Temperature effects on pathogenicity of selected Edwardsiella tarda strain to Japanese eel, Anguilla japonica

Temperature effect on the pathogenicity of selected Edwardsiella tarda V-1 strain to Japanese eel, Anguilla japonica was investigated. To evaluate the effects of both pathogen incubation temperature and fish cultivation temperature on pathogen pathogenicity a two-factor design was conducted. E. tarda was incubated at 15, 20, 25, 30 and 37±1°C, and the fish (mean weight: 100g) were reared at 15, 20, 25 and 28±1°C respectively. The fish reared at different temperatures were infected with the E. tarda incubated at different temperatures. The results of a 4-day LD50 test showed that temperature significantly affected the pathogenicity of E. tarda (p<0.01) and the interaction between the two factors was also significant (p<0.01). For fish reared at 20°C the pathogenicity of E. tarda was the highest at 30°C of pathogen incubation. When the fish rearing temperature was raised to 25 and 28°C, the pathogenicity of E. tarda incubated at all temperatures increased. Isolation testing demonstrated results similar to those of LD50. The selected isolate was virulent to eel, but pathogenicity varied with temperature.

Stress-facilitated LTD induces output plasticity through a synchronized-spikes and spontaneous unitary discharges the CA1 region of the hippocampus

Long-term potentiation (LTP) and long-term depression (LTD) of the excitatory synaptic inputs plasticity in the hippocampus is believed to underlie certain types of learning and memory. Especially, stressful experiences, well known to produce long-lasting strong memories of the event themselves, enable LTD by low frequency stimulation (LFS, 3 Hz) but block LTP induction by high frequency stimulation (HFS, 200 Hz). However, it is unknown whether stress-affected synaptic plasticity has an impact on the output plasticity. Thus, we have simultaneously studied the effects of stress on synaptic plasticity and neuronal output in the hippocampal CA1 region of anesthetized Wistar rats. Our results revealed that stress increased basal power spectrum of the evoked synchronized-spikes and enabled LTD induction by LFS. The induction of stress-facilitated LTD but not LFS induced persistent decreases of the power spectrum of the synchronized-spikes and the frequency of the spontaneous unitary discharges; However, HFS induced UP in non-stressed animals and increased the power spectrum of the synchronized-spikes, without affecting the frequency of the spontaneous unitary discharges, but HFS failed to induce UP in stressed animals without affecting the power spectrum of the synchronized-spikes and the frequency of the spontaneous unitary discharges. These observations that stress-facilitated LTD induces the output plasticity through the synchronized-spikes and spontaneous unitary discharges suggest that these types of stress-related plasticity may play significant roles in distribution, amplification and integration of encoded information to other brain structures under stressful conditions. (C) 2004 Elsevier Ireland Ltd and The Japan Neuroscience Society. All rights reserved.