Objective To study the effect of hyperbaric oxygen (HBO) on the proliferation and differentiation of neural stem cells (NSCs) in rats after middle cerebral artery occlusion (MCAO).Methods Seventy-two adult,male,Sprague-Dawley rats were randomly divided into a control (CON) group,a hyperbaric air (HBA) group,a normobaric oxygen (NBO) group and a hyperbaric oxygen (HBO) group.All were subjected to MCAO.Rats in the CON group did not receive any treatment; those in the other groups were treated with HBA,NBO or HBO daily beginning 2 hours after the operation.Western blotting was applied to detect the expression of nestin,MAP2 and GFAP at 2,3,7 and 14 days after the MCAO.Results The expression of nestin in the HBO group was significantly higher than in the other groups on the 3rd,7th and 14th days.It peaked at day 3 but remained high until day 14.Similarly,expression of MAP2 was significantly higher than in the other groups at least until day 14.GFAP expression was significantly lower than in the other groups.Conclusion HBO can increase neural stem cell proliferation and neuronal differentiation,and inhibit the proliferation of astrocytes.

Tweety-homolog 1 (Ttyh1) is expressed in neural tissue and has been implicated in the generation of several brain diseases. However, its functional significance in pain processing is not understood. By disrupting the gene encoding Ttyh1, we found a loss of Ttyh1 in nociceptors and their central terminals in Ttyh1-deficient mice, along with a reduction in nociceptor excitability and synaptic transmission at identified synapses between nociceptors and spinal neurons projecting to the periaqueductal grey (PAG) in the basal state. More importantly, the peripheral inflammation-evoked nociceptor hyperexcitability and spinal synaptic potentiation recorded in spinal-PAG projection neurons were compromised in Ttyh1-deficient mice. Analysis of the paired-pulse ratio and miniature excitatory postsynaptic currents indicated a role of presynaptic Ttyh1 from spinal nociceptor terminals in the regulation of neurotransmitter release. Interfering with Ttyh1 specifically in nociceptors produces a comparable pain relief. Thus, in this study we demonstrated that Ttyh1 is a critical determinant of acute nociception and pain sensitization caused by peripheral inflammation.