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Gas chromatographic analysis of coyote and magpie tissues for residues of compound 1080 (sodium fluoroacetate).

Tissues of coyotes and magpies administered known dosages of 1080 were analyzed for residues by an analytical method specifying gas chromatography and electron capture detection. The repeatability of the method was determined for the replicate analyses of coyote muscle tissue samples aged under different storage conditions. The average coefficient of variation (CV) was 6% for quadruplicate determinations of 1080 in fresh tissues, 12-14% for samples stored at - 10 degrees C for 30-60 days, and 24% for samples aged for 7 days at ambient temperatures. The larger CV value obtained for stored samples is attributed more to greater sample variability than to less precision of the analytical method. Residues of 1080 appear to be relatively stable in tissues; there was essentially no change in the concentration of 1080 in samples stored up to 28 days at ambient temperature. Residue levels in the muscle, heart, kidney, and intestine were comparable, slightly lower in the liver, and much higher in the stomach. The concentration of 1080 in the muscle tissue was related to the administered dosages. Correlation analyses of dosages and residue levels in coyote muscle tissue showed a correlation coefficient of 0.99 for 1080 administered by gavage, and 0.88 for 1080 administered by bait. A correlation coefficient of 0.99 was observed between dosages and mean residues in the breast muscle tissues of magpies. The average CV value was 3.5% for duplicate analyses of 1 g samples of magpie tissues.

Animals↗
PubMed1952

Effect of sodium monofluoroacetate on the multiplication of influenza viruses, mumps virus and pneumonia virus of mice (PVM).

Sodium fluoroacetate, given after virus inoculation in doses of 3 to 4 mg. per kg. in mice or 2 mg. in chick embryos, caused only a slight delay in the multiplication of the PR8 strain of influenza A virus in the mouse lung and of PR8 or the Lee strain of influenza B virus in the allantoic sac. The quantities of the compound used were sufficient to cause approximately 10 to 20 per cent mortality in mice and 100 per cent in chick embryos. The use of small virus inocula did not markedly increase the effect of sodium fluoroacetate on the multiplication of PR8 or Lee in the chick embryo and maximal titers were obtained in all cases. In contrast to the findings in the chick embryo, sodium fluoroacetate caused a definite delay in the multiplication of Lee virus in the mouse lung but did not affect the final virus titer. Sodium fluoroacetate in like amounts caused only a minimal delay in the multiplication of pneumonia virus of mice (PVM) in the mouse lung or of mumps virus in the chick embryo. With both PVM and mumps virus, maximal titers were obtained almost simultaneously in fluoroacetate and control animals. When three daily injections of the compound were given to mice infected previously with PVM, a definite diminution in the virus titer was demonstrable. However, pretreatment with three daily injections of the compound caused no alteration in the capacity of mice to support the multiplication of PVM. From the results of these experiments, it appears that the cellular metabolic processes blocked by sodium fluoroacetate are not essential for the multiplication of influenza viruses, mumps virus, or pneumonia virus of mice (PVM).

Animals↗
PubMed1998

Glial cells participate in histamine inactivation in vivo.

The ability of glial cells to take up histamine in vitro suggests that these cells may be involved in histamine inactivation. This prompted us to study the possible interactions between neuronal and glial processes which determine the histamine concentration in the synaptic cleft. In vitro experiments showed that the glial metabolic toxin, fluoroacetate (20 and 40 mmol/l) depressed histamine uptake into cultured astroglial cells and dissociated hypothalamic cells of rats. For in vivo experiments, the push-pull superfusion technique was used. In anaesthetized rat, the anterior hypothalamic area was superfused through the push-pull cannula with artificial cerebrospinal fluid (aCSF) or with aCSF which contained fluoroacetate and the release of endogenous histamine was determined in the superfusate. Hypothalamic superfusion with fluoroacetate (20 mmol/l) led to a pronounced increase in extracellular histamine. The effect of fluoroacetate was inhibited by 5 micromol/l tetrodotoxin. Superfusion with Ca++-free, Mg++-rich (12 mmol/l) aCSF inhibited the basal release rate of histamine. Under these conditions, 20 mmol/l fluoroacetate did not modify the level of the amine in the superfusate. These data demonstrate that depression of glial function enhances the concentration of histamine in the extracellular space by slowing down the uptake of the amine into the glial cells. Thus, under in vivo conditions, glial cells are directly involved in the continuous removal of neuronal histamine from the synaptic cleft.

Animals↗
PubMed2003

Blockade of astrocyte metabolism causes delayed excitation as revealed by voltage-sensitive dyes in mouse brainstem slices.

Fluoroacetate is known to block cell metabolism and to change potassium conductances selectively in astrocytes. In a functional neuronal network with ongoing activity, we investigated the effects of such a blockade of the astrocytic metabolism by fluoroacetate on neuronal signal propagation. Transverse 400- microm slices were prepared from the caudal medulla of mice of postnatal day 3-8, which contained the hypoglossal nucleus receiving excitatory synaptic input from the ventral respiratory group. Propagation of excitation within this network was measured by optical imaging using the voltage-sensitive dye RH 795. A 464-element photodiode array allowed fast recordings of voltage changes within a small population of cells. The spatial and temporal resolution was advanced to 32 microm and 1.27 ms, respectively. Changes of cellular membrane potential levels were expressed as relative changes of fluorescence (DeltaI/I). Stimulus-evoked excitation of neurons propagating from the ventral respiratory group to the hypoglossal nucleus peaked after 7.2+/-0.6 ms ( n=6). The latency of this early excitatory response is consistent with the time course of stimulus-evoked EPSPs in whole-cell recordings. Mean changes of fluorescence in the hypoglossal nucleus were -2.1+/-0.5 x 10(-3) (DeltaI/I). After incubation in 1 mM fluoroacetate, the early depolarization was reduced to 69.1+/-9.8% of control ( n=6, p=0.034). Additionally, fluoroacetate induced a delayed excitatory response, such that fluorescence intensity did not return to baseline within 1s. Propagation velocity and spatial distribution of the voltage signal were not affected by fluoroacetate. Our results suggest that blockade of astrocyte metabolism impairs fast synaptic transmission and induces a delayed excitation, probably resulting from the combination of reduced repolarization of neurons and persistent depolarization of astrocytes.

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