Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0040822 (tremor)
 18,428 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Nicotine levels in blood and whole brain were measured as a function of sex and age in C57BL/6J and DBA/2J mice and compared to the behavioral responses following an intraperitoneal injection of nicotine. The results indicate that blood levels of nicotine alone do not accurately predict either brain levels of nicotine or the behavioral responses to a single injection of nicotine. In general, brain levels of nicotine proved to be a fairly accurate predictor of the behavioral responses to nicotine. The data indicate that the sexes differ in their sensitivity to nicotine. Forty-two-day-old male mice of both strains given comparable doses of nicotine were found to concentrate the drug in the brain more than females. However, there was no corresponding increase in sensitivity to this increased brain concentration as measured by LD50, ED50, latency to tremor or latency to death.
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PMID:Relations between nicotine-induced convulsive behavior and blood and brain levels of nicotine as a function of sex and age in two inbred strains of mice. 45 Sep 47

During an experiment of shaking in El mice, a strain which was less susceptible to convulsion was found out. In this strain (ASK), the mortality to anaphylactic shock and susceptibility to audiogenic seizure were compared with five other strains of mice. Six strains of mice (ASK, EL, IDT, JCC-ICR, dd, C57BL/6J) were sensitized by two subcutaneous injections with 2 mg/head of crystalline egg albumin at five and six weeks of age, and then challenged by the intravenous injection of 0.125, 1, 8, 64, 512 and 4096 mug/head at seven weeks of age. In both sexes of ASK strain, the mortality was the maximum (75--95%) after the challenge of 8--4096 mug egg albumin. The mortality of the female El and IDT and the both sexes of JCL-ICR strains was middle (55--70%) after the challenge with 64 mug egg albumin, while that of other strains (dd and C57BL/6J) was very low (0--20%). The susceptibility of 3-weeks-old mice of ASK, El, IDT, JCL-ICR and dd strains was low (1.9--19.0%), whereas mice of DBA/2 strain showed a very high susceptibility (80%) to 110 phons.
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PMID:[A few characteristics of mouse having high sensibility to anaphylatic shock separated from El mouse (author's transl)]. 123 61

When given a two-bottle choice between gradually increasing morphine concentrations (in 0.2% saccharin) and plain tap water, C57BL/6J mice consumed almost 90% of their daily fluid intake from the morphine-saccharin bottle, while the DBA/2J strain, in contrast, consumed 13% or less from the morphine-saccharin solution. The C57BL/6J strain consistently consumed mean daily doses of morphine sulfate in excess of 200 mg/kg, which was sufficient to induce an easily discernable withdrawal syndrome upon removal of the morphine solution, either with or without naloxone challenge. Hypothermia, tremor, wet dog shakes, jumping, and diarrhea were prominent withdrawal signs. In separate experiments, the saccharin was removed from the morphine-containing bottle, yet the C57BL/6J mice continued to prefer the morphine solution over tap water. In complete contrast to the above, mice of the DBA/2J strain rejected the morphine-saccharin solution at the lowest concentration employed, and at no time did their mean daily morphine dose exceed 20 mg/kg. Thus, morphine-saccharin preference is strongly genetically determined, and a high degree of physical dependence can result in the morphine-preferring strain. Palatability differences appear not to be the predominant explanation for these differences in morphine-saccharin consumption.
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PMID:Physical dependence induced by the voluntary consumption of morphine in inbred mice. 232 Jun 38

Cas-Br-M is an ecotropic murine leukemia virus (MuLV) of wild-mouse origin that causes neurogenic hind-limb paralysis. By virtue of its N-tropism, the virus replicates well in tissues of mice bearing the n but not the b allele at the Fv-1 locus. To determine if different Fv-1n strains of mice were equally susceptible to virus-induced neurological disease, we inoculated NFS, C3H, DBA/2, CBA, AKR, C58, and NZB mice at birth with Cas-Br-M murine leukemia virus and observed them for the development of tremor and hind-limb paralysis. Three patterns of disease were observed: NFS and C3H mice developed disease within 3 months postinoculation; DBA/2 and CBA mice became affected between 8 and 15 months postinoculation; and no disease was observed in AKR, C58, or NZB mice up to 15 months after infection with Cas-Br-M murine leukemia virus. Studies of genetic crosses between intermediate-latency (DBA/2) or long-latency (AKR) strains with short-latency (NFS) strains showed that intermediate latency and long latency were semidominant traits determined by two or more interacting but independently assorting loci. These genes appear to determine the rate at which the virus replicates and at which viral gene products accumulate in the central nervous system.
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PMID:Host genetic determinants of neurological disease induced by Cas-Br-M murine leukemia virus. 298 60

The acute effects of diisopropylfluorophosphate (DFP) were assessed in DBA/2Ibg, C57BL/6Ibg and C3H/2Ibg mice. The DFP was administered by intraperitoneal injection in saline. Brain acetylcholinesterase (AChE) activity was maximally inhibited within 5 min after injection. All mice showed signs of organophosphate intoxication including salivation, lacrimation, diarrhea, respiratory distress, tremor and, at high doses, seizures. The C57BL mice were most susceptible to these effects of DFP. The LD50 values for DFP were 8.0, 7.6, and 6.8 mg/kg for male DBA, C3H, and C57BL mice, respectively. The LD50 values for females were nearly the same. Body temperature and brain AChE activity decreased in a dose-dependent manner following injections of DFP of 3.17, 4.22, 5.28, and 6.33 mg/kg. Maximum temperature depression occurred 2 hours after DFP administration; by 24 hours temperatures had returned to normal except for C57BL mice treated with the highest dose of DFP. The C57BL strain was most susceptible to the DFP-induced hypothermia, the C3H strain was the most resistant, and the DBA strain was intermediate. Maximum temperature depression and residual AChE activity, as measured 24 hours after injection, were linearly related. These strain differences do not seem to be explained easily by a differential inhibition of AChE activity.
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PMID:Genetically determined differences in acute responses to diisopropylfluorophosphate. 399 71

Vibrator (gene symbol vb), an autosomal recessive mutation, occurred spontaneously in the DBA/2J strain of mice, was rescued by a single cross to C57BL/6J and subsequent brother X sister mating, and has been mapped near shaker-2 (sh-2) and vestigial tail (vt) on chromosome 11. The name emphasizes the unusually rapid (18-20 Hz) postural action tremor expressed in juvenile homozygotes. Selected neurons in spinal cord, and later in brainstem and cerebellum, show progressive degenerative changes featuring dilated cisternae of endoplasmic reticulum in cell bodies, dendrites and axons, with eventual severe intracellular vacuolation and some cell death.
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PMID:Vibrator (vb): a spinocerebellar system degeneration with autosomal recessive inheritance in mice. 713 32

To elucidate the neurochemical mechanism of epilepsy, we investigated the role of neurotransmitter systems in the animal models of epilepsy, the mechanism of anticonvulsants and proconvulsants, the neurotransmitters in the CSF of children with epilepsy, and the new therapy for epilepsy. The main results are as follows. 1) In El mice, the increased activity of excitatory amino acids system in cortex and decreased activity of noradrenergic system in striatum and hippocampus were related to the increased seizure susceptibility. 2) GABA sensitivity was reduced in young DBA 2 J mice which are susceptible to audiogenic seizures. 3) Lower benzodiazepine receptor densities were found in hippocampus of 4 and 16 weeks-old tremor rats. GABA concentrations in the cerebral cortex and hippocampus of the tremor rats increased at 5 weeks-old and decreased at 15 weeks-old. These changes may be related to the absence-like seizures in tremor rats. 4) Anticonvulsant mechanism of ACTH may be due to antagonizing glutamate binding. Proconvulsant mechanism of thyroid hormone may be related to the decrease in number of cerebral cortical neuronal benzodiazepine receptors. Penicillin acts its proconvulsant effect through inhibiting GABA-gated chloride ion influx. 5) CSF GABA level in children with infantile spasms was lower than in controls. The combination of vitamin B6 and valproic acid is effective and safe therapy in the treatment of infantile spasms. Further investigations by the neurochemical approaches are necessary to understand the mechanisms of epilepsy and develop the new therapy.
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PMID:[Neurochemical approach to epilepsy]. 790 87

Our previous studies showed that the passage of the Friend virus complex through rats generated variant MuLVs, designated PVC111, PVC211, PVC321 and PVC441, that induced neurological disorders associated with tremor and paralysis. In this study, we tested the pathogenicity of four different PVC viruses in mice. Although histopathological studies revealed spongiform degeneration in the spinal cords of NFS mice infected with each PVC virus, only PVC441 frequently induced tremor and paralysis. After a long latency, all of these viruses induced leukemia associated with severe anemia. Further studies with PVC441 revealed dose- and age-dependence for tremor induction. In contrast to NFS mice, BALB/c, DBA/2 and C57BL/6 mice infected with PVC441 virus showed no neurological symptoms, although the virus could be isolated from the tissues of central nervous system. Despite the absence of neurological symptoms, a high degree of neuronal degeneration in the lumbar spinal cord was found in PVC441-infected BALB/c mice. A low degree of neuronal degeneration was found in PVC441-infected DBA/2 or C57BL/6 mice. Genetic crosses of these resistant mice with susceptible NFS mice indicated that resistance to tremor induction by PVC441 was dominant in all mouse strains and suggested that various host genes may control the susceptibility of mice to tremor induction by PVC441 virus.
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PMID:Factors affecting induction of neurological disorders in mice by paralysis-inducing Friend-related PVC viruses. 874 Dec 58

This study investigated the behavioural and anticonvulsant effects of voltage-sensitive calcium channel blockers in DBA/2 mice. Omega-Conotoxin MVIIC (0.1, 0.3 micrograms ICV/mouse) and omega-agatoxin IVA (0.1, 0.3, 1 micrograms ICV), which act predominantly at P- and/or Q-type calcium channels, prevented clonic and tonic sound-induced seizures in this animal model of reflex epilepsy (ED50 values with 95% confidence limits for protection against clonic sound-induced seizures were 0.09 (0.04-0.36) micrograms ICV and 0.09 (0.05-0.15) micrograms ICV respectively and against tonic seizures 0.07 (0.03-0.16) micrograms ICV and 0.08 (0.04-0.13) micrograms ICV, respectively). The N-type calcium channel antagonists omega-conotoxin GVIA and omega-conotoxin MVIIA were also tested in this model. Omega-Conotoxin GVIA was anticonvulsant in DBA/2 mice, but only at high doses (3 micrograms ICV prevented tonic seizures in 60% of the animals; 10 micrograms ICV prevented clonic seizures in 60% and tonic seizures in 90% of the animals), whereas omega-conotoxin MVIIA did not inhibit sound-induced seizures in doses up to 10 micrograms ICV. Both omega-conotoxin GVIA and omega-conotoxin MVIIA induced an intense shaking syndrome in doses as low as 0.1 microgram ICV, whereas omega-conotoxin MVIIC and omega-agatoxin IVA did not produce shaking at any of the doses examined. Finally, omega-conotoxin GI (0.01-1 microgram ICV) and alpha-conotoxin SI (0.3-30 micrograms ICV), which both act at acetylcholine nicotinic receptors, were not anticonvulsant and did not induce shaking in DBA/2 mice. These results confirm that blockers of N- and P-/Q-type calcium channels produce different behavioural responses in animals. The anticonvulsant effects of omega-conotoxin MVIIC and omega-agatoxin IVA in DBA/2 mice are consistent with reports that P- and/or Q-type calcium channel blockers inhibit the release of excitatory amino acids and are worthy of further exploration.
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PMID:Behavioural and anticonvulsant effects of Ca2+ channel toxins in DBA/2 mice. 885 21

PVC111, PVC211, PVC321 and PVC441 cause neurological disorders associated with tremor and paralysis in rats. We tested the pathogenicity of these viruses in mice. Although histopathological studies revealed spongiform degeneration in the spinal cords of NFS mice infected with each PVC virus, only PVC441 caused a high incidence of tremor and paralysis. Further studies with PVC441 revealed dose and age dependence for tremor induction. In contrast to NFS mice, BALB/c, DBA/2 and C57BL/6 mice infected with PVC441 virus showed no neurological symptoms, although the virus replicated in each strain to titers within 5-fold of the titer in NFS mice. Despite absence of neurological symptoms, high degree of neuronal degeneration in the lumbar spinal cord was found in PVC441-infected BALB/c mice. Low degree of neuronal degeneration was found in PVC441-infected DBA/2 or C57BL/6 mice. Genetic crosses of these resistant mice with susceptible NFS mice indicated that resistance to PVC441-induced tremor induction was dominant in all strains and suggested that various host genes may control the susceptibility of mice to tremor induction by PVC441 virus. Sequencing of env-LTR region of PVC441 revealed an intermediate character between PVC211 and F-MuLV.
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PMID:Factors affecting induction of neurological disorder in mice by PVC viruses and the sequence of env-LTR region of PVC441. 920 52


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