Sigma receptor type 1 knockout mice show a mild deficit in plasticity but no significant change in synaptic transmission in the CA1 region of the hippocampus.

The sigma-1 receptor (σ-1R) is a chaperone protein located at the endoplasmic reticulum (ER) mitochondrial interface with roles in neuroprotection and cognition. Increasing evidence suggests that loss of σ-1R function could contribute to neurological disease states making it a target for therapeutic intervention. Our objective was to elucidate the consequences to synaptic transmission and plasticity when σ-1R is absent. We utilized a knockout mouse in which the gene encoding for σ-1R was deleted (σ-1R-KO mouse). Using whole-cell patch-clamp recordings from CA1 pyramidal neurons in the hippocampus, we examined neuronal excitability and glutamatergic synaptic function. Surprisingly, we detected no significant change in action potential firing and basic cellular characteristics. Furthermore, we found no significant change to pre-synaptic function as indicated by a similar paired-pulse ratio and miniature excitatory post-synaptic current frequency in σ-1R-KO compared to wild-type (WT) mice. Similarly, the glutamate gated AMPA receptor and NMDA receptors were unaffected with no significant difference in AMPA/NMDA ratio or decay kinetics in σ-1R-KO compared to WT mice. We further examined long-term potentiation in extracellular field recordings in CA1 stratum radiatum following Schaffer collateral stimulation. Interestingly, we found a small but significant reduction in the magnitude of long-term potentiation in mutant compared to WT mice. The results of this investigation suggest that basic cellular physiology is unaffected by σ-1R loss, however the neuronal network is partially compromised. The sigma-1 receptor (σ-1R) is a chaperone protein with roles in neuroprotection and cognition. We determined the consequences to synaptic transmission and plasticity when σ-1R was absent. Utilizing the σ-1R knockout mouse and electrophysiological recordings, we found no change in neuronal excitability and glutamatergic synaptic function. However, we found a significant reduction in long-term potentiation.

The New Zealand national junior doctors' strike: implications for the provision of acute hospital medical services.

The New Zealand junior doctors' strike provided an opportunity to consider strategies that might be employed to overcome the international shortage of junior doctors. This article reports the experience of the emergency department (ED) and internal medicine (IM) services at Wellington Hospital during the national strike, in which medical services were primarily provided by specialist consultants in addition to, or as part of, their routine work. During the strike, elective admissions and outpatient clinics were mostly cancelled. In the ED, the waiting times and length of stay were markedly reduced. In IM, the proportion of patients admitted to the short stay unit rather than the general medical wards increased. Notwithstanding the different work circumstances, in both services one senior doctor carried the workload of at least two junior doctors. The deployment of additional senior medical staff to acute hospital services could greatly reduce the total number of doctors required. This strategy would have implications in terms of supporting acute medicine specialty initiatives, training, quality of care and funding.