Phosphorylation of GluA1-Ser831 by CaMKII Activation in the Caudate and Putamen Is Required for Behavioral Sensitization After Challenge Nicotine in Rats

Kim, Sung-Hyun; Sohn, Sumin; Choe, Eun Sang

doi:10.1093/ijnp/pyac034

Cited by 4 publications

(3 citation statements)

References 52 publications

(65 reference statements)

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“…Behavioral sensitization to repeated psychostimulant administration has been proposed to reflect many of the neurochemical changes that are characteristic for drug addiction ( Robinson and Berridge, 1993 ; Steketee and Kalivas, 2011 ), and is in this regard a well-established model to outline behavioral transformations elicited by drugs of abuse. Behavioral sensitization elicited by psychostimulants has been proposed to be driven by an interplay between dopaminergic and glutamatergic neuroadaptations ( Robinson and Becker, 1982 ; Vezina, 1996 ; Kim and Vezina, 2002 ; Bamford et al, 2008 ; Yoon et al, 2008 ; Jing et al, 2018 ; Kim et al, 2022 ), and neuroplasticity in the dorsal striatum appears to be especially important for establishing these behavioral transformations ( Durieux et al, 2012 ; Kim et al, 2022 ; Lotfi et al, 2022 ). The neurophysiological data presented here demonstrated a sensitized response to nicotine with respect to both dopaminergic-and glutamatergic signaling, thereby supporting a role for striatal neuroplasticity in behavioral sensitization.…”

Section: Discussionmentioning

confidence: 99%

Acute and chronic effects by nicotine on striatal neurotransmission and synaptic plasticity in the female rat brain

Lucente

Söderpalm

Ericson

et al. 2023

Front. Mol. Neurosci.

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IntroductionTobacco use is in part a gendered activity, yet neurobiological studies outlining the effect by nicotine on the female brain are scarce. The aim of this study was to outline acute and sub-chronic effects by nicotine on the female rat brain, with special emphasis on neurotransmission and synaptic plasticity in the dorsolateral striatum (DLS), a key brain region with respect to the formation of habits.MethodsIn vivo microdialysis and ex vivo electrophysiology were performed in nicotine naïve female Wistar rats, and following sub-chronic nicotine exposure (0.36 mg/kg free base, 15 injections). Locomotor behavior was assessed at the first and last drug-exposure.ResultsAcute exposure to nicotine ex vivo depresses excitatory neurotransmission by reducing the probability of transmitter release. Bath applied nicotine furthermore facilitated long-term synaptic depression induced by high frequency stimulation (HFS-LTD). The cannabinoid 1 receptor (CB1R) agonist WIN55,212-2 produced a robust synaptic depression of evoked potentials, and HFS-LTD was blocked by the CB1R antagonist AM251, suggesting that HFS-LTD in the female rat DLS is endocannabinoid mediated. Sub-chronic exposure to nicotine in vivo produced behavioral sensitization and electrophysiological recordings performed after 2-8 days abstinence revealed a sustained depression of evoked population spike amplitudes in the DLS, with no concomitant change in paired pulse ratio. Rats receiving sub-chronic nicotine exposure further demonstrated an increased neurophysiological responsiveness to nicotine with respect to both dopaminergic- and glutamatergic signaling. However, a tolerance towards the plasticity facilitating property of bath applied nicotine was developed during sub-chronic nicotine exposure in vivo. In addition, the dopamine D2 receptor agonist quinpirole selectively facilitate HFS-LTD in slices from nicotine naïve rats, suggesting that the tolerance may be associated with changes in dopaminergic signaling.ConclusionNicotine produces acute and sustained effects on striatal neurotransmission and synaptic plasticity in the female rat brain, which may contribute to the establishment of persistent nicotine taking habits.

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Section: Discussionmentioning

confidence: 99%

Acute and chronic effects by nicotine on striatal neurotransmission and synaptic plasticity in the female rat brain

Lucente

Söderpalm

Ericson

et al. 2023

Front. Mol. Neurosci.

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“…Nicotine hydrogen tartrate salt was purchased from Aladdin (Cat. 6019‐06‐3, Aladdin) dissolved in sterile 0.9% physiological saline and adjusted to pH 7.2–7.4 with sodium hydroxide 42 . Nicotine exposure group: Nicotine was administered subcutaneously in a volume of 0.1 mL, and the concentration of nicotine (3 mg/kg) was determined in previous studies 43 .…”

Section: Methodsmentioning

confidence: 99%

Demystifying the impact of prenatal tobacco exposure on the placental immune microenvironment: Avoiding the tragedy of mending the fold after death

Zhao,

Jiang,

et al. 2023

J Cellular Molecular Medi

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Prenatal tobacco exposure (PTE) correlates significantly with a surge in adverse pregnancy outcomes, yet its pathological mechanisms remain partially unexplored. This study aims to meticulously examine the repercussions of PTE on placental immune landscapes, employing a coordinated research methodology encompassing bioinformatics, machine learning and animal studies. Concurrently, it aims to screen biomarkers and potential compounds that could sensitively indicate and mitigate placental immune disorders. In the course of this research, two gene expression omnibus (GEO) microarrays, namely GSE27272 and GSE7434, were included. Gene set enrichment analysis (GSEA) and immune enrichment investigations on differentially expressed genes (DEGs) indicated that PTE might perturb numerous innate or adaptive immune‐related biological processes. A cohort of 52 immune‐associated DEGs was acquired by cross‐referencing the DEGs with gene sets derived from the ImmPort database. A protein–protein interaction (PPI) network was subsequently established, from which 10 hub genes were extracted using the maximal clique centrality (MCC) algorithm (JUN, NPY, SST, FLT4, FGF13, HBEGF, NR0B2, AREG, NR1I2, SEMA5B). Moreover, we substantiated the elevated affinity of tobacco reproductive toxicants, specifically nicotine and nitrosamine, with hub genes through molecular docking (JUN, FGF13 and NR1I2). This suggested that these genes could potentially serve as crucial loci for tobacco's influence on the placental immune microenvironment. To further elucidate the immune microenvironment landscape, consistent clustering analysis was conducted, yielding three subtypes, where the abundance of follicular helper T cells (p < 0.05) in subtype A, M2 macrophages (p < 0.01), neutrophils (p < 0.05) in subtype B and CD8+ T cells (p < 0.05), resting NK cells (p < 0.05), M2 macrophages (p < 0.05) in subtype C were significantly different from the control group. Additionally, three pivotal modules, designated as red, blue and green, were identified, each bearing a close association with differentially infiltrated immunocytes, as discerned by the weighted gene co‐expression network analysis (WGCNA). Functional enrichment analysis was subsequently conducted on these modules. To further probe into the mechanisms by which immune‐associated DEGs are implicated in intercellular communication, 20 genes serving as ligands or receptors and connected to differentially infiltrating immunocytes were isolated. Employing a variety of machine learning techniques, including one‐way logistic regression, LASSO regression, random forest and artificial neural networks, we screened 11 signature genes from the intersection of immune‐associated DEGs and secretory protein‐encoding genes derived from the Human Protein Atlas. Notably, CCL18 and IFNA4 emerged as prospective peripheral blood markers capable of identifying PTE‐induced immune disorders. These markers demonstrated impressive predictive power, as indicated by the area under the curve (AUC) of 0.713 (0.548–0.857) and 0.780 (0.618–0.914), respectively. Furthermore, we predicted 34 potential compounds, including cyclosporine, oestrogen and so on, which may engage with hub genes and attenuate immune disorders instigated by PTE. The diagnostic performance of these biomarkers, alongside the interventional effect of cyclosporine, was further corroborated in animal studies via ELISA, Western blot and immunofluorescence assays. In summary, this study identifies a disturbance in the placental immune landscape, a secondary effect of PTE, which may underlie multiple pregnancy complications. Importantly, our research contributes to the noninvasive and timely detection of PTE‐induced placental immune disorders, while also offering innovative therapeutic strategies for their treatment.

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“…Intracerebroventricular infusion of CaMKII antagonists blocked CPP establishment and CaMKII activation in the NAc and VTA of mice [ 23 ]. GluA1-Ser831 phosphorylation induced by CaMKII activation is necessary for nicotine-induced behavioral sensitization in rat caudate-putamen [ 24 ]. Furthermore, phosphorylation of ΔFosB Thr149 by CaMKIIα is enhanced by chronic cocaine use [ 25 ].…”

Section: Introductionmentioning

confidence: 99%

Amelioration of Nicotine-Induced Conditioned Place Preference Behaviors in Mice by an FABP3 Inhibitor

Jia

Kawahata

Cheng

et al. 2023

IJMS

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We previously demonstrated that fatty acid-binding protein 3 null (FABP3−/−) mice exhibit resistance to nicotine-induced conditioned place preference (CPP). Here, we confirm that the FABP3 inhibitor, MF1 ((4-(2-(1-(2-chlorophenyl)-5-phenyl-1H-pyrazol-3-yl)phenoxy) butanoic acid), successfully reduces nicotine-induced CPP scores in mice. MF1 (0.3 or 1.0 mg/kg) was orally administered 30 min before nicotine, and CPP scores were assessed in the conditioning, withdrawal, and relapse phases. MF1 treatment decreased CPP scores in a dose-dependent manner. Failure of CPP induction by MF1 (1.0 mg/kg, p.o.) was associated with the inhibition of both CaMKII and ERK activation in the nucleus accumbens (NAc) and hippocampal CA1 regions. MF1 treatment reduced nicotine-induced increases in phosphorylated CaMKII and cAMP-response element-binding protein (CREB)-positive cells. Importantly, the increase in dopamine D2 receptor (D2R) levels following chronic nicotine exposure was inhibited by MF1 treatment. Moreover, the quinpirole (QNP)-induced increase in the level of CaMKII and ERK phosphorylation was significantly inhibited by MF1 treatment of cultured NAc slices from wild type (WT) mice; however, QNP treatment had no effect on CaMKII and ERK phosphorylation levels in the NAc of D2R null mice. Taken together, these results show that MF1 treatment suppressed D2R/FABP3 signaling, thereby preventing nicotine-induced CPP induction. Hence, MF1 can be used as a novel drug to block addiction to nicotine and other drugs by inhibiting the dopaminergic system.

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Phosphorylation of GluA1-Ser831 by CaMKII Activation in the Caudate and Putamen Is Required for Behavioral Sensitization After Challenge Nicotine in Rats

Cited by 4 publications

References 52 publications

Acute and chronic effects by nicotine on striatal neurotransmission and synaptic plasticity in the female rat brain

Acute and chronic effects by nicotine on striatal neurotransmission and synaptic plasticity in the female rat brain

Demystifying the impact of prenatal tobacco exposure on the placental immune microenvironment: Avoiding the tragedy of mending the fold after death

Amelioration of Nicotine-Induced Conditioned Place Preference Behaviors in Mice by an FABP3 Inhibitor

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