Faglige interesser
- Eksponering i fosterlivet
- Nevrobiologi
- Nevrotoksikologi
- Opoidavhengighet.
Undervisning
Bakgrunn
Utdanning
- Dr. scient i nevrobiologi, Biologisk institutt, UiO, 2003
Arbeidserfaring
- Førsteamanuensis, Farmasøytisk institutt, UiO, 2017-
- Seniorforsker, Oslo universitetssykehus, 2017-
- Seniorforsker, Folkehelseinstituttet, 2015-2016
- Forsker, Folkehelseinstituttet, 2005-2014
- Forsker, Oslo universitetssykehus, 2004
- Forsker, Forsvarets forskningsinstitutt, 2003
Publikasjoner
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Lumor, Josephine Sena; Nyberg, Henriette Eckhardt; Nerem, Elisabeth; Andersen, Jannike Mørch & Bogen, Inger Lise
(2026).
Long-term effects of adolescent THC exposure on anxiety-like behavior and cognitive function in male rats.
Psychopharmacology.
ISSN 0033-3158.
doi:
10.1007/s00213-026-07067-y.
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Rationale
As cannabis legalization and decriminalization have expanded, it is increasingly perceived as a low-risk substance. Concurrently, the potency of cannabis products and the number of young adults seeking treatment for cannabis use disorder have risen markedly. A growing body of research links early onset, frequent use, and high potency cannabis products to a range of adverse outcomes.
Objective
This study aimed to examine whether frequent cannabis use during late adolescence affects cognitive functioning and increases the risk of developing anxiety in adulthood.
Methods
Male Sprague-Dawley rats were administered tetrahydrocannabinol (THC; 5 mg/kg/day) or vehicle from postnatal day (PND) 42 to 62. After a drug-free period, anxiety-like behavior was assessed in the elevated plus maze (EPM) and Light-Dark transition tests, while cognitive function was evaluated in the novel object recognition and Morris water maze (MWM) tests. THC concentrations in blood and brain tissue were quantified using ultra-high-performance liquid chromatography-tandem mass spectrometry (UHPLC-MS/MS).
Results
The rats displayed blood THC concentrations comparable to human cannabis users and reduced body weight during the exposure period – an effect that persisted for over two months following the final injection. Adolescent THC exposure impaired novelty preference in young adult animals, whereas effects on spatial memory were less definitive. THC-exposed rats showed anxiety-like behavior in the EPM test, but not in the Light-Dark transition test.
Conclusion
Our findings suggest that frequent cannabis exposure during adolescence may lead to long-term reductions in body weight, reduced novel object recognition, and increased vulnerability to certain aspects of anxiety-related behavior in adulthood.
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Baarset, Anne Marte; Steinsland, Synne; Nerem, Elisabeth; Andersen, Jannike Mørch; Baumann, Michael H. & Bogen, Inger Lise
(2025).
Pharmacological effects and pharmacokinetics of the novel synthetic cathinone α-pyrrolidinoisohexanophenone (α-PiHP) compared with α-pyrrolidinovalerophenone (α-PVP) in mice.
Neurotoxicology.
ISSN 0161-813X.
108,
s. 412–421.
doi:
10.1016/j.neuro.2025.05.005.
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Digranes, Nora; Pettersson, Emma Ulrika; Lervik, Andreas; Bogen, Inger Lise; Andersen, Jannike Mørch & Nordgreen, Janicke
[Vis alle 7 forfattere av denne artikkelen]
(2025).
Reversal of fentanyl-induced laryngospasm with ketanserin and naloxone: A prospective randomized blinded study in rats.
Drug and Alcohol Dependence.
ISSN 0376-8716.
277,
s. 112969–112969.
doi:
10.1016/j.drugalcdep.2025.112969.
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Fentanyl kan gi opphav til muskelaktivering av larynks musklatur, noe som resulterer i laryngospasme. I en randomisert, blindet, kontrollert studie utført på 75 rotter viste vi at en serotonin antagonist, ketanserin, sammen med en opioid antagonist, nalokson, kunne reversere denne effekten bedre enn nalokson alene eller kontroll behandling. Studien viser til en sammenheng mellom det serotonerge systemet og laryngospasme utløst av fentanyl.
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Arabaci, Öyküm Kaplan; Zosen, Denis; Domanska, Diana; Bjørnstad, Sigrid; Santini, Simone & Karaca, Umut
[Vis alle 12 forfattere av denne artikkelen]
(2025).
The antidepressant venlafaxine induces upregulation of miR-92 and histological alterations in a chicken embryo model.
Neurochemistry International.
ISSN 0197-0186.
190,
s. 1–11.
doi:
10.1016/j.neuint.2025.106056.
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Antidepressants are commonly prescribed for treating anxiety disorders and depression, including pregnant patients. These medications influence the absorption and metabolism of key neurotransmitters such as serotonin, norepinephrine, and dopamine. However, many aspects of antidepressant function remain unclear, especially regarding their impact on neurodevelopment when used during pregnancy. To explore this, we employed a 3R-friendly chicken embryo model to investigate the cellular and molecular implications of antidepressants use. We focused on commonly used antidepressants for the study: escitalopram, which is a selective serotonin reuptake inhibitor; and venlafaxine, a serotonin and noradrenaline reuptake inhibitor, both of which are frequently prescribed during pregnancy.
Drug distribution analysis showed that both antidepressant drugs reached clinical concentrations in the brain of developing chicken embryos and persisted for several hours. High-throughput miRNA-sequencing showed that venlafaxine upregulated 13 different miRNAs in the chicken cerebellum. Specifically, miR-92 and its human ortholog, miR-363, were significantly upregulated in chicken cerebellum and neuronally differentiated human SH-SY5Y cells, respectively. Neurite metrics showed a significant reduction in neurite outgrowth with venlafaxine, but not with escitalopram. Furthermore, venlafaxine caused histological alterations, such as increased white matter and reduced thickness of the cortical and molecular layer in the cerebellum. Both drugs reduced the thickness of the external granular layer and the number of mitotic events, impacting this crucial germinal zone of the brain.
These findings highlight distinct neurodevelopmental effects of escitalopram and venlafaxine and raise awareness for potential adverse neurological effects in offspring exposed to antidepressants in utero.
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Nyberg, Henriette Eckhardt; Bogen, Inger Lise; Duale, Nur & Andersen, Jannike Mørch
(2025).
Prenatal exposure to methadone or buprenorphine alters transcriptional networks associated with synaptic signaling in newborn rats.
Neuropharmacology.
ISSN 0028-3908.
270.
doi:
10.1016/j.neuropharm.2025.110368.
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Nyberg, Henriette Eckhardt; Bogen, Inger Lise; Nygaard, Egil & Andersen, Jannike Mørch
(2024).
Effects of prenatal exposure to methadone or buprenorphine and maternal separation on anxiety-like behavior in rats.
Drug and Alcohol Dependence.
ISSN 0376-8716.
262(111367),
s. 2–13.
doi:
10.1016/j.drugalcdep.2024.111367.
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Nyberg, Henriette Eckhardt; Bogen, Inger Lise; Nygaard, Egil; Achterberg, Marijke & Andersen, Jannike Mørch
(2024).
Maternal exposure to buprenorphine, but not methadone, during pregnancy reduces social play behavior across two generations of offspring.
Psychopharmacology.
ISSN 0033-3158.
241(12).
doi:
10.1007/s00213-024-06718-2.
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Rajalingam, Dhaksshaginy; Boix, Fernando; Khoder, Ala Zaim; Andersen, Jannike Mørch & Paulsen, Ragnhild Elisabeth Heimtun
(2023).
Distribution of morphine and methadone to the brain in a developmental chicken embryo model.
Toxicology and Applied Pharmacology.
ISSN 0041-008X.
479.
doi:
10.1016/j.taap.2023.116731.
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The use and/or misuse of opioids by pregnant women would expose the fetuses to these drugs during critical stages of development with serious effects for the newborn, like the neonatal abstinence syndrome (NAS). We have revisited an established chicken model for NAS to describe the distribution of morphine and methadone to the brain and explore its validity as a valuable alternative to rodent models. For this purpose, chicken eggs were injected with a single dose of 10 mg/kg or 20 mg/kg morphine or 20 mg/kg methadone onto the chorioallantoic membrane (CAM) on embryonal day 13. Whole brains and lungs were harvested and the concentrations of morphine, methadone and their subsequent metabolites (morphine-3-glucuronide and EDDP, respectively) determined in the brain and lungs at different time points using LC-MS/MS. Morphine and methadone, as well as their metabolites, were detected both in the brain and lungs, with significantly higher concentrations in the lungs. Pharmacokinetic modelling showed that the distribution of morphine to the brain followed a first-order absorption with transit compartments and linear elimination, with concentrations linearly dependent on dose. Moreover, methadone, but not morphine, reduced μ receptor (the main morphine receptor) binding, which can be of relevance for opioid tolerance. The present study is the first to report the brain distribution of morphine, which can be described by standard pharmacokinetic processes, and methadone in the developing chicken embryo. The present findings supplement the already established model and support the use of this chicken model to study NAS.
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Nygaard, Egil & Andersen, Jannike Mørch
(2023).
Prenatal exposure to opioids.
I Brown, Gregory G.; King, Tricia Z.; Haaland, Kathleen Y & Crosson, Bruce (Red.),
APA Handbook of Neuropsychology. Volume 1. Neurobehavioral Disorders and Condictions: Accepted Science and Open Questions.
American Psychological Association (APA).
ISSN 9781433833168.
s. 649–668.
doi:
10.1037/0000307-000.
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Bogen, Inger Lise; Boix, Fernando; Andersen, Jannike Mørch; Steinsland, Synne; Nerem, Elisabeth & Mørland, Jørg Gustav
(2023).
Heroin metabolism in human blood and its impact for the design of an immunotherapeutic approach against heroin effects.
Basic & Clinical Pharmacology & Toxicology.
ISSN 1742-7835.
133(4),
s. 418–427.
doi:
10.1111/bcpt.13926.
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Abstract Immunotherapeutic interventions that block drug effects by binding drug molecules to specific antibodies in the bloodstream have shown promising effects in animal studies. For heroin, which effects are mainly mediated by the metabolites 6‐acetylmorphine (6‐AM; also known as 6‐monoacetylmorphine or 6‐MAM) and morphine, the optimal antibody specificity has been discussed. In rodents, 6‐AM specific antibodies have been recommended based on the rapid metabolism of heroin to 6‐AM in the bloodstream. Since the metabolic rate of heroin in blood is unsettled in humans, we examined heroin metabolism with state‐of–the‐art analytical methodology (UHPLC–MS/MS) in freshly drawn human whole blood incubated with a wide range of heroin concentrations (1–500 μM). The half‐life of heroin was highly concentration dependent, ranging from 1.2–1.7 min for concentrations at or above 25 μM, and gradually increasing to approximately 20 min for 1 μM heroin. At concentrations that can be attained in the bloodstream shortly after an i.v. injection, approximately 70% was transformed into 6‐AM within 3 min, similar to previous observations in vivo. Our results indicate that blood enzymes play a more important role for the rapid metabolism of heroin in humans than previously assumed. This points to 6‐AM as an important target for an efficient immunotherapeutic approach to block heroin effects in humans.
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Skottvoll, Frøydis Sved; Aizenshtadt, Aleksandra; Hansen, Frederik Andre; Martinez, Mikel Amirola; Andersen, Jannike Mørch & Bogen, Inger Lise
[Vis alle 11 forfattere av denne artikkelen]
(2022).
Direct Electromembrane Extraction-Based Mass Spectrometry: A Tool for Studying Drug Metabolism Properties of Liver Organoids.
Analysis & Sensing.
2(2).
doi:
10.1002/anse.202100051.
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This work introduces a strategy for organoid analysis - direct Electromembrane Extraction based Mass Spectrometry (dEME-MS) – for coupling liver organoids with mass spectrometry (MS). dEME-MS comprises electrophoresis of selected small molecules from a culture chamber across an oil membrane, and to a MS compatible solution. This enables clean micro-extraction of drugs and their metabolites as produced in the liver organoids to capillary liquid chromatography-mass spectrometry. Applying dEME-MS, proof-of-concept of directly measuring methadone metabolism is demonstrated on adult liver organoids. With 50 liver organoids and 1 μM methadone, methadone metabolism was monitored from 0 to 24 hours (11 time points). All analytes had <0.4 % variance in retention times with >100 measurements. dEME-MS is capable of automated and selective monitoring of drug metabolism in liver organoids, and could serve as a valuable tool for automated drug discovery efforts.
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Zosen, Denis; Hadera, Mussie Ghezu; Lumor, Josephine Sena; Andersen, Jannike Mørch & Paulsen, Ragnhild Elisabeth Heimtun
(2021).
Chicken embryo as animal model to study drug distribution to the developing brain.
Journal of pharmacological and toxicological methods.
ISSN 1056-8719.
112,
s. 1–5.
doi:
10.1016/j.vascn.2021.107105.
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Andersen, Jannike Mørch; Bogen, Inger Lise; Karinen, Ritva Anneli; Brochmann, Gerd-Wenche; Mørland, Jørg Gustav & Vindenes, Vigdis
[Vis alle 7 forfattere av denne artikkelen]
(2021).
Does the preparation for intravenous administration affect the composition of heroin injections? A controlled laboratory study.
Addiction.
ISSN 0965-2140.
116(11),
s. 3104–3112.
doi:
10.1111/add.15492.
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Aims To study whether the preparation procedure, and its acidic and heating conditions, used by heroin users to prepare heroin for intravenous administration affects the final composition of the fluid to be injected. Methods Samples from different seizures of illegal heroin provided by the Norwegian police were prepared by adding water and ascorbic acid before heating under controlled conditions in the laboratory. Further, three seizures were prepared with different amounts of ascorbic or citric acid relative to their diacetylmorphine content. Pure diacetylmorphine base or salt was also submitted to the procedure applying two different heating intensities. The seizures and the final product after preparation were analysed for diacetylmorphine, 6-acetylmorphine and morphine using liquid chromatography with tandem mass spectrometry (LC-MS-MS). Results After preparation, a decrease of 19.8% (25th and 75th percentiles = −29.2 and −15.3) in the initial diacetylmorphine content was observed. Both the 6-acetylmorphine and morphine content increased but, due to their low content in the initial product, diacetylmorphine still represented 83.9% (25th and 75th percentiles = 77.3 and 88.0) of the sum of these three opioids in the final solution. The loss of water during preparation caused an increase in the concentration of diacetylmorphine, 6-acetylmorphine and morphine, depending on the heating intensity applied. The content of these opioids was affected by the quantity and type of acid added in relation to the heroin purity and the level of diacetylmorphine dissolved being proportional to the amount of ascorbic acid, but not citric acid, in the sample with high heroin purity. Conclusions Preparation of heroin for intravenous injection appears to change the amount or concentration of diacetylmorphine and its active metabolites, 6-acetylmorphine and morphine in the final product, depending on heroin purity, amount and type of acid used or heating conditions. These circumstances can contribute to unintentional variations in the potency of the final injected solution, and therefore affect the outcome after injection.
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Tuv, Silja Skogstad; Bergh, Marianne Skov-Skov; Andersen, Jannike Mørch; Steinsland, Synne; Vindenes, Vigdis & Baumann, Michael H.
[Vis alle 8 forfattere av denne artikkelen]
(2021).
Comparative neuropharmacology and pharmacokinetics of methamphetamine and its thiophene analog methiopropamine in rodents.
International Journal of Molecular Sciences.
ISSN 1661-6596.
22(21),
s. 1–16.
doi:
10.3390/ijms222112002.
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Andersen, Jannike Mørch; Høiseth, Gudrun & Nygaard, Egil
(2020).
Prenatal exposure to methadone or buprenorphine and long-term outcomes: A meta-analysis.
Early Human Development.
ISSN 0378-3782.
143:104997,
s. 1–13.
doi:
10.1016/j.earlhumdev.2020.104997.
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Aim To combine meta-analyses of multiple long-term outcomes in children prenatally exposed to methadone or buprenorphine through their mothers' Opioid maintenance therapy (OMT) with a systematic review of similar outcomes in experimental animals. Method The Medline, Embase, Web of Science, CINAHL, Cochrane and Epistemonikos databases were searched through August 30, 2018. Clinical studies measuring effects on cognitive, behavioral or visual outcomes in 3 months or older children prenatally exposed to OMT and control group(s) were included for meta-analyses. Experimental animal studies with similar exposures and outcomes were included in a systematic review. The three authors independently performed abstract screenings and full-text reviews, and extracted the data. One author performed the meta-analyses. Results The pooled results of the meta-analyses showed worse cognitive, psychomotor, behavioral, attentional and executive functioning, and affected vision in children born to mothers who were in OMT during pregnancy compared to children without prenatal drug exposure (overall effect size = 0.49, 95% confidence interval = 0.38, 0.59, p < 0.00001). Many of the experimental animal studies showed impaired outcomes after prenatal exposure to methadone or buprenorphine. The clinical results may be biased, e.g., with the OMT group having more concurrent risk factors than the unexposed comparison group. There are few studies of older children. Conclusion Children born to mothers in OMT show worse outcomes for a number of different behaviors and impaired vision compared to children born to nonusers. Experimental animal studies indicate that there might be a causal relationship between prenatal methadone or buprenorphine exposure and subsequent negative outcomes.
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Kongstorp, Mette; Bogen, Inger Lise; Stiris, Tom & Andersen, Jannike Mørch
(2020).
Prenatal exposure to methadone or buprenorphine impairs cognitive performance in young adult rats.
Drug and Alcohol Dependence.
ISSN 0376-8716.
212(108008),
s. 1–9.
doi:
10.1016/j.drugalcdep.2020.108008.
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Background Concerns have been raised about the use of opioid maintenance treatment (OMT) during pregnancy and negative effects for the offspring. While neonatal outcomes and short-term effects are relatively well described, studies examining long-term effects in adolescents and adults are absent. The aim of the present study was to examine effects on learning and memory in young adult rats prenatally exposed to methadone or buprenorphine. Methods Female rats were implanted with a 28-day osmotic minipump delivering methadone (10 mg/kg/day), buprenorphine (1 mg/kg/day) or vehicle 5 days prior to mating. To examine possible effects on cognitive functioning, young adult offspring were included in three different behavioral tests that examine recognition memory, nonspatial, and spatial learning and memory. In addition, offspring growth and maternal behavior after birh were investigated. Results Prenatal exposure to methadone or buprenorphine caused impaired recognition memory and nonspatial reference learning and memory in young adult rats compared with the vehicle-treated group. Methadone-exposed offspring, but not the buprenorphine-exposed, also showed reduced long-term spatial memory. We did not observe any changes in maternal behavior or offspring growth after prenatal exposure to methadone or buprenorphine, suggesting that the impaired cognitive functioning is due to the opioid exposure rather than reduced maternal caregiving. Conclusion The present findings of long-term cognitive impairments in methadone- and buprenorphine-exposed offspring points to a negative impact of OMT on neurobiological development.
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Andersen, Jannike Mørch; Opdal, Siri Hauge; Müller, Christian P. & Boix, Fernando
(2020).
CaMKII is activated in opioid induced conditioned place preference, but αCaMKII Thr286 autophosphorylation is not necessary for its establishment.
Behavioural Brain Research.
ISSN 0166-4328.
390,
s. 1–14.
doi:
10.1016/j.bbr.2020.112676.
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Kongstorp, Mette; Bogen, Inger Lise; Steinsland, Synne; Nerem, Elisabeth; Salih, Triske Woshyar & Stiris, Tom
[Vis alle 7 forfattere av denne artikkelen]
(2020).
Prenatal exposure to methadone or buprenorphine alters µ-opioid receptor binding and downstream signaling in the rat brain.
International Journal of Developmental Neuroscience.
ISSN 0736-5748.
80(5),
s. 443–453.
doi:
10.1002/jdn.10043.
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There is a growing concern related to the use of opioid maintenance treatment during pregnancy. Studies in both humans and animals have reported reduced cognitive functioning in offspring prenatally exposed to methadone or buprenorphine; however, little is known about the neurobiological mechanisms underlying these impairments. To reveal possible neurobiological effects of such in utero exposure, we examined brain tissue from methadone‐ and buprenorphine‐exposed rat offspring previously shown to display impaired learning and memory. We studied µ‐opioid receptor (MOR) and N‐methyl‐D‐aspartate receptor (NMDAR) binding in the rat offspring cerebrum during development and in the hippocampus at young adulthood. Moreover, we examined activation of the Ca2+/calmodulin‐dependent protein kinase II (CaMKII) and the extracellular signal‐regulated kinase (ERK), which are central in the downstream signaling of these receptors. The methadone‐ and buprenorphine‐exposed rat pups displayed reduced MOR binding up to two weeks after birth, whereas the NMDAR binding was unaffected. Prenatal exposure to methadone or buprenorphine also resulted in decreased activation of CaMKII and/or ERK during development, while young adult offspring displayed increased hippocampal ERK activation. In conclusion, our findings suggest that prenatal exposure to exogenous opioids, such as methadone or buprenorphine, may disturb the endogenous opioid system during development, with long‐term effects on proteins important for cognitive functioning.
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Kongstorp, Mette; Bogen, Inger Lise; Stiris, Tom & Andersen, Jannike Mørch
(2019).
High accumulation of methadone compared with buprenorphine in fetal rat brain after maternal exposure.
Journal of Pharmacology and Experimental Therapeutics.
ISSN 0022-3565.
371(1),
s. 130–137.
doi:
10.1124/jpet.119.259531.
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Kvello, Anne Marte Sjursen; Andersen, Jannike Mørch; Øiestad, Elisabeth Leere; Steinsland, Synne; Aase, Audun & Mørland, Jørg
[Vis alle 7 forfattere av denne artikkelen]
(2019).
A monoclonal antibody against 6-acetylmorphine protects female mice offspring from adverse behavioral effects induced by prenatal heroin exposure.
Journal of Pharmacology and Experimental Therapeutics.
ISSN 0022-3565.
368(1),
s. 106–115.
doi:
10.1124/jpet.118.251504.
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Kvello, Anne Marte Sjursen; Andersen, Jannike Mørch; Boix, Fernando; Mørland, Jørg & Bogen, Inger Lise
(2019).
The role of 6-acetylmorphine in heroin-induced reward and locomotor sensitization in mice.
Addiction Biology.
ISSN 1355-6215.
s. 1–10.
doi:
10.1111/adb.12727.
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We have previously demonstrated that heroin's first metabolite, 6‐acetylmorphine (6‐AM), is an important mediator of heroin's acute effects. However, the significance of 6‐AM to the rewarding properties of heroin still remains unknown. The present study therefore aimed to examine the contribution of 6‐AM to heroin‐induced reward and locomotor sensitization. Mice were tested for conditioned place preference (CPP) induced by equimolar doses of heroin or 6‐AM (1.25‐5 μmol/kg). Psychomotor activity was recorded during the CPP conditioning sessions for assessment of drug‐induced locomotor sensitization. The contribution of 6‐AM to heroin reward and locomotor sensitization was further examined by pretreating mice with a 6‐AM specific antibody (anti–6‐AM mAb) 24 hours prior to the CPP procedure. Both heroin and 6‐AM induced CPP in mice, but heroin generated twice as high CPP scores compared with 6‐AM. Locomotor sensitization was expressed after repeated exposure to 2.5 and 5 μmol/kg heroin or 6‐AM, but not after 1.25 μmol/kg, and we found no correlation between the expression of CPP and the magnitude of locomotor sensitization for either opioid. Pretreatment with anti–6‐AM mAb suppressed both heroin‐induced and 6‐AM–induced CPP and locomotor sensitization. These findings provide evidence that 6‐AM is essential for the rewarding and sensitizing properties of heroin; however, heroin caused stronger reward compared with 6‐AM. This may be explained by the higher lipophilicity of heroin, providing more efficient drug transfer to the brain, ensuring rapid increase in the brain 6‐AM concentration.
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Bergh, Marianne Skov-Skov; Bogen, Inger Lise; Andersen, Jannike Mørch; Øiestad, Åse Marit Leere & Berg, Thomas
(2017).
Determination of adrenaline, noradrenaline and corticosterone in rodent blood by ion pair reversed phase UHPLC–MS/MS.
Journal of chromatography. B.
ISSN 1570-0232.
1072,
s. 161–172.
doi:
10.1016/j.jchromb.2017.11.016.
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Kvello, Anne Marte Sjursen; Andersen, Jannike Mørch; Øiestad, Elisabeth Leere; Mørland, Jørg & Bogen, Inger Lise
(2016).
Pharmacological Effects of a Monoclonal Antibody against
6-Monoacetylmorphine upon Heroin-Induced Locomotor Activity
and Pharmacokinetics in Mice.
Journal of Pharmacology and Experimental Therapeutics.
ISSN 0022-3565.
358(2),
s. 181–189.
doi:
10.1124/jpet.116.233510.
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Eriksen, Guro Søe; Andersen, Jannike Mørch; Boix, Fernando; Bergh, Marianne Skov-Skov; Vindenes, Vigdis & Rice, Kenner C.
[Vis alle 8 forfattere av denne artikkelen]
(2016).
Comparison of (+)- and (-)-Naloxone on the acute psychomotor-stimulating effects of heroin, 6-acetylmorphine, and morphine in mice.
Journal of Pharmacology and Experimental Therapeutics.
ISSN 0022-3565.
358(2),
s. 209–215.
doi:
10.1124/jpet.116.233544.
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Thaulow, Cecilie Hasselø; Høiseth, Gudrun; Andersen, Jannike Mørch; Handal, Marte & Mørland, Jørg
(2014).
Pharmacokinetic interactions between ethanol and heroin: a study on post-mortem cases.
Forensic Science International.
ISSN 0379-0738.
242,
s. 127–134.
doi:
10.1016/j.forsciint.2014.06.032.
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Bogen, Inger Lise; Boix, Fernando; Nerem, Elisabeth; Mørland, Jørg & Andersen, Jannike Mørch
(2014).
A monoclonal antibody specific for 6-monoacetylmorphine reduces acute heroin effects in mice.
Journal of Pharmacology and Experimental Therapeutics.
ISSN 0022-3565.
349(3),
s. 568–576.
doi:
10.1124/jpet.113.212035.
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Eriksen, Guro Søe; Andersen, Jannike Mørch; Boix, Fernando & Mørland, Jørg
(2014).
3-Methoxynaltrexone is not a selective antagonist for the acute psychomotor stimulating effects of heroin and 6-monoacetylmorphine in mice.
Pharmacology, Biochemistry and Behavior.
ISSN 0091-3057.
122,
s. 82–88.
doi:
10.1016/j.pbb.2014.03.018.
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Andersen, Jannike Mørch; Haugen, Karianne Slåtta; Ripel, Åse & Mørland, Jørg
(2014).
The interference of ethanol with heroin-stimulated psychomotor activation in mice is not related to changed brain concentrations of the active metabolites 6MAM or morphine.
Basic & Clinical Pharmacology & Toxicology.
ISSN 1742-7835.
114(2),
s. 197–201.
doi:
10.1111/bcpt.12133.
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Boix, Fernando; Andersen, Jannike Mørch & Mørland, Jørg
(2013).
Pharmacokinetic modeling of subcutaneous heroin and its metabolites in blood and brain of mice.
Addiction Biology.
ISSN 1355-6215.
18(1),
s. 1–7.
doi:
10.1111/j.1369-1600.2010.00298.x.
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Høiseth, Gudrun; Andersen, Jannike Mørch & Mørland, Jørg
(2013).
Less glucuronidation of morphine in the presence of ethanol in vivo.
European Journal of Clinical Pharmacology.
ISSN 0031-6970.
69(9),
s. 1683–1687.
doi:
10.1007/s00228-013-1533-5.
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Sankararaman, Aparna; Masiulis, Irene; Richardson, Devon; Andersen, Jannike Mørch; Mørland, Jørg & Eisch, Amelia
(2012).
Methadone does not alter key parameters of adult hippocampal neurogenesis in the heroin-naive rat.
Neuroscience Letters.
ISSN 0304-3940.
516(1),
s. 99–104.
doi:
10.1016/j.neulet.2012.03.066.
Fulltekst i vitenarkiv
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Andersen, Jannike Mørch; Klykken, Christine & Mørland, Jørg
(2012).
Long-term methadone treatment reduces phosphorylation of CaMKII in rat brain.
Journal of Pharmacy and Pharmacology (JPP).
ISSN 0022-3573.
64(6),
s. 843–847.
doi:
10.1111/j.2042-7158.2012.01469.x.
Fulltekst i vitenarkiv
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Boix, Fernando; Andersen, Jannike Mørch & Mørland, Jørg
(2011).
Pharmacokinetic modeling of subcutaneous heroin and its metabolites in blood and brain of mice.
Addiction Biology.
ISSN 1355-6215.
18(1),
s. 1–7.
doi:
10.1111/j.1369-1600.2010.00298.x.
Fulltekst i vitenarkiv
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Andersen, Jannike Mørch; Olaussen, Christine Fostveit; Ripel, Åse & Mørland, Jørg
(2011).
Long-term methadone treatment impairs novelty preference in rats both when present and absent in brain tissue.
Pharmacology, Biochemistry and Behavior.
ISSN 0091-3057.
98(3),
s. 412–416.
doi:
10.1016/j.pbb.2011.02.017.
Fulltekst i vitenarkiv
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Andersen, Jannike Mørch; Ripel, Åse; Boix, Fernando; Normann, Per Trygve & Mørland, Jørg
(2009).
Increased locomotor activity induced by heroin in mice: pharmacokinetic demonstration of heroin acting as a prodrug for the mediator 6-monoacetylmorphine in vivo.
Journal of Pharmacology and Experimental Therapeutics.
ISSN 0022-3565.
331(1),
s. 153–161.
doi:
10.1124/jpet.109.152462.
Fulltekst i vitenarkiv
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Karinen, Ritva Anneli; Andersen, Jannike Mørch; Ripel, Åse; Hasvold, Inger; Hopen, Anita Braute & Mørland, Jørg
[Vis alle 7 forfattere av denne artikkelen]
(2009).
Determination of heroin and its main metabolites in small sample volumes of whole blood and brain tissue by reversed-phase liquid chromatography-tandem mass spectrometry.
Journal of Analytical Toxicology.
ISSN 0146-4760.
33(7),
s. 345–350.
Fulltekst i vitenarkiv
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Zahl, Per Henrik; Gøtzsche, Peter C; Andersen, Jannike Mørch & Mæhlen, Jan
(2006).
Results of the Two-County trial of mammography screening are not compatible with contemporaneous official Swedish breast cancer statistics.
Danish Medical Bulletin.
ISSN 0907-8916.
53(4),
s. 438–440.
Fulltekst i vitenarkiv
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Andersen, Jannike Mørch; Myhre, Oddvar; Aarnes, Halvor; Vestad, Tor Arne & Fonnum, Frode
(2003).
Identification of the Hydroxyl Radical and Other Reactive Oxygen Species in Human Neutrophil Granulocytes Exposed to a Fragment of the Amyloid Beta Peptide.
Free radical research.
ISSN 1071-5762.
37(3),
s. 269–279.
Fulltekst i vitenarkiv
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Myhre, Oddvar; Andersen, Jannike Mørch; Aarnes, Halvor & Fonnum, Frode
(2003).
Evaluation of the probes 2´,7´-dichlorofluorescin diacetate, luminol, and lucigenin as indicatos of reactive species formation.
Biochemical Pharmacology.
ISSN 0006-2952.
65,
s. 1575–1582.
Fulltekst i vitenarkiv
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Fonnum, Frode; Myhre, Oddvar; Voie, Øyvind Albert; Andersen, Jannike Mørch & Dreiem, Anne
(2001).
The formation of free radicals in human granulocytes in cerebellar granule cells.
ATLA (Alternatives to Laboratory Animals).
ISSN 0261-1929.
29(3),
s. 283–285.
Fulltekst i vitenarkiv
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Nygaard, Egil; Andersen, Jannike Mørch & Høiseth, Gudrun
(2019).
Long-term outcomes after prenatal exposure to methadone or buprenorphine: A meta-analysis.
Fulltekst i vitenarkiv
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Handal, Marte; Andersen, Jannike Mørch & Nygaard, Egil
(2019).
Barn født av mødre som bruker opioider under svangerskapet.
Fulltekst i vitenarkiv
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Kongstorp, Mette; Andersen, Jannike Mørch; Bogen, Inger Lise & Stiris, Tom
(2019).
Prenatal exposure to opioid maintenance treatment (OMT) reduces cognitive performance in young adult rats.
Fulltekst i vitenarkiv
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Kongstorp, Mette; Andersen, Jannike Mørch & Bogen, Inger Lise
(2018).
Prenatal exposure to opioid maintenance treatment (OMT) reduced cognitive performance in young adult rats.
Fulltekst i vitenarkiv
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Kongstorp, Mette; Andersen, Jannike Mørch & Bogen, Inger Lise
(2018).
The effect on neonatal rat offspring born to dams exposed to methadone or buprenorphine during pregnancy.
Fulltekst i vitenarkiv
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Andersen, Jannike Mørch; Opdal, Siri Hauge; Müller, Christian P. & Boix, Fernando
(2017).
Phosphorylation of alpha-CaMKII at Thr286 is not required for the acquisition of morphine-induced condition place preference in mice.
Fulltekst i vitenarkiv
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Kongstorp, Mette; Andersen, Jannike Mørch & Bogen, Inger Lise
(2017).
Neurobiological development in rat pups exposed to methadone or buprenorphine during gestation.
Fulltekst i vitenarkiv
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Hadera, Mussie Ghezu; Andersen, Jannike Mørch & Paulsen, Ragnhild Elisabeth
(2017).
Effects of methadone in the developing chicken embryo as a model of neurodevelopmental toxicity.
Reproductive Toxicology.
ISSN 0890-6238.
72,
s. 216–217.
doi:
10.1016/j.reprotox.2017.06.030.
Fulltekst i vitenarkiv
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Eriksen, Guro Søe; Andersen, Jannike Mørch; Boix, Fernando & Mørland, Jørg
(2013).
Vil vi i fremtiden kunne utvikle smertelindrende opioidbaserte preparater uten ruspotensial?
Fulltekst i vitenarkiv
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Andersen, Jannike Mørch; Haugen, Karianne Slåtta; Ripel, Åse & Mørland, Jørg
(2013).
Hvorfor er kombinasjonen alkohol og heroin farlig?
Fulltekst i vitenarkiv
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Bogen, Inger Lise; Boix, Fernando; Nerem, Elisabeth; Mørland, Jørg & Andersen, Jannike Mørch
(2013).
Preklinisk studie av en passiv heroinvaksine.
Fulltekst i vitenarkiv
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Bogen, Inger Lise; Boix, Fernando; Nerem, Elisabeth; Mørland, Jørg & Andersen, Jannike Mørch
(2013).
Prekliniske studier av en heroin-vaksine.
Fulltekst i vitenarkiv
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Andersen, Jannike Mørch; Haugen, Karianne Slåtta; Ripel, Åse & Mørland, Jørg
(2013).
Hvorfor er alkohol og heroin en farlig kombinasjon?
Fulltekst i vitenarkiv
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Boix, Fernando & Andersen, Jannike Mørch
(2013).
Avhengighet: en læringsprosess som setter avtrykk i hjernen.
Fulltekst i vitenarkiv
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Boix, Fernando & Andersen, Jannike Mørch
(2013).
Avhengighet: en læringsprosess som setter avtrykk i hjernen.
Fulltekst i vitenarkiv
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Sankararaman, Aparna; Richardson, Devon; Andersen, Jannike Mørch; Mørland, Jørg & Eisch, Amelia
(2012).
Effect of methadone on neurogenesis in rats.
Fulltekst i vitenarkiv
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Bogen, Inger Lise; Andersen, Jannike Mørch; Boix, Fernando; Nerem, Elisabeth; Normann, Per Trygve & Mørland, Jørg
(2012).
Heroin abuse and addiction: Heroin metabolism as a key player and possible target for new pharmacotherapy.
Fulltekst i vitenarkiv
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Eriksen, Guro Søe; Andersen, Jannike Mørch; Boix, Fernando & Mørland, Jørg
(2012).
Ulike µ-opioide subreseptorer medierer den stimulerende- og smertestillende effekten av heroin, 6MAM og morfin.
Fulltekst i vitenarkiv
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Haugen, Karianne Slåtta; Ripel, Åse & Andersen, Jannike Mørch
(2011).
Påvirker etanol metabolismen av heroin?
Fulltekst i vitenarkiv
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Andersen, Jannike Mørch; Olaussen, Christine Fostveit; Ripel, Åse & Mørland, Jørg
(2011).
Langvarig metadonbehandling svekker kognitiv funksjonsevne hos rotter.
Fulltekst i vitenarkiv
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Sankararaman, Aparna; Richardson, Devon; Andersen, Jannike Mørch; Mørland, Jørg & Eisch, Amelia
(2011).
Effect of methadone on neurogenesis in rats.
Fulltekst i vitenarkiv
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Andersen, Jannike Mørch; Ripel, Åse; Boix, Fernando; Normann, Per Trygve & Mørland, Jørg
(2011).
Glem heroin og morfin! - Det er 6MAM som medierer den umiddelbare heroinresponsen.
Fulltekst i vitenarkiv
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Eriksen, Guro Søe; Andersen, Jannike Mørch; Boix, Fernando & Mørland, Jørg
(2011).
Medieres den lokomotoriske effekten av heroin, 6MAM, morfin og M6G gjennom forskjellige µ-opioide subreseptorer?
Fulltekst i vitenarkiv
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Boix, Fernando; Andersen, Jannike Mørch & Mørland, Jørg
(2011).
Heroin: det er 6-MAM som ”går rett i hodet”.
Fulltekst i vitenarkiv
Vis sammendrag
Heroins effekt gjennom opioidreseptorer i hjernen er veldig svak og kan ikke forklare heroins høye
avhengighetspotensial sammenliknet med andre opiater som f.eks. morfin. I kroppen, omdannes
heroin først til 6-monoacetylmorfin (6-MAM), som omdannes videre til morfin. Siden heroin er et
meget lipofilt stoff som lett krysser blod-hjerne barrieren har man antatt at heroins rolle er å raskt
levere høye konsentrasjoner av morfin til hjernen. I en studie i mus (Andersen et al J Pharmacol
Exp Ther 331:153-161.2009), har vi vist at konsentrasjonen av 6-MAM i blod og hjerne var mye
høyere enn heroin og morfin etter subkutan injeksjon av heroin. Parallelle atferdsstudier viste at den
akutte effekten av heroin falt sammen med tilstedeværelsen av 6-MAM i hjernen og ikke morfin.
Med hjelp av farmakologisk modellering har vi beregnet hastighetskonstanter som beskriver
overføring mellom blod og hjerne, metabolisme og utskillelse - prosesser som bestemmer
distribusjonen av heroin og metabolittene i blod og hjerne.
Den lave heroinkonsentrasjonen i blod er et resultat av høy utskillelse og lynrask omdannelse til 6-
MAM som akkumuleres i blod pga. lav omdannelse til morfin. Heroins opptak til og metabolisme i
hjernen kan ikke forklare den høye 6-MAM konsentrasjonen i hjernen, som i høy grad må skyldes
opptak av 6-MAM fra blodet der stoffet foreligger i høye konsentrasjoner.
I motsetning til hva en har trodd, viser resultatene at,heroin omdannes umiddelbart i blod hvor
stoffet foreligger med en så lav konsentrasjon at bare en liten fraksjon er tilgjengelig for opptak til
hjernen. Høye konsentrasjoner av den aktive metabolitten 6-MAM i hjernen gjenspeiler dette
stoffets høye konsentrasjon i blod.
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Andersen, Jannike Mørch; Ripel, Åse; Boix, Fernando; Normann, Per Trygve & Mørland, Jørg
(2010).
Glem morfin! – 6-monoacetylmorfin medierer den umiddelbare heroinresponsen.
Fulltekst i vitenarkiv
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Boix, Fernando; Andersen, Jannike Mørch & Mørland, Jørg
(2010).
Farmakokinetikk av heroin i blod og hjerne i mus.
Fulltekst i vitenarkiv
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Olaussen, Christine Fostveit; Lieng, Nina; Normann, Per Trygve & Andersen, Jannike Mørch
(2009).
Påvirker metadon kognitive funksjoner hos rotte?
Fulltekst i vitenarkiv
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Andersen, Jannike Mørch; Ripel, Åse; Boix, Fernando; Normann, Per Trygve & Mørland, Jørg
(2009).
The acute behavioural response to heroin in mice is mediated by the initial metabolite 6-acetylmorphine and not morphine.
Fulltekst i vitenarkiv
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Ripel, Åse; Hasvold, Inger; Karinen, Ritva Anneli; Andersen, Jannike Mørch & Christophersen, Asbjørg S.
(2008).
Determination of heroin and the metabolites in blood by LC-MS/MS.
Fulltekst i vitenarkiv
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Willoch, Frode; Lobmaier, Philipp Paul; Kunøe, Nikolaj; Waal, Helge; Andersen, Jannike Mørch & Sundet, Kjetil Søren
[Vis alle 7 forfattere av denne artikkelen]
(2008).
”Kognitiv evne og nevrobiologiske prosesser hos heroinavhengige i behandling”.
Fulltekst i vitenarkiv
Vis sammendrag
Mange heroinavhengige har nedsatt kognitiv evne og svekket hukommelse. Dette kan relateres til nevrobiologiske effekter av agonisten heroin, som stimulerer opioidreseptorer. Agonistene metadon og buprenorfin brukes som erstatning for heroin i legemiddelassistert rehabilitering (LAR). Det antas at også disse legemidlene påvirker kognitiv evne og hukommelse negativt.
Relaterte nevrobiologiske prosesser i LAR-behandling over tid er ikke kartlagt.
Naltrekson er en antagonist som blokkerer opioidreseptorer. I implantatform forhindrer naltrekson effektivt tilbakefall til heroinbruk og overdose etter gjennomgått avrusning. Det er uklart hvordan kognitiv evne og hukommelse utvikler seg i langtids naltreksonbehandling. Sammenhengen mellom konsentrasjonen av naltrekson i blod og grad av reseptormetning er ikke undersøkt og har umiddelbar betydning for hvor lenge implantatet virker og for faren for overdoser.
Denne prospektive studien skal kartlegge kognitiv evne og nevrobiologiske prosesser blant pasienter i LAR og naltrekson implantatbehandling sammenlignet med pasienter i avholdenhetsorientert behandling og friske kontrollpersoner.
Følgende problemstillinger undersøkes:
1. Kognitiv evne hos avholdne heroinavhengige med eller uten naltrekson implantat og relasjon til metning av opioidreseptorer og evt. strukturelle forandringer påvist ved hhv. PET og MR:
a. Tidlig i avrusingen?
b. Etter 6 måneders avholdenhet?
2. Hvilken effekt har metadon, buprenorfin og naltrekson på kognitiv evne:
a. Ved oppstart og etter 6 måneder?
b. Forskjeller mellom gruppene?
c. Sammenhengen med funn fra hjerneavbildning?
20 pasienter i institusjon og 20 i naltrekson implantatbehandling gjennomgår kognitiv testing og hjerneavbildning med MR og PET etter avrusning. Gruppen i institusjon undersøkes igjen etter 6, gruppen med naltrekson igjen etter 3 og 5 måneder. 20 pasienter på henholdsvis metadon og buprenorfin gjenomgår de samme undersøkelsene ved innleggelse til langtidsbehandling og etter 6 måneder. Alle sammenlignes med friske kontrollpersoner.
Prosjektmidler er søkt NFR 2008. Undersøkelsen av friske kontroller og etablering av egnet PET tracer er påbegynt med midler innvilget av NevroNor (NFR).
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Andersen, Jannike Mørch; Billington, Camilla & Normann, Per Trygve
(2007).
Hvorfor er heroin et mye mer potent rusmiddel sammenliknet med morfin?
Fulltekst i vitenarkiv
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Andersen, Jannike Mørch; Boix, Fernando; Billington, Camilla; Normann, Per Trygve & Mørland, Jørg
(2007).
Heroin, 6MAM and morphine: locomotor activity and pharmacokinetic in mice.
Fulltekst i vitenarkiv
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Andersen, Jannike Mørch; Myhre, Oddvar; Vestad, Tor Arne; Aarnes, Halvor & Fonnum, Frode
(2000).
bA(25-35) produces free radicals in human neutrophil granulocytes. A study including fluorescence, electron paramagnetic resonance (EPR) spectroscopy and aromatic acid hydroxylation.
Fulltekst i vitenarkiv
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Andersen, Jannike Mørch & Olaussen, Christine Fostveit
(2009).
Does long-term methadone exposure affect cognitive functions in rats? : Effects on novelty exploration and phosphorylation of CaMKII and ERK.
Universitetet i Oslo.
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Numerous studies have explored the effects of morphine on cognitive function, while knowledge concerning methadone is scarce. This study is the first in line, being part of a newly started project. The aim of this study was to examine whether long-term administration of methadone results in deficits in performance in the Novelty-test and changes in phosphorylation of calcium/calmodulin kinase II (CaMKII) and extracellular signal-regulated kinase (ERK) in the hippocampus. Rats were administrated (sc) methadone, morphine or saline once per day for three weeks (2.5-10 mg/kg), and novelty-tested one hour and one week after the last injection. Western blotting was performed on homogenate from hippocampus, taken out directly after the novelty-testing, to detect levels of phosphorylated CaMKII (p-CaMKII) and ERK (p-ERK). p-CaMKII was significantly down-regulated one week after the last injection of methadone, while no significant difference in p-ERK was observed. There were no significant differences between the groups in the novelty-test one week after the last injection, while one hour after the last injection the animals were to affected by the methadone to perform the test. Our findings indicate that long-term methadone exposure may specifically affect protein phosphorylation, but don’t seem to have a persistent effect on novelty-exploration. This may also be due to the Novelty-test not being sensitive enough to pick up small differences between the exposed groups and the control group.
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Publisert
25. sep. 2017 10:56
- Sist endret
5. sep. 2022 09:12