Mechanisms of firing patterns in fast-spiking cortical interneurons

Cortical fast-spiking (FS) interneurons display highly variable electrophysiological properties. Their spike responses to step currents occur almost immediately following the step onset or after a substantial delay, during which subthreshold oscillations are frequently observed. Their firing patterns include high-frequency tonic firing and rhythmic or irregular bursting (stuttering). What is the origin of this variability? In the present paper, we hypothesize that it emerges naturally if one assumes a continuous distribution of properties in a small set of active channels. To test this hypothesis, we construct a minimal, single-compartment conductance-based model of FS cells that includes transient Na(+), delayed-rectifier K(+), and slowly inactivating d-type K(+) conductances. The model is analyzed using nonlinear dynamical system theory. For small Na(+) window current, the neuron exhibits high-frequency tonic firing. At current threshold, the spike response is almost instantaneous for small d-current conductance, gd, and it is delayed for larger gd. As gd further increases, the neuron stutters. Noise substantially reduces the delay duration and induces subthreshold oscillations. In contrast, when the Na(+) window current is large, the neuron always fires tonically. Near threshold, the firing rates are low, and the delay to firing is only weakly sensitive to noise; subthreshold oscillations are not observed. We propose that the variability in the response of cortical FS neurons is a consequence of heterogeneities in their gd and in the strength of their Na(+) window current. We predict the existence of two types of firing patterns in FS neurons, differing in the sensitivity of the delay duration to noise, in the minimal firing rate of the tonic discharge, and in the existence of subthreshold oscillations. We report experimental results from intracellular recordings supporting this prediction.     

Severe hepatopathy in geese and broilers associated with ochratoxin in their feed

The feeding of a shipment of imported corn was associated with a severe reduction in growth and increased mortality in geese, and increased mortality in broilers. Pathological examinations revealed hepatopathy, visceral gout and mild nephropathy in geese, and in broilers an hepatopathy, which was often severe, and ascites. Samples of feed from affected geese farms were examined for up to 24 mycotoxins, and ochratoxin was found in 6 of 15 samples at levels up to 930 ng/g. The syndrome was experimentally reproduced by feeding geese and broilers suspect feeds with the natural ochratoxin contamination. It is believed that another, unidentified, mycotoxin was the major cause of the hepatotoxicity, and that ochratoxin served in this case as an indicator of a multi-mycotoxin involvement. This revised version was published online in June 2006 with corrections to the Cover Date.     

Aspergillus clavatus as the probable cause of a lethal mass neurotoxicosis in sheep

Sprouted barley grains, the waste product of malt extract production, were incriminated as the cause of a lethal (96% mortality) neurotoxic syndrome in sheep fed the grains. Clinical manifestations, comprising tremors, lameness, abnormal gait, paralysis and death indicated a tremorgenic mycotoxicosis. Whilst 50% of the flock died within 17 days, mortality continued over more than 5 months. Pathological findings were limited to neuronal degeneration and necrosis in the midbrain. Germinating grains were shown to be contaminated with growth of Aspergillus clavatus.     

Lethality of T-2 toxin,as applied by various methods,in adultAedes aegypti (Diptera: Culicidae) mosquitoes

The lethality of T-2 toxin to adult femaleAedes aegypti mosquitoes was investigated using various methods of application: Topically, by injection, and by natural feeding. The technique of topical application was found to be the most precise, whereby an LD₅₀ of 565 ng T-2 toxin/mosquito was determined.     

Fluoroacetamide (1081) oisoning in wild birds.

An outbreak of poisoning in four greylag geese (Anser anser) and 35-45 teal (Anas crecca) is described. Laboratory findings led to the conclusion that a wheat bait containing the rodenticide fluoracetamide (1081) caused the poisoning. Circumstantial evidence incriminated fluoracetamide as the cause of death in white-fronted geese (Anser albifrons), mallards (Anas platyrhynchos), and chukars (Alectoris chukar).