Sequence comparisons indicated that the RELIK ancestor may have integrated into the rabbit lineage more than 7 million years ago. We have substantiated this by producing sequence data certifying the sharing of RELIK sequences among leporid lineages that diverged some 12 million years ago.”
“Breathing
is controlled by inspiratory pre-Botzinger complex (preBotC) networks that remain active in transversal brainstem slices from perinatal rodents. In 600 mu m thick preBotC slices, inspiratory-related bursting in physiological (3 mM) [K+] is depressed by <1 mM elevation of superfusate [Ca2+]. Here, we studied underlying cellular mechanisms in whole-cell-recorded neurons of 400 mu m thin newborn rat slices with the <200 mu m thin preBotC in
the middle (“”m-preBotC[400]“” slices). Extracellular activity in the ventrolateral slice area in 3 mM K+ and a most common physiological Ca2+ range (1-1.2 mM) stopped spontaneously within 2 h (“”in vitro apnea”"). Contrary, rhythm was stable for >3 h at 6-8 bursts/min in 7 mM K+ and 1.2 mM Ca2+ solution. In non-pacemaker preBotC inspiratory cells and neighboring inspiratory or tonically active neurons. block or frequency depression by >90% of rhythm in the latter solution by 2-3 mM Ca2+ changed neither resting potential nor input resistance. High Ca2+ silenced inspiratory neurons and depressed tonic discharge of non-respiratory neurons. However, in both cell types current injection evoked normal action potentials with unchanged threshold potential. The findings show that m-preBotC[400] slices represent a good
compromise between long term viability of rhythmogenic preBotC neurons and minimal modulation of these cells by adjacent tissue, but need to be studied in elevated K+. The lack of postsynaptic K+ channel-mediated hyperpolarization suggests that saturation of surface charges, presynaptic block of transmission and/or inhibition of postsynaptic burst-promoting conductances such as Ca2+ activated non-selective cation channels are involved in inspiratory depression by high Ca2+. (C) 2009 Elsevier Ireland Ltd. All rights reserved.”
“Caspase 3 staining in Schwann cells was investigated with immunohistochemistry, as a measure of Schwann cell apoptosis, after transection and immediate (day 0) or delayed rat sciatic nerve repair (30, 90 and 180 days post injury). Cleaved caspase 3 stained Schwann cells significantly increased at the site of lesion (SNL; median [IQR], 15.2 [7.0] %) and in the distal nerve segment (SND; 9.5 [3.6] %) 10 days after immediate repair. The number of cleaved caspase stained Schwann cells also increased significantly after delayed repair, irrespective of length of delay, at both locations (SNL: 22.0-27.1%; SND: 18.5-22.1%; p < 0.05).