ArticleNeuropsychopharmacology : official publication of the American College of Neuropsychopharmacology2014
CaMKII activity in the ventral tegmental area gates cocaine-induced synaptic plasticity in the nucleus accumbens.
Article in Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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19 citing papers in PubMed, 33 citations in OpenAlex.
- Article
- Sevoflurane anaesthesia induces cognitive impairment in young mice through sequential tau phosphorylation.British journal of anaesthesia · 2023Article
- cAMP-mediated upregulation of HCN channels in VTA dopamine neurons promotes cocaine reinforcement.Molecular psychiatry · 2023Article
- CaNeuropharmacology · 2023Article
- Article
- Enhanced psychostimulant response, but not social avoidance, depends on GluA1 AMPA receptors in VTA dopamine neurons following intermittent social defeat stress in rats.The European journal of neuroscience · 2022Article
- A high-affinity cocaine binding site associated with the brain acid soluble protein 1.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- TAAR1 regulates drug-induced reinstatement of cocaine-seeking via negatively modulating CaMKIIα activity in the NAc.Molecular psychiatry · 2022Article
- Article
- Effects of nicotine on DARPP-32 and CaMKII signaling relevant to addiction.Advances in pharmacology (San Diego, Calif.) · 2021Review
- Article
- CaMKII antagonism in the ventral tegmental area impairs acquisition of conditioned approach learning in rats.Neurobiology of learning and memory · 2020Article
- Multidimensional Top-Down Proteomics of Brain-Region-Specific Mouse Brain Proteoforms Responsive to Cocaine and Estradiol.Journal of proteome research · 2019Article
- Extinction of Contextual Cocaine Memories Requires CaThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2017Article
- A New Insight into the Role of CART in Cocaine Reward: Involvement of CaMKII and Inhibitory G-Protein Coupled Receptor Signaling.Frontiers in cellular neuroscience · 2017Review
- Phosphodiesterase 4 inhibitors and drugs of abuse: current knowledge and therapeutic opportunities.Frontiers in biology · 2016Article
- CaMKII mediates stimulus specificity in early odor preference learning in rats.Journal of neurophysiology · 2016Article
- BDNF interacts with endocannabinoids to regulate cocaine-induced synaptic plasticity in mouse midbrain dopamine neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015Article
- αCaMKII controls the establishment of cocaine's reinforcing effects in mice and humans.Translational psychiatry · 2014Article
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
Addictive drugs such as cocaine induce synaptic plasticity in discrete regions of the reward circuit. The aim of the present study is to investigate whether cocaine-evoked synaptic plasticity in the ventral tegmental area (VTA) and nucleus accumbens (NAc) is causally linked. Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) is a central regulator of long-term synaptic plasticity, learning, and drug addiction. We examined whether blocking CaMKII activity in the VTA affected cocaine conditioned place preference (CPP) and cocaine-evoked synaptic plasticity in its target brain region, the NAc. TatCN21 is a CaMKII inhibitory peptide that blocks both stimulated and autonomous CaMKII activity with high selectivity. We report that intra-VTA microinjections of tatCN21 before cocaine conditioning blocked the acquisition of cocaine CPP, whereas intra-VTA microinjections of tatCN21 before saline conditioning did not significantly affect cocaine CPP, suggesting that the CaMKII inhibitor blocks cocaine CPP through selective disruption of cocaine-cue-associated learning. Intra-VTA tatCN21 before cocaine conditioning blocked cocaine-evoked depression of excitatory synaptic transmission in the shell of the NAc slices ex vivo. In contrast, intra-VTA microinjection of tatCN21 just before the CPP test did not affect the expression of cocaine CPP and cocaine-induced synaptic plasticity in the NAc shell. These results suggest that CaMKII activity in the VTA governs cocaine-evoked synaptic plasticity in the NAc during the time window of cocaine conditioning.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.