Dark neurons were produced in the cortex of the rat brain by hypoglycemic convulsions. In the somatodendritic domain of each affected neuron, the ultrastructural elements, except for disturbed mitochondria, were remarkably preserved during the acute stage, but the distances between them were reduced dramatically (ultrastructural compaction). Following a 1-min convulsion period, only a few neurons were involved and their environment appeared undamaged. In contrast, 1-h convulsions affected many neurons and caused swelling of astrocytic processes and neuronal dendrites (excitotoxic neuropil). A proportion of dark neurons recovered the normal structure in 2 days. The non-recovering dark neurons were removed from the brain cortex through two entirely different pathways. In the case of 1-h convulsions, their organelles swelled, then disintegrated and finally dispersed into the neuropil through large gaps in the plasma membrane (necrotic-like removal). Following a 1-min convulsion period, the non-recovering dark neurons fell apart into membrane-bound fragments that retained the compacted interior even after being engulfed by astrocytes or microglial cells (apoptotic-like removal). Consequently, in contrast to what is generally accepted, the dark neurons produced by 1-min hypoglycemic convulsions do not die as a consequence of necrosis. As regards the case of 1-h convulsions, it is assumed that a necrotic-like removal process is imposed, by an excitotoxic environment, on dark neurons that previously died through a non-necrotic pathway. Apoptotic neurons were produced in the hippocampal dentate gyrus by intraventricularly administered colchicine. After the biochemical processes had been completed and the chromatin condensation in the nucleus had reached an advanced phase, the ultrastructural elements in the somatodendritic cytoplasm of the affected cells became compacted. If present in an apparently undamaged environment such apoptotic neurons were removed from the dentate gyrus through the apoptotic sequence of morphological changes, whereas those present in an impaired environment were removed through a necrotic-like sequence of morphological changes. This suggests that the removal pathway may depend on the environment and not on the death pathway, as also assumed in the case of the dark neurons produced by hypoglycemic convulsions. 相似文献
The focus of treatment of faciocervical scar contractures includes cervical reconstruction and elimination of hypertrophic scars. Unfortunately, most previous studies have neglected the esthetic appearance of scars. In this study, we tried to combine surgical therapy and ultrapulse fractional CO2 laser (UFCL) to eliminate facial scars while restoring neck reconstruction and to establish the optimal conventional management for faciocervical contracture. Thirty-eight individuals were enrolled and divided into two groups. After received cervical release surgeries, comprehensive UFCL therapy group received treatment of UFCL at 3-month intervals, silicone sheets, and pressure garments, while another group only received treatment of silicone sheeting and compression. Twelve months after the termination of therapy, faciocervical scars of both two groups were assessed by two uninvolved physicians according to the Vancouver Scar Scale (VSS), and patients’ satisfaction survey was also recorded by the study participants using a patient four-point satisfaction scale. Thirty-six patients completed the treatment and follow-up. The results show that the VSS scores of both two groups decreased after 12 months, but comprehensive UFCL therapy group dropped more significantly than the conventional treatment group at follow-up session, which was statistically significant (P?<?0.001), and the patient satisfaction was higher than that of the conventional treatment group. This comprehensive treatment combined of surgery, UFCL, silicone sheets, and pressure garments works as an effective and esthetic reconstruction for moderate to severe postburn faciocervical scar contractures.
