| 1. |
- 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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| 2. |
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| 3. |
- 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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| 4. |
- 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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| 5. |
- Adermark, Louise, 1974, et al.
(författare)
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Brain region specific modulation of ethanol-induced depression of GABAergic neurons in the brain reward system by the nicotine receptor antagonist mecamylamine
- 2014
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Ingår i: Alcohol. - : Elsevier BV. - 0741-8329. ; 48:5, s. 455-461
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Tidskriftsartikel (refereegranskat)abstract
- The mechanisms underlying ethanol-induced activation of the mesolimbic dopamine system are not fully understood, but increased extracellular dopamine in the nucleus accumbens (nAc) has been shown to involve nicotinic acetylcholine receptors (nAChRs). Basal activity of dopaminergic neurons in the ventral tegmental area (VTA) is under the influence of GABAergic neurotransmission, and the aim of this study was to characterize the involvement of nAChRs in mediating acute ethanol effects on GABAergic activity in subregions of the brain reward system. Multi-electrode in vivo recordings were made in the VTA and nAc of awake and behaving C57BL6/J mice receiving intraperitoneal injections of saline or ethanol (2.0 g/kg), combined with, or without, pre-injection of the non-competitive nAChR antagonist mecamylamine (1.0 mg/kg). Ethanol significantly decreased the activity of quinpirole-insensitive slow-spiking and fast-spiking units in both the VTA and the nAc as compared to saline injection. Pre-treatment with mecamylamine inhibited the rate-inhibiting properties of ethanol in the VTA, but not in the nAc. The data presented here show that ethanol depresses the activity of quinpirole-insensitive, putative GABAergic neurons, in the mesolimbic dopamine system of mice, and that nAChRs contribute to this modulation. This finding, taken together with previous microdialysis studies, supports an involvement of GABAergic neurons and nAChRs in ethanol's interaction with the mesolimbic dopamine system. (C) 2014 The Authors. Published by Elsevier Inc. All rights reserved.
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| 6. |
- Adermark, Louise, 1974, et al.
(författare)
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Ethanol-induced modulation of synaptic output from the dorsolateral striatum in rat is regulated by cholinergic interneurons.
- 2011
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Ingår i: Neurochemistry international. - : Elsevier BV. - 1872-9754 .- 0197-0186. ; 58:6, s. 693-9
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Tidskriftsartikel (refereegranskat)abstract
- The striatum is the largest input nucleus to the basal ganglia and associated with reward-based behavior. We assessed whether acute ethanol (EtOH) exposure could modulate synaptic efficacy in the dorsolateral striatum of juvenile Wistar rats. Since acute EtOH administration can both increase and decrease the probability of release of different neurotransmitters from synaptic terminals, we used field potential recordings to evaluate the net effect of EtOH on striatal output. We showed that 50mM EtOH but not 20, 80 or 100mM, depresses population spike (PS) amplitude in the dorsolateral striatum. This depression of synaptic output is insensitive to the N-methyl-d-aspartic acid (NMDA) receptor inhibitor DL-2-amino-5-phosphonopentanoic acid (AP-5, 50μM), but is blocked in slices treated with glycine receptor antagonists (strychnine, 1μM; PMBA, 50μM), nicotinic acetylcholine receptor antagonists (mecamylamine, 10μM; methyllycaconitine citrate (MLA), 40nM), or GABA(A) receptor inhibitors (picrotoxin, 100μM; bicuculline, 2μM, 20μM). A long-term facilitation of synaptic output, which is more pronounced in slices from adult Wistar rats, is detected following EtOH washout (50, 80, 100mM). This long-term enhancement of PS amplitude is regulated by cholinergic interneurons and completely blocked by mecamylamine, MLA or the non-selective muscarinic antagonist scopolamine (10μM). Administration of 100mM EtOH significantly depresses PS amplitude in scopolamine-treated slices, suggesting that EtOH exerts dual actions on striatal output that are initiated instantly upon drug wash-on. In conclusion, EtOH modulates striatal microcircuitry and neurotransmission in a way that could be of importance for understanding the intoxicating properties as well as the acute reward sensation of EtOH.
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| 7. |
- Adermark, Louise, 1974, et al.
(författare)
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Implications for glycine receptors and astrocytes in ethanol-induced elevation of dopamine levels in the nucleus accumbens.
- 2011
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Ingår i: Addiction biology. - : Wiley. - 1369-1600 .- 1355-6215. ; 16:1, s. 43-54
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Tidskriftsartikel (refereegranskat)abstract
- ABSTRACT Elevated dopamine levels are believed to contribute to the rewarding sensation of ethanol (EtOH), and previous research has shown that strychnine-sensitive glycine receptors in the nucleus accumbens (nAc) are involved in regulating dopamine release and in mediating the reinforcing effects of EtOH. Furthermore, the osmoregulator taurine, which is released from astrocytes treated with EtOH, can act as an endogenous ligand for the glycine receptor, and increase extracellular dopamine levels. The aim of this study was to address if EtOH-induced swelling of astrocytes could contribute to elevated dopamine levels by increasing the extracellular concentration of taurine. Cell swelling was estimated by optical sectioning of fluorescently labeled astrocytes in primary cultures from rat, and showed that EtOH (25-150 mM) increased astrocyte cell volumes in a concentration- and ion-dependent manner. The EtOH-induced cell swelling was inhibited in cultures treated with the Na(+)/K(+)/2Cl(-) cotransporter blocker furosemide (1 mM), Na(+)/K(+)-ATPase inhibitor ouabain (0.1 mM), potassium channel inhibitor BaCl(2) (50 microM) and in cultures containing low extracellular sodium concentration (3 mM). In vivo microdialysis performed in the nAc of awake and freely moving rats showed that local treatment with EtOH enhanced the concentrations of dopamine and taurine in the microdialysate, while glycine and beta-alanine levels were not significantly modulated. EtOH-induced dopamine release was antagonized by local treatment with the glycine receptor antagonist strychnine (20 microM) or furosemide (100 microM or 1 mM). Furosemide also prevented EtOH-induced taurine release in the nAc. In conclusion, our data suggest that extracellular concentrations of dopamine and taurine are interconnected and that swelling of astrocytes contributes to the acute rewarding sensation of EtOH.
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| 8. |
- Adermark, Louise, 1974, et al.
(författare)
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Intermittent ethanol consumption depresses endocannabinoid-signaling in the dorsolateral striatum of rat.
- 2011
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Ingår i: Neuropharmacology. - : Elsevier BV. - 1873-7064 .- 0028-3908. ; https://gup.ub.gu.se/publications/sho61:7, s. 1160-1165
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Tidskriftsartikel (refereegranskat)abstract
- Recent research suggests that adaptations elicited by drugs of abuse share common features with traditional learning models, and that drugs of abuse cause long-term changes in behavior by altering synaptic function and plasticity. In this study, endocannabinoid (eCB) signaling in the dorsolateral striatum, a brain region vital for habit formation, was evaluated in acutely isolated brain slices from ethanol (EtOH)-consuming rats and control rats. EtOH-consuming rats had free access to a 20% EtOH solution for three 24hour sessions a week during seven weeks and consumed an average of 3.4g/kg per session. eCB-mediated long-lasting disinhibition (DLL) of population spike (PS) amplitude induced by moderate frequency stimulation was impaired in EtOH-consuming rats, and was not restored by the muscarinic receptor antagonist scopolamine (10μM). The lack of DLL could be linked to a reduced GABA(A) receptor tone, since bicuculline-mediated disinhibition of striatal output was significantly reduced in slices from EtOH-consuming rats. However, eCB signaling induced by high frequency stimulation (HFS) was also impaired in slices from EtOH-consuming rats and isolated control rats. Activation of presynaptic cannabinoid 1 receptors (CB1R) with WIN55,212-2 (250nM, 1μM) significantly modulated PS amplitude in slices from age-matched control rats while slices from EtOH-consuming rats remained unaffected, indicating that eCB signaling is inhibited at a level that is downstream from CB1R activation. Intermittent alcohol intake for seven weeks might thus be sufficient to modulate a presynaptic mechanism that needs to be synergized with CB1R activation for induction of long-term depression (LTD). In conclusion, alcohol consumption inhibits striatal eCB signaling in a way that could be of importance for understanding the neurological underpinnings of addictive behavior.
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| 9. |
- Adermark, Louise, 1974, et al.
(författare)
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Region-specific depression of striatal activity in Wistar rat by modest ethanol consumption over a ten-month period
- 2013
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Ingår i: Alcohol. - : Elsevier BV. - 0741-8329. ; 47:4, s. 289-298
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Tidskriftsartikel (refereegranskat)abstract
- The nucleus accumbens (nAc) is the primary target for the mesolimbic dopamine system and a key brain region for the reinforcing effects displayed by drugs of abuse, including ethanol. During the. transition from recreational to compulsive consumption of reinforcing drugs, however, the dorsal striatum seems to be recruited. Understanding how synaptic activity is altered in a sub-region specific manner in the striatum during the course of long-term drug consumption thus could be essential for understanding the long-lasting changes produced by addictive substances, including ethanol. Here we evaluated synaptic activity in the dorsolateral striatum (DLS) and ventral Striatum (nucleus accumbens, nAc) of single-housed Wistar rats consuming water, or water and ethanol, for up to 10 months. Even though ethanol intake was moderate, it was sufficient to decrease input/output function in response to stimulation intensity in the DLS, while recorded population spike (PS) amplitudes in the nAc were unaffected. Striatal disinhibition induced by the GABA(A) receptor antagonist bicuculline had a slower onset in rats that had consumed ethanol for 2 months, and was significantly depressed in slices from rats that had Consumed ethanol for 4 months. Bicuculline-induced disinhibition in the nAc, on the other hand, was not significantly altered by long-term ethanol intake. Changes in PS amplitude induced by taurine or the glycine receptor antagonist strychnine were not significantly altered by ethanol in any brain region. Even though input/output function was not significantly affected by age, there was a significant decline in antagonist-induced disinhibition in brain slices from aged rats. The data presented here suggest that even modest consumption of ethanol is sufficient to alter neurotransmission in the striatum, while synaptic activity appears to be relatively well-preserved in the nAc during the course of long-term ethanol consumption. (C) 2013 Elsevier Inc. All rights reserved.
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| 10. |
- Adermark, Louise, 1974, et al.
(författare)
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Subregion-Specific Modulation of Excitatory Input and Dopaminergic Output in the Striatum by Tonically Activated Glycine and GABA(A) Receptors.
- 2011
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Ingår i: Frontiers in systems neuroscience. - : Frontiers Media SA. - 1662-5137. ; 5
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Tidskriftsartikel (refereegranskat)abstract
- The flow of cortical information through the basal ganglia is a complex spatiotemporal pattern of increased and decreased firing. The striatum is the biggest input nucleus to the basal ganglia and the aim of this study was to assess the role of inhibitory GABA(A) and glycine receptors in regulating synaptic activity in the dorsolateral striatum (DLS) and ventral striatum (nucleus accumbens, nAc). Local field potential recordings from coronal brain slices of juvenile and adult Wistar rats showed that GABA(A) receptors and strychnine-sensitive glycine receptors are tonically activated and inhibit excitatory input to the DLS and to the nAc. Strychnine-induced disinhibition of glutamatergic transmission was insensitive to the muscarinic receptor inhibitor scopolamine (10μM), inhibited by the nicotinic acetylcholine receptor antagonist mecamylamine (10μM) and blocked by GABA(A) receptor inhibitors, suggesting that tonically activated glycine receptors depress excitatory input to the striatum through modulation of cholinergic and GABAergic neurotransmission. As an end-product example of striatal GABAergic output in vivo we measured dopamine release in the DLS and nAc by microdialysis in the awake and freely moving rat. Reversed dialysis of bicuculline (50μM in perfusate) only increased extrasynaptic dopamine levels in the nAc, while strychnine administered locally (200μM in perfusate) decreased dopamine output by 60% in both the DLS and nAc. Our data suggest that GABA(A) and glycine receptors are tonically activated and modulate striatal transmission in a partially subregion-specific manner.
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