Morphine-Induced Dendritic Spine Remodeling in Rat Nucleus Accumbens Is Corticosterone Dependent

Geoffroy, H; Canestrelli, Corinne; Marie, Nicolas; Noble, Florence

doi:10.1093/ijnp/pyz014

Cited by 11 publications

(8 citation statements)

References 42 publications

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“…A 3D image was reconstructed with NIH ImageJ software 1 . The number of dendritic protrusions were calculated based on the morphology: thin spines have thin head and long neck; mushroom spines come with large head and short neck; stubby spines also have large head but no apparent neck (Montalbano et al, 2013; Geoffroy et al, 2019). For morphological quantification, one dendrite per neuron and 5–8 neurons per rat were analyzed in five rats in each group.…”

Section: Methodsmentioning

confidence: 99%

Traumatic Stress Produces Delayed Alterations of Synaptic Plasticity in Basolateral Amygdala

et al. 2019

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Acute traumatic event exposure is a direct cause of post-traumatic stress disorder (PTSD). Amygdala is suggested to be associated with the development of PTSD. In our previous findings, different activation patterns of GABAergic neurons and glutamatergic neurons in early or late stages after stress were found. However, the neural plastic mechanism underlying the role of basolateral amygdala (BLA) in post-traumatic stress disorder remains unclear. Therefore, this study mainly aimed at investigating time-dependent morphologic and electrophysiological changes in BLA during the development of PTSD. We used single prolonged stress (SPS) procedure to establish PTSD model of rats. The rats showed no alterations in anxiety behavior as well as in dendritic spine density or synaptic transmission in BLA 1 day after SPS. However, 10 days after SPS, rats showed enhancement of anxiety behavior, and spine density and frequency of miniature excitatory and inhibitory postsynaptic currents in BLA. Our results suggested that after traumatic stress, BLA displayed delayed increase in both spinogenesis and synaptic transmission, which seemed to facilitate the development of PTSD.

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Section: Methodsmentioning

confidence: 99%

Traumatic Stress Produces Delayed Alterations of Synaptic Plasticity in Basolateral Amygdala

et al. 2019

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“…Geoffroy et al ( 2019 ) investigated the effects of chronic low-dose morphine treatment (14 days) on medium spiny neurons of the core and shell of rat NAc. Analysis of spine morphology showed a selective increase in the density of thin spines and a decrease in stubby spines in the shell of morphine-treated rats.…”

Section: Opioids In General Anesthesia and Spine Remodelingmentioning

confidence: 99%

“…Removal of the effects of corticosteroids caused a significant increase of mushroom spines in the shell and stubby spines in the core after morphine treatment. The increase of thin spines in adrenalectomized rats was lower when compared to morphine-treated intact rats, with no change detected in stubby spines within the shell of NAc (Geoffroy et al 2019 ). These findings agree with the results of another report investigating the impact of morphine in the post-traumatic stress disorder (PTSD) model (RaiseAbdullahi et al 2019 ).…”

Section: Opioids In General Anesthesia and Spine Remodelingmentioning

confidence: 99%

Dendritic spine remodeling and plasticity under general anesthesia

2021

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Ever since its first use in surgery, general anesthesia has been regarded as a medical miracle enabling countless life-saving diagnostic and therapeutic interventions without pain sensation and traumatic memories. Despite several decades of research, there is a lack of understanding of how general anesthetics induce a reversible coma-like state. Emerging evidence suggests that even brief exposure to general anesthesia may have a lasting impact on mature and especially developing brains. Commonly used anesthetics have been shown to destabilize dendritic spines and induce an enhanced plasticity state, with effects on cognition, motor functions, mood, and social behavior. Herein, we review the effects of the most widely used general anesthetics on dendritic spine dynamics and discuss functional and molecular correlates with action mechanisms. We consider the impact of neurodevelopment, anatomical location of neurons, and their neurochemical profile on neuroplasticity induction, and review the putative signaling pathways. It emerges that in addition to possible adverse effects, the stimulation of synaptic remodeling with the formation of new connections by general anesthetics may present tremendous opportunities for translational research and neurorehabilitation.

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“…Both chronic stress and opioid exposure cause structural changes in the nucleus accumbens (NAc) that are thought to drive stress-susceptibility or increased drug intake (Matsubara et al, 1999;Robinson et al, 2002;Spiga et al, 2005;Diana et al, 2006;Christoffel et al, 2011bChristoffel et al, , 2011aPal and Das, 2013;Golden et al, 2013;Guegan et al, 2016;Kobrin et al, 2016;Graziane et al, 2016;Francis et al, 2017;Cahill et al, 2018;Geoffroy et al, 2019;Fox et al, 2020aFox et al, , 2020b. We thus examined the consequences of our combined stress and fentanyl paradigm on genes associated with dendritic remodeling (Nakayama et al, 2000;Negishi and Katoh, 2005;Newey et al, 2005;Chen and Firestein, 2007).…”

Section: Chronic Stress and Fentanyl Exposure Downregulate Dendritic Complexity Molecules In The Nucleus Accumbensmentioning

confidence: 99%

Chronic Physical and Vicarious Psychosocial Stress Alter Fentanyl Consumption and Nucleus Accumbens Rho GTPases in Male and Female C57BL/6 Mice

Franco

Wulff

Lobo

et al. 2021

Preprint

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Chronic stress can increase the risk of developing a substance use disorder in vulnerable individuals. Numerous models have been developed to probe the underlying neurobiological mechanisms, however most prior work has been restricted to male rodents, conducted only in rats, or introduces physical injury that can complicate opioid studies. Here we sought to establish how chronic psychosocial stress influences fentanyl consumption in male and female C57BL/6 mice. We used chronic social defeat stress (CSDS), or the modified vicarious chronic witness defeat stress (CWDS), and used social interaction to stratify mice as stress-susceptible or resilient. We then subjected mice to a 15 day fentanyl drinking paradigm in the home cage that consisted of alternating forced and choice periods with increasing fentanyl concentrations. Male mice susceptible to either CWDS or CSDS consumed more fentanyl relative to unstressed mice, and exhibited increased preference for fentanyl. CWDS-susceptible female mice did not differ from unstressed mice during the forced periods, but showed increased preference for fentanyl. We also found decreased expression of nucleus accumbens Rho GTPases in male, but not female mice following stress and fentanyl drinking. We also compare fentanyl drinking behavior in mice that had free access to plain water throughout. Our results indicate that stress-sensitized fentanyl consumption is dependent on both sex and behavioral outcomes to stress.

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Morphine-Induced Dendritic Spine Remodeling in Rat Nucleus Accumbens Is Corticosterone Dependent

Cited by 11 publications

References 42 publications

Traumatic Stress Produces Delayed Alterations of Synaptic Plasticity in Basolateral Amygdala

Traumatic Stress Produces Delayed Alterations of Synaptic Plasticity in Basolateral Amygdala

Dendritic spine remodeling and plasticity under general anesthesia

Chronic Physical and Vicarious Psychosocial Stress Alter Fentanyl Consumption and Nucleus Accumbens Rho GTPases in Male and Female C57BL/6 Mice

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