RESUMO
Post-traumatic stress disorder(PTSD) caused by various natural disasters and man-made events has gradually become the highlight of neuroscientists. Sleep disorders after PTSD can impair the effect of treatment and affect the patient's prognosis. In addition, treatment for sleep problems can be effective in improving outcomes for people with PTSD, which indicates that it is significant to pay attention to sleep disorders after PTSD. However, current studies have focused more on the incidence of PTSD and severity of related symptoms after a traumatic event, and less on the occurrence and mechanism of sleep disorders after PTSD. A number of articles on stress and sleep disorders published in recent years provide reliable clues to understand the probable mechanisms of sleep disorders after PTSD. After summarizing the latest research results, this article finds that the occurrence of sleep disorder after PTSD may be related to the changes of connectivity between insula, hippocampus and medial-prefrontal cortex. Apart from that, decline in the mean phase difference of slow spindles in PTSD patients may reflect pathological changes in the thalamic cortical circuit, which may contribute to the objective diagnosis of PTSD and the development of sleep-focused interventions. This paper provides a systematic review of changes in sleep characteristics and possible neural circuitry mechanisms after PTSD from clinical and basic perspectives, which may provide potential directions for future researches on the pathological mechanism of sleep disorders after PTSD and screening novel intervention targets.
RESUMO
Selective labeling of small populations of neurons of a given phenotype for conventional neuronal tracing is difficult because tracers can be taken up by all neurons at the injection site, resulting in nonspecific labeling of unrelated pathways. To overcome these problems, genetic approaches have been developed that introduce tracer proteins as transgenes under the control of cell-type-specific promoter elements for visualization of specific neuronal pathways. The aim of this study was to explore the use of tracer gene expression for neuroanatomical tracing to chart the complex interconnections of the central nervous system. Genetic tracing methods allow for expression of tracer molecules using cell-type-specific promoters to facilitate neuronal tracing. In this study, the rat tyrosine hydroxylase (TH) promoter and an adenoviral delivery system were used to express tracers specifically in dopaminergic and noradrenergic neurons. Region-specific expression of the transgenes was then analyzed. Initially, we characterized cell-type-specific expression of GFP or RFP in cultured cell lines. We then injected an adenovirus carrying the tracer transgene into several brain regions using a stereotaxic apparatus. Three days after injection, strong GFP expression was observed in the injected site of the brain. RFP and WGA were expressed in a cell-type-specific manner in the cerebellum, locus coeruleus, and ventral tegmental regions. Our results demonstrate that selective tracing of catecholaminergic neuronal circuits is possible in the rat brain using the TH promoter and adenoviral expression.