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  • 1
    Digitale Medien
    Digitale Medien
    Effects of Cold Exposure on Rat Adrenal Tyrosine Hydroxylase: An Analysis of RNA, Protein, Enzyme Activity, and Cofactor Levels (1990)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 54 (1990), S. 0 
    Details
    ISSN: 1471-4159
    Quelle: Blackwell Publishing Journal Backfiles 1879-2005
    Thema: Medizin
    Notizen: Abstract: Long-term cold exposure (5–7 days) is known to induce concomitant increases in the levels of adrenomedullary tyrosine hydroxylase (TH) RNA, protein, and enzyme activity. In this report, we compare the time courses of these changes and investigate the effects of cold exposure on the levels of biopterin, the cofactor required for tyrosine hydroxylation. After only 1 h of cold exposure, TH mRNA abundance increased 71% compared with nonstressed controls. Increases in total cellular TH RNA levels were maximal (threefold over control values) within 3–6 h of cold exposure and remained elevated throughout the duration of the experiment (72 h). TH protein levels increased rapidly after 24 h of cold exposure and reached a maximal value threefold above that of controls at 48–72 h. Despite the relatively rapid and large elevations in TH RNA and protein content, only modest increases in TH activity were detected during the initial 48 h of cold exposure. Adrenomedullary biopterin increased rapidly after the onset of cold exposure, rising to a level approximately twofold that of the nonstressed controls at 24 h, and remained at this level throughout the duration of the stress period. Taken together, the results of this time course study indicate that cold-induced alterations in adrenal TH activity are mediated by multiple cellular control mechanisms, which may include pre- and posttranslational regulation. Our findings also suggest that cold stress-induced increases in the levels of the TH cofactor may represent another key event in the sympathoadrenal system's response to cold stress.
    Materialart: Digitale Medien
    URL: http://dx.doi.org/10.1111/j.1471-4159.1990.tb01232.x
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  • 2
    Digitale Medien
    Digitale Medien
    Stimulation of Autoimmune Helper T Lymphocytes from Patients with Myasthenia Gravis with Synthetic Peptides of the Acetylcholine Receptor Alpha Subunit (1988)
    Oxford, UK : Blackwell Publishing Ltd
    Annals of the New York Academy of Sciences 540 (1988), S. 0 
    Details
    ISSN: 1749-6632
    Quelle: Blackwell Publishing Journal Backfiles 1879-2005
    Thema: Allgemeine Naturwissenschaft
    Materialart: Digitale Medien
    URL: http://dx.doi.org/10.1111/j.1749-6632.1988.tb27154.x
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  • 3
    Digitale Medien
    Digitale Medien
    The effect of chronic nicotine treatment on nicotine-induced seizures (1988)
    Springer
    Psychopharmacology 95 (1988), S. 52-55 
    Details
    ISSN: 1432-2072
    Schlagwort(e): Nicotine ; Tolerance ; Seizures ; Nicotinic receptors
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Medizin
    Notizen: Abstract Tolerance to nicotine occurs in mice after its chronic administration. This tolerance is accompanied by an up-regulation of nicotinic receptors as assessed by the binding of (3H)-nicotine and α-(125I)-bungarotoxin (BTX). Past studies (Marks et al. 1983, 1986) have shown that the increase in BTX binding sites is most evident in the hippocampus. Mice that have a greater concentration of BTX binding sites in the hippocampus are more sensitive to the convulsant effects of nicotine (Miner et al. 1984, 1985, 1986). In the study reported here, mice from the DBA/2Ibg strain, which are relatively resistant to nicotine-induced seizures and have a relatively low concentration of hippocampal BTX binding sites (Miner et al. 1984), were infused with nicotine for 10 days. At various time points after cessation of nicotine administration, sensitivity to the convulsant effects of nicotine was assessed. Mice were then sacrificed and BTX binding was determined in three regions: cortex, midbrain, and hippocampus. As expected, chronic treatment with nicotine resulted in a significant up-regulation of BTX binding sites in the hippocampus. Chronic nicotine treatment also produced significant tolerance to nicotine-induced seizures. Hippocampal BTX binding sites returned to control levels within 2 days after stopping nicotine infusion, whereas tolerance was not lost until 5 days. These results suggest that factors other than the number of hippocampal BTX binding sites affect nicotine-induced seizure sensitivity, at least following chronic nicotine treatment.
    Materialart: Digitale Medien
    URL: http://dx.doi.org/10.1007/BF00212766
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  • 4
    Digitale Medien
    Digitale Medien
    Aggression modulates genetic influences on morphine analgesia as assessed using a classical mendelian cross analysis (1993)
    Springer
    Psychopharmacology 111 (1993), S. 17-22 
    Details
    ISSN: 1432-2072
    Schlagwort(e): Analgesia ; Aggression ; Morphine ; Pharmacogenetics
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Medizin
    Notizen: Abstract Pharmacogenetic techniques allow for the examination of genetic and environmental factors underlying phenotypes associated with drug response. Initial studies of mice bred at Jackson Laboratories (JAX) indicated that C57BL/6J mice were more sensitive to morphine-induced analgesia, as measured by latency to paw lick, than SJL/J mice. A classical Mendelian cross breeding program was initiated in which F1, F2 and backcross generations were derived from C57BL/6J and SJL/J breeding pairs purchased from JAX to examine the genetic factors underlying morphine analgesia. Genetic analysis indicated significant dominance or heterosis for a reduced drug response. The F1 generation was less sensitive to morphine-induced analgesia than either parental strain. Mathematical analysis of the generation means revealed that a simple dominance model with no epistatic interaction between genes best described the data. Environmental factors also affected sensitivity to morphine analgesia, in that C57BL and SJL mice raised in our facility did not differ in latency to paw lick. SJL mice from JAX exhibit a high degree of aggression, while SJL mice raised in our facilities show little or no aggression. The levels of aggression among groups of SJL mice were characterized and found to correlate with sensitivity to morphine analgesia. Mice exposed to increasingly greater levels of aggression were the least sensitive to morphine. Thus, the changes observed in sensitivity to morphine-induced analgesia appear to be related to the degree of aggression to which these mice are exposed, possibly resulting from the stress and/or prolonged exposure to painful stimuli associated with aggressive encounters.
    Materialart: Digitale Medien
    URL: http://dx.doi.org/10.1007/BF02257401
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  • 5
    Digitale Medien
    Digitale Medien
    Chromosomal mapping of loci influencing sensitivity to cocaine-induced seizures in BXD recombinant inbred strains of mice (1995)
    Springer
    Psychopharmacology 117 (1995), S. 62-66 
    Details
    ISSN: 1432-2072
    Schlagwort(e): Cocaine ; Quantitative trait loci ; Seizure ; Recombinant inbred strains ; Genetics
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Medizin
    Notizen: Abstract Among inbred mice, genetic factors mediate differences in sensitivity to the convulsant properties of cocaine; however, the gene(s) underlying cocaine's effects have not been identified. To help elucidate the gene(s) responsible for cocaine seizure susceptibility, we used recombinant inbred-quantitative trait loci (RI-QTL) analyses to identify chromosomal loci associated with cocaine-induced seizures. RI-QTL analyses seek to identify associations between a quantitative measure of a particular phenotype and one or more previously mapped marker genes across a panel of RI strains. This report describes an RI-QTL analysis of cocaine seizure susceptibility among 26 BXD RI strains. These strains showed a skewed, bimodal range of seizure susceptibility which could be the result of one or more modifying genes acting in concert with a major gene to influence cocaine sensitivity. Correlating the percent seizures displayed by each strain following 60 mg/kg cocaine with chromosomal marker data for these strains revealed a number of significant correlations clustered in two regions on chromosomes 12 and 6. This is the first identification of putative chromosomal loci associated with a cocaine-related phenotype and should facilitate identification of the gene(s) underlying cocaine toxicity and other cocaine-related phenotypes.
    Materialart: Digitale Medien
    URL: http://dx.doi.org/10.1007/BF02245099
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  • 6
    Digitale Medien
    Digitale Medien
    Behavioral phenotypes of inbred mouse strains: implications and recommendations for molecular studies (1997)
    Springer
    Psychopharmacology 132 (1997), S. 107-124 
    Details
    ISSN: 1432-2072
    Schlagwort(e): Key words Mouse ; Inbred strains ; Behavior ; Genetics ; Locomotion ; Open field activity ; Learning ; Memory ; Aggression ; Parental behaviors ; Acoustic startle ; Prepulse inhibition ; Alcohol ; Nicotine ; Cocaine ; Opiates ; Haloperidol ; Diazepam ; Breeding ; Embryonic stem cell lines ; Transgenic ; Knockouts ; Null mutation
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Medizin
    Notizen: Abstract  Choosing the best genetic strains of mice for developing a new knockout or transgenic mouse requires extensive knowledge of the endogenous traits of inbred strains. Background genes from the parental strains may interact with the mutated gene, in a manner which could severely compromise the interpretation of the mutant phenotype. The present overview summarizes the literature on a wide variety of behavioral traits for the 129, C57BL/6, DBA/2, and many other inbred strains of mice. Strain distributions are described for open field activity, learning and memory tasks, aggression, sexual and parental behaviors, acoustic startle and prepulse inhibition, and the behavioral actions of ethanol, nicotine, cocaine, opiates, antipsychotics, and anxiolytics. Using the referenced information, molecular geneticists can choose optimal parental strains of mice, and perhaps develop new embryonic stem cell progenitors, for new knockouts and transgenics to investigate gene function, and to serve as animal models in the development of novel therapeutics for human genetic diseases.
    Materialart: Digitale Medien
    URL: http://dx.doi.org/10.1007/s002130050327
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  • 7
    Digitale Medien
    Digitale Medien
    Cold-induced increases in phenylethanolamine N-methyltransferase (PNMT) mRNA are mediated by non-cholinergic mechanisms in the rat adrenal gland (1993)
    Springer
    Neurochemical research 18 (1993), S. 759-766 
    Details
    ISSN: 1573-6903
    Schlagwort(e): Cold stress ; adrenal gland ; PNMT mRNA ; neural modulation ; cholinergic receptors ; chlorisondamine
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Medizin
    Notizen: Abstract Previously, we reported that cold stress induces a rapid increase in adrenomedullary PNMT mRNA levels, followed by concomitant increases in PNMT immunoreactivity (10). In the present study, the extracellular signals mediating this adaptive response to stress were investigated using northern analysis and RNA slot-blot hybridization. Although adrenal denervation significantly diminished cold-induced increments in adrenomedullary PNMT mRNA levels, it did not completely abolish the cold stress response. In contrast to these results, splanchnectomy completely inhibited cold-induced increments in TH mRNAs in the same tissue samples. These findings indicate that the effects of cold exposure on PNMT mRNA levels are mediated by both neural and non-neural mechanisms, and that adrenal PNMT and TH are differentially regulated in response to cold stress. Surprisingly, the neural component of the PNMT stress response could not be attenuated by peripheral administration of chlorisondamine, a powerful nicotinic ganglionic blocking agent. In contrast, chlorisondamine was effective in inhibiting sympathetic neural activity, as judged by the drug's ability to completely block increases in blood pressure, heart rate, and plasma catecholamines resulting from spinal cord stimulation in pithed rats. The administration of atropine, a muscarinic receptor antagonist, also failed to inhibit cold-induced alterations in adrenal PNMT mRNA. These results suggest that the trans-synaptic induction of adrenal PNMT mRNA involves a non-cholinergic component, and that cold-induced increases in PNMT mRNA are not coupled to acetylcholine-mediated adrenal catecholamine release.
    Materialart: Digitale Medien
    URL: http://dx.doi.org/10.1007/BF00966770
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