Jannike Mørch Andersen

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We investigated the relative importance of heroin and its metabolites in eliciting a behavioral response in mice by studying the relationship between concentrations of heroin, 6-monoacetylmorphine (6MAM), and morphine in brain tissue and the effects on locomotor activity. Low doses (subcutaneous) of heroin (< or =5 micromol/kg) or 6MAM (< or =15(More)
Methadone is a synthetic opiate that is useful in a variety of clinical settings, including in maintenance therapy of heroin dependence and as an analgesic. However, methadone can have negative effects on cognition in humans and in rodents. The mechanisms underlying methadone-induced disruption in cognition are unknown. One possibility is that methadone(More)
High blood-brain permeability and effective delivery of morphine to the brain have been considered as explanations for the high potency of heroin. Results from Andersen et al. indicate that 6-monoacetylmorphine (6-MAM), and not morphine, is the active metabolite responsible for the acute effects observed for heroin. Here, we use pharmacokinetic modeling on(More)
OBJECTIVES To reveal a possible relationship between a previously reported impairment of novelty seeking in rats exposed to methadone and changes in intracellular molecules related to learning and memory. METHODS Expression of phosphorylated Ca²⁺-calmodulin kinase II (pCaMKII), extracellular-signal-regulated kinase 2 (pERK2) and cAMP-responsive element(More)
Behavioral consequences of long-term methadone treatment have received little attention either in humans or experimental animals. In this work, we show that methadone (2.5-10 mg/kg) administered (sc) once daily for three weeks with repeated withdrawal on Saturday and Sunday impairs the novelty preference in rats. One hour after the last injection, when(More)
Toll-like receptor 4 (TLR4) signaling is implied in opioid reinforcement, reward, and withdrawal. Here, we explored whether TLR4 signaling is involved in the acute psychomotor-stimulating effects of heroin, 6-acetylmorphine (6-AM), and morphine as well as whether there are differences between the three opioids regarding TLR4 signaling. To address this, we(More)
Immunotherapy can provide a supplemental treatment strategy against heroin use on the principle of sequestering the active drug in the bloodstream, thereby reducing its distribution to the brain. Previous studies have shown that heroin's first metabolite, 6-monoacetylmorphine (6-MAM), is the main mediator of acute heroin effects. The objective of the(More)
The opioid receptor antagonist 3-methoxynaltrexone (3-MeONtx) has previously been shown in rodents to selectively reverse the analgesic actions of heroin and its metabolites 6-monoacetylmorphine (6-MAM), and morphine-6-glucuronide (M6G), but not that of morphine. Based on these and other results, a heroin/6-MAM/M6G μ-opioid receptor binding site or(More)
Ethanol and morphine are both substrates of uridine diphosphate glucuronosyl transferases (UGTs). A pharmacokinetic interaction between ethanol and morphine is suggested from in vitro studies, but to our knowledge not documented in vivo. The aim of this study was to compare the ratios between M6G and morphine and between M3G and morphine in blood samples(More)
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