation as a model for developmental drug exposure. This perinatal drug-exposure is sufficient to impact mitochondrial copy number in circulating blood leukocytes, as well as mitochondrial-related gene expression in the nucleus accumbens (NAc), a reward-related brain structure, in a sex-dependent manner in adolescent offspring. Specific NAc gene expression is correlated with both blood mitochondrial copy number and with anxiety related behaviors dependent on developmental exposure to fentanyl and sex. These data indicate that developmental fentanyl exposure impacts mitochondrial function in both the brain and body in ways that can impact neuronal signaling and may prime the brain for altered reward-related behavior in adolescence and later into adulthood.

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