Aims:  To evaluate the cross‐protected Salmonella enterica cells under acid and cold stress conditions. Methods and Results:  The acid‐adapted S. enterica cells were exposed to pH 4·0 at 4 and 20°C. Recovery of sublethally injured cells was estimated by the difference between the counts obtained on trypticase soy agar (TSA) and xylose lysine desoxycholate (XLD) agar. The survival curves of nonadapted and acid‐adapted S. enterica cells at pH 4·0 were fitted with Weibull distribution model. The recovery behaviour of injured S. enterica cells was estimated by the modified Gompertz parameters. Acid‐adapted S. enterica were more resistant to subsequent acid shock than the nonadapted cells. The numbers of nonadapted S. enterica cells were decreased by 4·57 and 7·55 log CFU ml−1 at 4 and 20°C after 12‐day acid challenge, respectively. The acid adaptation induced cross‐protection and viable nonculturable (VBNC) state against low acid and cold stresses. The 7‐h adaptation showed the least recovery of injured cells. Conclusion:  The results suggest that acid‐adapted S. enterica cells induced acid tolerance response and VBNC state. Significance and Impact of the Study:  These results provide useful information for understanding the induction of cross‐protected and VBNC pathogens under various stresses, which might be needed in designing new food preservation strategies.

Somatostatin is found in the olfactory system, including the main olfactory bulb (MOB), and is thought to be one of the neuroactive substances for olfaction. However, somatostatin immunoreactivity in the olfactory system has not been determined during ageing. Hence, we examined the age-related changes of somatostatin-immunoreactive (IR) neurones in the rat MOB over a period of 2 years, at the following various ageing stages: post-natal month 1 (PM 1), PM 3, PM 6, PM 12 and PM 24. In PM 1 group, a few somatostatin-IR neurones were detected in the granule cell layer (GCL), and had slender or oval somata and short processes. At PM 3, somatostatin-IR neurones were observed in the glomerular, external plexiform and GCL. The size of somatostatin-IR somata was larger than that at PM 1. In PM 6 group, the number and size of somatostatin-IR neurones increased, and their processes became longer while running in various directions. At PM 12, somatostatin-IR neurones increased in number, and their processes became markedly longer than those at PM 6. At this stage, somatostatin-IR neurones had multipolar somata, and were the largest in size. In PM 24 group, somatostatin-IR neurones were most numerous. However, the processes of somatostatin-IR neurones were shorter than those at PM 12. This study suggests that the increased number of somatostatin-IR neurones in the MOB of aged rats may play a role to compensate for any decrease of olfactory function.

Calbindin D-28k (CB), a calcium-binding protein, containing neurons in the hippocampus plays an important role in hippocampal excitability in epilepsy. In the present study, we investigated changes of CB immunoreactivity after adrenalectomy (ADX) in the hippocampus and dentate gyrus of the seizure sensitive gerbil, which is susceptible to seizure to identify roles of CB in epileptogenesis. The changes of the CB immunoreactivity after ADX were significant in the hippocampal CA1 region. By 24 h after ADX, CB-immunoreactive CA1 pyramidal cells and CB immunoreactivity increased. At this time, well-stained dendrites projected to the stratum radiatum. Thereafter, the CB immunoreactivity decreased time dependently by 96 h after ADX. In the dentate gyrus, the changes of CB-immunoreactive neurons were mainly observed in the granule cell layer. The number and immunoreactivity of CB-immunoreactive neurons was high at 24 h after ADX, thereafter, those decreased by 96 h after ADX. These results suggest that glucocorticoid has an important role in modulating the seizure activity and CB serves an inhibitory function, which regulates the seizure activity and output signals from the hippocampus.

P2X receptors play a role in the transduction of sensory signals like pain. Few studies have been undertaken on altered P2X(3) receptor (P2X3) expression in sensory neurones after peripheral nerve injury. In the present study, we investigated chronological alterations in P2X3 immunoreactivity and its protein content in the trigeminal ganglion after ischaemic insult in the Mongolian gerbil. In the sham-operated group, P2X3-immunoreactive neurones were found abundantly in small- and medium-sized neurones. From 1 day after ischaemic insult, the number of P2X3-immunoreactive neurones decreased significantly. At 5 days after ischaemic insult, P2X3 immunoreactivity was observed in few neurones, but its immunoreactivity was weak. However, the number of cresyl violet-positive neurones was unchanged throughout this period in all groups. These results suggest that transient trigeminal ganglion ischaemia may provoke a decrease of P2X3 expression and its protein content, and that this down-regulation of P2X3 may be related to the altered pain and thermal sensation without being associated with a transient ischaemic insult.

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