| 1. |
- Lundqvist, Thomas, et al.
(författare)
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Frontal lobe dysfunction in long-term cannabis users
- 2001
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Ingår i: Neurotoxicology and Teratology. - 0892-0362 .- 1872-9738. ; 23:5, s. 437-443
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Tidskriftsartikel (refereegranskat)abstract
- This study examined the neurophysiological effects of cannabis. Cerebral blood flow (CBF) was measured in 12 long-term cannabis users shortly after cessation of cannabis use (mean 1.6 days). The findings showed significantly lower mean hemispheric blood flow values and significantly lower frontal values in the cannabis subjects compared to normal controls. The results suggest that the functional level of the frontal lobes is affected by long-term cannabis use.
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| 8. |
- Niklasson, Magnus, et al.
(författare)
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Effects of toluene, styrene, trichloroethylene, and trichloroethane on the vestibulo- and opto-oculo motor system in rats
- 1993
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Ingår i: Neurotoxicology and Teratology. - 0892-0362 .- 1872-9738. ; 15:5, s. 327-334
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Tidskriftsartikel (refereegranskat)abstract
- The acute effects of inhalation of four solvents on the central vestibular system of rats were analyzed by recording eye movements upon different stimuli. The dose-response relationship was investigated. Optokinetic stimulation was obtained by placing the animals in front of a surrounding visual pattern, moving at different velocities. The slow-phase eye velocity (SPV) of nystagmus was calculated and divided by the stimulus velocity, giving the gain. All the solvents caused a decrease of the gain. Vestibular stimulation was performed on a turntable by an angular acceleration/deceleration in darkness. The SPV and the duration of the post-stimulatory nystagmus were calculated. The shape of the SPV dose-response curves differed among the four solvents. Toluene, styrene, and trichloroethylene prolonged the duration of nystagmus while trichloroethane did not. A conflicting vestibular and optokinetic stimulation was performed by an angular acceleration/deceleration with a surrounding visual pattern moving with the turntable. All solvents decreased the ability to cancel nystagmus, elicited by vestibular stimulation in conflict with a visual input. Quick movements of the eyes, saccades, were elicited by tactile stimulation. Toluene, styrene, and trichloroethylene changed the generation of the saccades while trichloroethane did not. Most of the findings indicate a common site of action in the central vestibular system, viz., the cerebellar-vestibular circuit. However, within this domain, there are evident differences in the effects among the solvents. This finding, together with previous results obtained in other experimental models of the central nervous system (CNS), suggest that different solvents should be considered as individual compounds. While the current results are consistent with the notion that solvents affect cerebellar-vestibular function, they also demonstrate differences on selected components of this system which may be of concern.
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| 9. |
- Tham, Richard, et al.
(författare)
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The effect of toluene on the vestibulo- and opto-oculomotor system in rats, pretreated with GABAergic drugs
- 1990
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Ingår i: Neurotoxicology and Teratology. - : Elsevier. - 0892-0362 .- 1872-9738. ; 12:4, s. 307-311
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Tidskriftsartikel (refereegranskat)abstract
- Toluene, an aromatic solvent, prolongs the duration of nystagmus induced by a rotatory acceleration or by an optokinetic stimulation in the pigmented rat. Baclofen, an agonist of GABAB receptors, and 4,5,6,7-tetrahydroisoxazolo[5,4-c]-pyridin-3-ol (THIP), an agonist of GABAA receptors are able to block this toluene effect on the vestibular system. On the contrary diazepam, which by itself causes an evident reduction of the duration of acceleratory nystagmus, is not able to block the toluene effect. The results indicate that the toluene effect is related to GABA transmission and that the solvent interacts by a rather receptor specific mechanism of action.
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| 11. |
- Carpenter, Jessica M., et al.
(författare)
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Delayed treatment with the immunotherapeutic LNFPIII ameliorates multiple neurological deficits in a pesticide-nerve agent prophylactic mouse model of Gulf War Illness
- 2021
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Ingår i: Neurotoxicology and Teratology. - : Elsevier. - 0892-0362 .- 1872-9738. ; 87
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Tidskriftsartikel (refereegranskat)abstract
- Residual effects of the 1990-1991 Gulf War (GW) still plague veterans 30 years later as Gulf War Illness (GWI). Thought to stem mostly from deployment-related chemical overexposures, GWI is a disease with multiple neurological symptoms with likely immunological underpinnings. Currently, GWI remains untreatable, and the long-term neurological disease manifestation is not characterized fully. The present study sought to expand and evaluate the long-term implications of prior GW chemicals exposure on neurological function 6-8 months post GWI-like symptomatology induction. Additionally, the beneficial effects of delayed treatment with the glycan immunotherapeutic lacto-Nfucopentaose III (LNFPIII) were evaluated. Male C57BL/6J mice underwent a 10-day combinational exposure (i.p.) to GW chemicals, the nerve agent prophylactic pyridostigmine bromide (PB) and the insecticide permethrin (PM; 0.7 and 200 mg/kg, respectively). Beginning 4 months after PB/PM exposure, a subset of the mice were treated twice a week until study completion with LNFPIII. Evaluation of cognition/memory, motor function, and mood was performed beginning 1 month after LNFPIII treatment initiation. Prior exposure to PB/PM produced multiple locomotor, neuromuscular, and sensorimotor deficits across several motor tests. Subtle anxiety-like behavior was also present in PB/PM mice in mood tests. Further, PB/PM-exposed mice learned at a slower rate, mostly during early phases of the learning and memory tests employed. LNFPIII treatment restored or improved many of these behaviors, particularly in motor and cognition/memory domains. Electrophysiology data collected from hippocampal slices 8 months post PB/PM exposure revealed modest aberrations in basal synaptic transmission and long-term potentiation in the dorsal or ventral hippocampus that were improved by LNFPIII treatment. Immunohistochemical analysis of tyrosine hydroxylase (TH), a dopaminergic marker, did not detect major PB/PM effects along the nigrostriatal pathway, but LNFPIII increased striatal TH. Additionally, neuroinflammatory cells were increased in PB/PM mice, an effect reduced by LNFPIII. Collectively, long-term neurobehavioral and neurobiological dysfunction associated with prior PB/PM exposure was characterized; delayed LNFPIII treatment provided multiple behavioral and biological beneficial effects in the context of GWI, highlighting its potential as a GWI therapeutic.
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| 14. |
- Dow-Edwards, DL, et al.
(författare)
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Neuroimaging of prenatal drug exposure
- 2006
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Ingår i: Neurotoxicology and teratology. - : Elsevier BV. - 0892-0362. ; 28:3, s. 386-402
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Forskningsöversikt (övrigt vetenskapligt/konstnärligt)
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| 15. |
- Eriksson, Per, 1951-, et al.
(författare)
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Perfluorinated chemicals (PFOA) can, by interacting with highly brominated diphenyl ethers (PBDE 209) during a defined period of neonatal brain development, exacerbate neurobehavioural defects
- 2023
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Ingår i: Neurotoxicology and Teratology. - : Elsevier. - 0892-0362 .- 1872-9738. ; 96
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Tidskriftsartikel (refereegranskat)abstract
- Perfluorinated compounds (PFCs) and polybrominated diphenyl ethers (PBDEs) are ubiquitous persistent environmental compounds, present in humans and at higher levels in infants/children than in adults. This study shows that co-exposure to pentadecafluorooctanoic acid (PFOA) and 2,2 ',3,3 ',4,4 ',5,5 ',6,6'-decaBDE (PBDE 209) can significantly exacerbate developmental neurobehavioural defects. Neonatal male NMRI mice, 3 and 10 days old, were exposed perorally to PBDE 209 (1.4 or 8.0 mu mol/kg bw), PFOA (1.4 or 14 mu mol/kg bw), co-exposed to PBDE 209 and PFOA (at the given doses), or a vehicle (20% fat emulsion) and observed for spontaneous behaviour in a novel home environment when 2 and 4 months old. The behavioural defects observed included hyperactivity and reduced habituation indicating cognitive defects. This interaction appears most likely dependent on the presence of PBDE 209 and/or its metabolites together with PFOA, during a defined critical period of neonatal brain development, corresponding to the perinatal and newborn period in humans.
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| 16. |
- Galofré, Mireia, et al.
(författare)
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GABA(A) receptor and cell membrane potential as functional endpoints in cultured neurons to evaluate chemicals for human acute toxicity
- 2010
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Ingår i: Neurotoxicology and Teratology. - : Elsevier BV. - 0892-0362 .- 1872-9738. ; 32, s. 52-61
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Tidskriftsartikel (refereegranskat)abstract
- Toxicity risk assessment for chemical-induced human health hazards relies mainly on data obtained from animal experimentation, human studies and epidemiology. In vitro testing for acute toxicity based on cytotoxicity assays predicts 70 - 80% of rodent and human toxicity. The nervous system is particularly vulnerable to chemical exposure which may result in different toxicity features. Acute human toxicity related to adverse neuronal function is usually a result of over-excitation or depression of the nervous system. The major molecular and cellular mechanisms involved in such reactions include GABAergic, glutamatergic and cholinergic neurotransmission, regulation of cell and mitochondrial membrane potential, and those critical for maintaining central nervous system functionality, such as controlling cell energy. In this work, a set of chemicals that are used in pharmacy, industry, biocide treatments or are often abused by drug users are tested for their effects on GABA(A) receptor activity, GABA and glutamate transport, cell membrane potential and cell viability in primary neuronal cultures. GABA(A) receptor function was inhibited by compounds for which seizures have been observed after severe human poisoning. Commonly abused drugs inhibit GABA uptake but not glutamate uptake. Most neurotoxins altered membrane potential. The GABA(A) receptor, GABA uptake and cell membrane potential assays were those that identified the highest number of chemicals as toxic at low concentrations. These results show that in vitro cell assays may identify compounds that produce acute neurotoxicity in humans, provided that in vitro models expressing neuronal targets relevant for acute neural dysfunctions are used.
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| 17. |
- Gui, Chuan-Zhi, et al.
(författare)
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Changes of learning and memory ability and brain nicotinic receptors of rat offspring with coal burning fluorosis
- 2010
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Ingår i: Neurotoxicology and Teratology. - : Elsevier BV. - 0892-0362 .- 1872-9738. ; 32:5, s. 536-541
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Tidskriftsartikel (refereegranskat)abstract
- The purpose of the investigation is to reveal the mechanism of the decreased ability of learning and memory induced by coal burning fluorosis. Ten offspring SD rats aged 30 days, who were born from the mothers with chronic coal burning fluorosis, and ten offspring with same age from the normal mothers as controls were selected. Spatial learning and memory of the rats were evaluated by Morris Water Maze test. Cholinesterase activity was detected by photometric method. The expressions of nicotinic acetylcholine receptors (nAChRs) at protein and mRNA levels were detected by Western blotting and Real-time PCR, respectively. The results showed that in the rat offspring exposed to higher fluoride as compared to controls, the learning and memory ability declined; the cholinesterase activities in the brains were inhibited; the protein levels of alpha 3, alpha 4 and alpha 7 nAChR subunits were decreased which showed certain significant correlations with the declined learning and memory ability: and the mRNA levels of alpha 3 and alpha 4 nAChRs were decreased, whereas the alpha 7 mRNA increased. The data indicated that coal burning fluorosis can induce the decreased ability of learning and memory of rat offspring, in which the mechanism might be connected to the changed nAChRs and cholinesterase.
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| 22. |
- Hougaard, K. S., et al.
(författare)
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No evidence for enhanced noise induced hearing loss after prenatal stress or dexamethasone
- 2007
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Ingår i: Neurotoxicol Teratol. - : Elsevier BV. - 0892-0362. ; 29:6, s. 613-21
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Tidskriftsartikel (refereegranskat)abstract
- It was recently implied that prenatal stress and fetal exposure to glucocorticoids may interfere with hearing ability and noise induced hearing loss in adulthood. In the present study pregnant Wistar rats were stressed during gestation by Chronic Mild Stress (CMS, a variable schedule of different stressors) or by dexamethasone (a synthetic glucocorticoid, i.e. a pharmacological stressor). At birth, but not at weaning, the dexamethasone offspring exhibited significantly decreased body weight compared to both control offspring and progeny from dams exposed to CMS during pregnancy. As adults, male offspring were exposed to 105 dB sound pressure level (SPL) wide band noise either continuously for eight hours or for two hours per day on three consecutive days. Oto-acoustic emissions and auditory brainstem responses were recorded before and after exposure to noise. Neither prenatal chronic stress nor prenatal dexamethasone exposure was associated with significantly enhanced noise induced hearing loss compared to controls, and these results were consistent in both subsets of animals. Our data do not support previous reports that prenatal exposure to mild stress nor to dexamethasone is detrimental to the hearing organ per se. However, hearing may be modulated by prenatal stressors under certain circumstances, of which the timing and degree are probably the most important.
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| 29. |
- Wastensson, Gunilla, 1956, et al.
(författare)
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Quantitative tremor assessment in workers with current low exposure to mercury vapor.
- 2006
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Ingår i: Neurotoxicology and Teratology. - : Elsevier BV. - 0892-0362. ; 28:6, s. 681-93
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Tidskriftsartikel (refereegranskat)abstract
- Measurement of tremor has been used in several occupational studies of workers with long-term exposure to mercury vapor (Hg(0)). Recent studies indicate an adverse effect even at relatively low exposure levels. In the present study, we used sensitive quantitative methods to assess tremor in chloralkali workers with current low exposure to Hg(0). Neurological examinations and recordings of tremor using both an accelerometer and a laser-based system were conducted in 43 mercury-exposed workers and 22 age-matched referents. The median urinary mercury concentration in exposed workers was 5.9 (1.3-25) microg/g creatinine (microg/gC), while it was 0.7 (0.2-4.1) microg/gC in referents. The mean exposure time was 15 years, and the median cumulative mercury index was 161 years x microg/gC in exposed workers. There were no differences between the exposed workers and the referents in the clinical evaluation of tremor. In the quantitative tremor tests, no associations were found with current or cumulative mercury exposure for the majority of tremor measures. There were indications that exposure to Hg(0) was associated with a lowering of tremor frequency in the non-dominant hand, and a possible interaction with smoking. The differences were small, however, and overall, this study indicates no significant adverse effects on tremor at these exposure levels.
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