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Inflammatory cells and their mediators are known to contribute to neuropathic pain following nerve injury. Mast cells play a key role in non-neural models of inflammation and we propose that mast cells and their mediators (in particular histamine) are important in the development of neuropathic pain. In rats, where the sciatic nerve was partially ligated, we showed that stabilisation of mast cells with sodium cromoglycate reduced the recruitment of neutrophils and monocytes to the injured nerve and suppressed the development of hyperalgesia. Treatment with histamine receptor antagonists suppressed the development of hyperalgesia following nerve injury and alleviated hyperalgesia once it was established. These results suggest that mast cell mediators such as histamine released within hours of nerve injury contribute to the recruitment of leukocytes and the development of hyperalgesia.

Summary Astrocytes are the most abundant glial cells in the central nervous system (CNS) and participate in synaptic, circuit, and behavioral functions. The well‐developed protoplasmic astrocytes contain numerous processes forming well‐delineated bushy territories that overlap by as little as 5% at their boundaries. This highly complex morphology, with up to approximately 80% of the cell's membrane constituted by fine processes with dimensions on the tens of nanometer scale and high surface area to volume ratios, comes in contact with synapses, blood vessels, and other glial cells. Recent progress is challenging the conventional view that astrocytes are morphologically homogeneous throughout the brain; instead, they display circuit‐ and region‐specific morphological diversity that may contribute to the heterogeneous astrocyte‐neuron spatiotemporal interplay in different brain areas. Further, the fine structure of astrocytes is found to be highly plastic and activity‐dependent. We are beginning to understand how astrocyte structural plasticity contributes to brain functions. The change/loss of astrocyte morphology, traditionally known as a hallmark for reactive astrogliosis, is a common pathological feature in many neurological disorders. However, recent data suggest the fine structural deficits preceding reactive astrogliosis may drive disease progression. This review summarizes recent advances in astrocyte morphological diversity, plasticity, and disease‐related deficits.

Similar to the original English version, the QoR-15C reveals satisfactory psychometric properties. Furthermore, it may be a more valid, reliable, and easy-to-use scale than the PQRS.

Aims: To determine the effect of choice of inhalational anaesthetic (sevoflurane vs propofol) on the incidence and severity of postoperative cognitive dysfunction (POCD) in elderly patients (aged ! 60 years) with mild cognitive impairment (MCI). Methods: Elderly patients with MCI undergoing radical rectal resection were randomly assigned to receive sevoflurane or propofol general anaesthesia. Cognitive function was assessed using neuropsychological testing before and 7 days after surgery. POCD severity was graded as mild, moderate or severe using standard deviation cut-offs. Results: At 7 days after surgery, the incidence of POCD was 29.7% in the propofol group (n ¼ 101) and 33.3% in the sevoflurane group (n ¼ 99). There was a signiEcant between-group difference for POCD severity: sevoflurane anaesthesia had a more severe impact on cognitive function than propofol anaesthesia. Conclusions: There was no difference in the incidence of POCD at 7 days after radical rectal resection under sevoflurane or propofol-based general anaesthesia. Both propofol and sevoflurane were associated with negative cognitive effects, but sevoflurane had a more severe impact on cognitive function than propofol, in elderly patients with MCI.