| 1. |
- Brkic, Sejla, et al.
(författare)
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A family history of Type 1 alcoholism differentiates alcohol consumption in high cortisol responders to stress
- 2015
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Ingår i: Pharmacology Biochemistry and Behavior. - : Elsevier BV. - 0091-3057. ; 130, s. 59-66
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Tidskriftsartikel (refereegranskat)abstract
- Background: The differentiation between high and low cortisol responders to stress is of interest in determining the risk factors which may, along with genetic vulnerability, influence alcohol intake. Study 1: Methods: Thirty-two healthy volunteers, family history positive to alcoholism (FHP, n = 16) and family history negative (FUN, n = 16) attended two laboratory sessions during which alcohol or placebo was offered. Results: There were no differences in consumption of alcohol or placebo between FHP and FHN subjects. Study 2: Methods: Fifty-eight healthy social drinkers, FHP (n = 27) and FUN (n = 31) attended two laboratory sessions. They were administered either alcohol or placebo in both sessions they attended. All subjects underwent either a stress task (the Trier Social Stress Test, TSST) or a stress-free period, at two separate occasions, before being offered beverage. After the salivary cortisol analysis, subjects in each group were divided into high (HCR) or low (LCR) cortisol responders. Results: After stress, subjects who were FHP-HCR consumed more alcohol than FHN-HCR. There were no differences in the placebo intake between FHP and FHN subjects regardless of their cortisol response. Conclusions: This result indicates that stress promotes alcohol consumption only in subjects with a family history of Type 1 alcoholism who show an increase in cortisol response to stress. This behaviour is similar to that previously observed in alcohol dependent individuals after stress and thus could represent an endophenotype posing a risk for future development of alcohol use disorders. (C) 2015 The Authors. Published by Elsevier Inc. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
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| 2. |
- Brkic, Sejla, et al.
(författare)
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High cortisol responders to stress show increased sedation to alcohol compared to low cortisol responders: An alcohol dose-response study
- 2016
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Ingår i: Pharmacology Biochemistry and Behavior. - : Elsevier BV. - 0091-3057. ; 143, s. 65-72
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Tidskriftsartikel (refereegranskat)abstract
- Aims: The present study was designed to examine the relationship between high and low cortisol response to an acute stressful situation and the subjective effects after different doses of alcohol, in healthy social drinkers. Method: Sixty-four subjects (32 men and 32 women) participated in one laboratory session. They performed a modified version of the Trier Social Stress Test (TSST) immediately before consumption of either placebo or alcohol (0.2, 0.4 or 0.8 g/kg). Subjects in each dose group were then divided into high (HCR; n = 32) or low (LCR; n = 32) cortisol responders. Primary dependent measures were self-report questionnaires of mood. Results: The HCR reported increased ratings on Sedation on the Biphasic Alcohol Effects Scale (BAES) with increased dose in comparison with the LCR. This increase in sedation also correlated to the increase in cortisol levels. Conclusion: We conclude that a high cortisol response to stress modulates the subjective response to alcohol, dose-dependently. HCR subjects experience increased sedative effects of alcohol after consumption of higher doses of alcohol following stress compared to LCR subjects.
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| 3. |
- Jacobsson, Lars, et al.
(författare)
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ADHD : Diagnostik och behandling, vårdens organisation och patientens delaktigheten systematisk litteraturöversikt
- 2013
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Rapport (refereegranskat)abstract
- ADHD En funktionsnedsättning med debut i baranåren. Kärmsymtom karaktäriseras av uppmärksamhetsproblem, impulsivitet ioch hyperaktivitet.I ett antal fall sker en normalisering eller mognadsprocess, i andra fall kan någon form av psykisk ohälsa förekommma samtidigt. Den diagnostiska utredningen är omfattande, och både instrument för diagnostik och den diagnostiska processen bör undersökas bättre.Många olika insatser och behandlingar, förutom läkemedel förekommer idag, men kunskapen om eras nytta, risker och kostnader måste förbättras. Vissa läkemedel lindrar ADHD symtom vid korttidsbehandling, men nyttan av långtidsbehandling går inte att bedöma. Vanliga biverjkningar av dessa läkemedel är illamående och nedsatt aptit, för barn viktminskning och pulsökning.
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| 4. |
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| 5. |
- Söderpalm, Bo, 1959, et al.
(författare)
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Stressas vi till missbruk?
- 2005
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Ingår i: Stress. Ed. Ekman R & Arnetz B. - Lund : Liber. - 9789147052585 ; , s. 181-93
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Bokkapitel (övrigt vetenskapligt/konstnärligt)
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| 6. |
- Söderpalm Gordh, Anna, 1971, et al.
(författare)
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Healthy subjects with a family history of alcoholism show increased stimulative subjective effects of alcohol.
- 2011
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Ingår i: Alcoholism, clinical and experimental research. - : Wiley. - 1530-0277 .- 0145-6008. ; 35:8, s. 1426-34
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Tidskriftsartikel (refereegranskat)abstract
- Background: Research has shown that subjects with a family history positive (FHP) of alcoholism are at increased risk for alcoholism and that this group reacts differently to alcohol than family history negative (FHN) subjects. These different levels of sensitivity may make FHP persons more likely to consume alcohol. Here, we tested the hypothesis that subjects FHP for type 1 alcoholism (according to Cloninger) are more sensitive than control subjects to the stimulative, properties of alcohol following a single moderate dose of alcohol. Methods: Fifty-one healthy men and women (22 FHP and 29 FHN) participated in 2 laboratory sessions, in which they consumed a beverage containing ethanol (0.6g/kg in juice) or placebo (juice alone) in a randomized order. Primary dependent measures were self-report questionnaires of mood states. Results: Subjects with family history of type 1 alcoholism showed increased stimulative responses and an elevated positive mood state after ethanol compared to controls. Conclusions: At this moderate dose, ethanol increased stimulative subjective responses in individuals who were "family history positive." This enhanced sensitivity could motivate to exaggerated drinking and thereby increase the risk for developing alcoholism.
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| 7. |
- Söderpalm Gordh, Anna, 1971, et al.
(författare)
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Stress increases consumption of alcohol in humans with a Type 1 Family History of alcoholism in an experimental laboratory setting
- 2011
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Ingår i: Pharmacology Biochemistry and Behavior. - : Elsevier BV. - 0091-3057. ; 99:4, s. 696-703
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: This paper investigates how stress interacts with alcohol consumption in subjects with a family history of alcoholism. One mechanism for increases in alcohol intake may be that stress alters the subjective effects produced by the drug. METHODS: 58 healthy volunteers, divided into two groups of family history positive (FHP) and two groups of family history negative (FHN) participated in two laboratory sessions, in which they performed in one out of two sessions a stress task. Then subjects were allowed to choose up to six additional drinks of ethanol or placebo depending on which session they were randomly assigned to start with. RESULTS: It was found that FHP subjects increased their consumption of alcohol after stress. CONCLUSIONS: It is possible that both stress and alcohol specifically exaggerate the feelings of the reward in the FHP individuals in such way that it may increase the likelihood of consuming more alcohol.
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| 8. |
- Ademar, Karin, et al.
(författare)
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Acamprosate reduces ethanol intake in the rat by a combined action of different drug components
- 2023
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Ingår i: Scientific Reports. - 2045-2322. ; 13:1
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Tidskriftsartikel (refereegranskat)abstract
- Alcohol misuse accounts for a sizeable proportion of the global burden of disease, and Campral (R) (acamprosate; calcium-bis-(N-acetylhomotaurinate)) is widely used as relapse prevention therapy. The mechanism underlying its effect has in some studies been attributed to the calcium moiety and not to the N-acetylhomotaurine part of the compound. We recently suggested that the dopamine elevating effect of acamprosate is mediated both by N-acetylhomotaurine and calcium in a glycine receptor dependent manner. Here we aimed to explore, by means of in vivo microdialysis, if our previous study using local administration was functionally relevant and if systemic administration of the sodium salt of N-acetylhomotaurine (sodium acamprosate; 200 mg/kg, i.p.) enhanced the effects of calcium chloride (CaCl2; 73.5 mg/kg, i.p.) on nucleus accumbens (nAc) dopamine and/or taurine levels in male Wistar rats. In addition, we investigated the impact of regular acamprosate and the combination of CaCl(2 )and N-acetylhomotaurine on the alcohol deprivation effect (ADE). Finally, we assessed if N-acetylhomotaurine potentiates the ethanol-intake reducing effect of CaCl(2 )in a two-bottle choice voluntary ethanol consumption model followed by an ADE paradigm. Systemic administration of regular acamprosate, sodium acamprosate and CaCl(2 )all trended to increase nAc dopamine whereas the combination of CaCl(2)and sodium acamprosate produced a significant increase. Sodium acamprosate elevated extracellular taurine levels without additional effects of CaCl2. Ethanol intake was significantly reduced by systemic administration of CaCl(2 )without additional effects of the combination of CaCl(2 )and sodium acamprosate. Both acamprosate and CaCl(2 )combined with sodium acamprosate blocked the ADE following acute treatment. The data presented suggest that CaCl(2 )and N-acetylhomotaurine act in concert on a neurochemical level, but calcium appears to have the predominant effect on ethanol intake.
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| 9. |
- Ademar, Karin, et al.
(författare)
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Sodium acamprosate and calcium exert additive effects on nucleus accumbens dopamine in the rat
- 2022
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Ingår i: Addiction Biology. - : Wiley. - 1355-6215 .- 1369-1600. ; 27:5
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Tidskriftsartikel (refereegranskat)abstract
- Acamprosate (Campral (R) - calcium-bis[N-acetylhomotaurinate]) is one of few available pharmacotherapies for individuals suffering from alcohol use disorder. Previously, we suggested that acamprosate reduces ethanol intake by increasing dopamine in the nucleus accumbens (nAc), thereby partly substituting for alcohol's dopamine releasing effect. An experimental study suggested the calcium moiety of acamprosate to be the active component of the drug and to mediate the relapse preventing effect. The aim of the present study was to, by means of reversed in vivo microdialysis, elucidate if the dopamine elevating properties of acamprosate are mediated by N-acetylhomotaurine or by the calcium moiety. Male rats were equipped with a microdialysis probe in the nAc and received acute local treatment with regular acamprosate (CaAcamp 0.5 mM), calcium chloride (CaCl2 0.5 mM), sodium acamprosate (NaAcamp 0.5-1 mM), the glycine receptor (GlyR) antagonist strychnine (Stry 20 mu M), or vehicle. In all experiments, extracellular levels of dopamine and taurine were examined. We found that local perfusion with both CaAcamp and CaCl2 increased dopamine levels in a GlyR-dependent manner. NaAcamp did not influence dopamine levels, but concomitant administration with CaCl2 resulted in an additive dopamine output compared to the drugs administrated alone. We also found CaAcamp and the combination of CaCl2 and NaAcamp to increase accumbal taurine levels, suggesting that CaAcamp may act indirectly on GlyRs via taurine release. The present results indicate that both N-acetylhomotaurine and the calcium moiety of acamprosate have dopamine elevating properties within the nAc and that, in this respect, these substances are beneficial in combination.
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| 10. |
- Adermark, Louise, 1974, et al.
(författare)
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Acute and chronic modulation of striatal endocannabinoid-mediated plasticity by nicotine.
- 2019
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Ingår i: Addiction biology. - : Wiley. - 1369-1600 .- 1355-6215. ; 24:3, s. 355-363
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Tidskriftsartikel (refereegranskat)abstract
- The endocannabinoid (eCB) system modulates several phenomena related to addictive behaviors, and drug-induced changes in eCB signaling have been postulated to be important mediators of physiological and pathological reward-related synaptic plasticity. Here, we studied eCB-mediated long-term depression (eCB-LTD) in the dorsolateral striatum, a brain region critical for acquisition of habitual and automatic behavior. We report that nicotine differentially affects ex vivo eCB signaling depending on previous exposure in vivo. In the nicotine-naïve brain, nicotine facilitates eCB-signaling and LTD, whereas tolerance develops to this facilitating effect after subchronic exposure in vivo. In the end, a progressive impairment of eCB-induced LTD is established after protracted withdrawal from nicotine. Endocannabinoid-LTD is reinstated 6months after the last drug injection, but a brief period of nicotine re-exposure is sufficient to yet again impair eCB-signaling. LTD induced by the cannabinoid 1 receptor agonist WIN55,212-2 is not affected, suggesting that nicotine modulates eCB production or release. Nicotine-induced facilitation of eCB-LTD is occluded by the dopamine D2 receptor agonist quinpirole, and by the muscarinic acetylcholine receptor antagonist scopolamine. In addition, the same compounds restore eCB-LTD during protracted withdrawal. Nicotine may thus modulate eCB-signaling by affecting dopaminergic and cholinergic neurotransmission in a long-lasting manner. Overall, the data presented here suggest that nicotine facilitates eCB-LTD in the initial phase, which putatively could promote neurophysiological and behavioral adaptations to the drug. Protracted withdrawal, however, impairs eCB-LTD, which may influence or affect the ability to maintain cessation.
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