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Repeated traumatic events induce long-lasting behavioral changes that are key to organism adaptation and that affect cognitive, emotional, and social behaviors. Rodents subjected to repeated instances of aggression develop enduring social aversion and increased anxiety. Such repeated aggressions trigger a stress response, resulting in glucocorticoid release(More)
RATIONALE The nicotine discriminative stimulus has been linked to beta2-containing (beta2*) nicotinic receptors, with little evidence of a role for alpha7 nicotinic receptors, because nicotine discrimination was very weak in beta2 null mutant mice but normal in alpha7 mutants. OBJECTIVES As both alpha7 and beta2* nicotinic receptors have been implicated(More)
The glucocorticoid receptor is a ubiquitous transcription factor mediating adaptation to environmental challenges and stress. Selective Nr3c1 (the glucocorticoid receptor gene) ablation in mouse dopaminoceptive neurons expressing dopamine receptor 1a, but not in dopamine-releasing neurons, markedly decreased the motivation of mice to self-administer(More)
Nicotinic acetylcholine receptors (nAChRs) can modulate transmitter release. Striatal [(3)H]dopamine ([(3)H]DA) release is regulated by presynaptic nAChR on dopaminergic terminals and alpha7 nAChR on neighboring glutamatergic afferents. Here, we explored the role of alpha7 nAChR in the modulation of [(3)H]noradrenaline ([(3)H]NA) release from rat(More)
Nicotine achieves its psychopharmacological effects by interacting with nicotinic acetylcholine receptors (nAChRs) in the brain. There are numerous subtypes of nAChR that differ in their properties, including their sensitivity to nicotine, permeability to calcium and propensity to desensitise. The nAChRs are differentially localised to different brain(More)
Neuronal nicotinic acetylcholine receptors (nAChRs) in the CNS appear to exert a predominantly modulatory influence on brain mechanisms, despite being fast-acting ligand-gated ion channels. Many nAChRs have an extrasynaptic location on somatodendritic regions or presynaptic terminals. They influence local excitability by depolarization and can initiate(More)
The activation of glucocorticoid receptors (GR) by glucocorticoids increases stress-related memory through the activation of the MAPK signaling pathway and the downstream transcription factor Egr-1. Here, using converging in vitro and in vivo approaches, respectively, GR-expressing cell lines, culture of hippocampal neurons, and GR genetically modified mice(More)
BACKGROUND Psychostimulants and opiates trigger similar enduring neuroadaptations within the reward circuitry thought to underlie addiction. Transcription factors are key to mediating these enduring behavioral alterations. The facilitation of these maladaptive changes by glucocorticoid hormones suggests that the glucocorticoid receptor (GR), a transcription(More)
In this study, we have examined cellular responses of neuroblastoma SH-SY5Y cells after chronic treatment with galantamine, a drug used to treat Alzheimer's disease that has a dual mechanism of action: inhibition of acetylcholinesterase and allosteric potentiation of nicotinic acetylcholine receptors (nAChR). Acute experiments confirmed that maximum(More)